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HMB202 midterm notes- lectures 2-5.docx

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Department
Human Biology
Course
HMB202H1
Professor
Rajni Lala
Semester
Winter

Description
HMB202- LEC 2 MICROORGANISMS • Microscopic, unicellular organisms • Includes: bacteria, archaea, unicellular eukaryotes (algi, fungi, protists), viruses (non-living) • Archaea and eukaryotes are more related. Eukaryotes: uni and multicellular organisms. Bacteria nad archaea are prokaryotes – all unicellular microbes IMPORTANCE OF MICROOGRANISMS: o Important for function of biosphere; they make the biosphere • The oldest form of life 30 • Large mass of living material on earth (5x10 cells) • Form microbial communities – communicate with eachother and change behavious to adjust to communites • Other forms require microbes to survive • Can live in places unsuitable for other organism-> in extreme environments: polyextremophiles o Live in hotsprings: temp >100°C, deep under the artic ice, hydrothermal vents, Mariana’s Trench -> can tolerate high pressure • Deinococcus radiodurans: worls’toughest bacterium – withstand extremes cold, dehydration, vacuum conditions, acidic, radioactivite environments PLAY IMPORTANT ROLES IN : • Agriculture: o Nitrogen-fixing bacteria in plant roots o Cellulose-degrading microbes in the herbivore’s rumen  Ex) grass has cellulose in cell wallsthat must be degraded in fermenting chambers. Humans cannot digust grass for this reason o Regeneration of nutrients in soil (decomposition) and water. Degradation of organic matter to make nutrients available to soil • Industry: o Microbial transformations, like fermentation – cheese, yogurt, pickles, beer, bread, wine o Biofuels production= natural gas (methane, ethano, hydrogen) o Cleaning up pollutants=bioremediation (toxic metals, raditation) – extraction of metal from their ores using living organisms – cleaner!  Oil spills, pesticides, toxic stuff, bioleaching • Medicine: o Models for understanding basic life processes- and human diseases o The production of antibiotics, enzymes, and various chemicals o Biotechnology= genetic engineering of microbes to generate products (insulin) – proced by yeast or bacteria through recombinant DNA o Probiotic Bacteria from yogurt good for brain function  Resting brain activity and more intense activites or emotional states are changed after consumptions os yogurt  Future dietary or drug interventions that can improve brain activity – change depression with yogurt NON-BENEFICIAL ROLES • Food spoilage- negative for human health, financial burden for food industry • Diseases in plants, animals, and humans 1 o Bacteria- most deadly diseases and widespread pidemics o Smallpox and malaria, TB, diarrhea =(non-bacterial microbes)- killed the most humans in the last century BACTERIA: prokaryotic • Unicellular. Multiply by binary fission- asexual reproduction CHARACTERITICS OF LIVING SYSTEMS: • Composed of cell(s)- fundamental unit of life • Reproduction: generation of 2 cells from one • Growth and development • Obtain and use energy (metabolism) • Respond to their environment (communication) – also with other organsims BINARY FISSIONAND GROWTH • Binary Fission= cell divison following enlargement of cell to twice it’s minimum size o Each daughter cell receives a chromosomes and sufficient copies of other cell cosnttuent to exist as an independent cell o Faster division because less work. Don’t need mitosis/meiosis, No need to build spindle or degradation of the nuclear envelope o Each daughter can repeat the process. Rapidly increase in numbers o One generation: cell elongation septum formation completion of sputum formation of walls; cell separation  Rod shaped bacteria havevery fast stages like round bacteria o Replicate DNAand attach to one side of membrane, cell elongates and seperates. Form a Sectum – separating 2 sections of a bacteria. 2 fully mature daughter cells that can continue the binary fission process • Bacterial growth = increasing the number of cells in a culture – not the size o Can form biofilms o Advantage for bacteria – can associate with biofilms ( bacterial cells and polysaccharides) that protects it from various drugs o Grows exponentially DIFFERENTIATION OF BACTERIALSPECIES • Morphology, hemical composition, nutritional requirements, biochemical activites, source of energy SIZE OF BACTERIAL CELLS • Most are: 0.20 -2.0 um in diameter = round • 2-8 um in length = Bacilli or rod • Life not possible in very small bacteria – need certain structure • Small size of bacteria allows it to invade human cells= 10X bigger • Signifcance of smallness: have more SArelative to cell volume than larger cells ( higher SA/V) o Greater nutrient exchange per unit cell volume o Tend to grow faster than larger cells o Same amount of resources support larger population of small cells SHAPE OF BACTERIAL CELLS • 3 basic cell shapes/morphologies: o coccus (cocci)  spheres o bacillus (bacilli)  rods 2 o spirillum (spirilla)  spiral/twisted rods  good for swimming motility • other cell morphologies: many variations on basic morphological types: o spirochetes – much longer and twisted spirilla. Motility o budding & appendadged bacteria - stalkes – help attach to substrate. Can have buds on one side. Stalks can be very long o filamentous bacteria – good for gliding motility.  Groups of filaments become really long. o pleomorphic – Can change shape according to environment  ex) heliobacterpilori found in human stomach ARRANGMENT OF BACTERIAL CELLS INTO GROUPS: • new properties different from single cell • Often encapsulated to resist drugs • Diplo – paired bacteria. Ex) diplococcic, diplobacilli • Strepto – really longe chains. Ex) streptococci: strept throat; streptobacilli • Sarcinae can for tetrad squares = cubes • Staphylococci – round spheres can divide in all places to ……….structures? • Palisade: rods that arrange self in fence like structures. • V-shaped CELL MORPHOLOGY: • Doesn’t typically predict physiology, ecology, phylogeny of bacteria • Selective forces may be involved in setting the morphology o Optimization for nutrient uptake (small cells and those with high SA/V ratio) o Swimming motility in viscous environment or near surfaces (helical or spiral-shaped cells) o Gliding motility (filamentous bacteria) – faster • Staphyloccus aureus – on skin and body. Usually beneficial, but can be bad in situations. grape- like structure (staphyloccus) • Bacillus anthtracis – rod like, but can form spores to change – short generation time. Grows fast. o streptobacillus o Depending on entry to body can do different damage  Through skin = black nicotic skin legions  Through lungs/ GI tracts = death • Camplyobacter jejuni – causes gastroenteritis (food-poisoning) o Spirilla shape helps swimming motility – move faster in medium o Prevented by cooking meat well o Found mostle in animal feces o More food poisoning cases than salmonella • Helicobacter pylori – rod shaped, but pleomorphic – can change shape to form caucus (spheres) or bacilli (round) – high morphological diversity o Found in stomach and destroys lining – leads to cancer o Hard to destroy because pleomorphic and in stomach forms biofilm o Studies show probiotics (yogurts) improves rate of it’s eradication in humans STRUCTURE OF BACTERIAL CELL 3 • Free chromosome in cytoplasm. Ribosomes in cytoplasm • Flagellum =motility; • Cell membrane – contacts cytoplasm. Cell wall. Have different proteins in different bacteria • Then gelatin-like capsule – capsule or slime layers CYTOPLASMIC MEMBRANE IN BACTERIA • Thin structure that surrounds the cell. 6-8 nm thick, somewhat fluid- not liquid • Vital barrier that seperates the cytoplasm from the environment • Highly selective and permeable barrier; enable concentration of specific metabolites and excretion of waste products – the layer is stabilized by hydrophobic interactions • Filter substances entering the cell – different composition, but similar functions • Composition of membranes: o General structure – phospholipid bilayer o Both hydrophobic and hydrophilic components – negative P head o FApoint inward to hydrophobic environment. Hydrophilic stuff point outward – FA blocks enterance of polar molecules o Have transmembrane proteins – stabilize the fluidity. Some act as receptors or channels • Membrane permeability – selective. Free diffusion of gas… MAJOR FUNCTIONS OF THE CYTOPLASMIC MEMBRANE 1. Permeability barrier – prevents leakage and functions as gateway for transports of nutrients in and out of cell 2. Protein anchor – site of many proteins involved in transport, bioenergetics and chemotaxis –on outside or inside 3. energy conservation – generation and use of proton motive force – negative on inside, positive on outside o OH- and H+ equally distributed to create proton forces o Transport across membrane is essential for bacteria!!! TRANSPORTAND TRANSPORT SYSTEMS • Simple diffusion – very slow • Carrier mediated transport systems – much faster (Assisted transport). Slows when carrier proteins become saturated. • Active transport is highly selective • 3 major classes in bacteria!All require energy fromATP or proton motive force: o simple transport – driven by energy in the proton motive force o group translocation – hemical modification of transported substance driven by phosphoenolpyruvate o ABC transporter – periplasmic binding proteins bind s pecific molecules and transport through TM proteins. Energy comes fromATP  High concentration of solutes increases the osmotic pressure inside the cell- bacterial nuclear envelope must be able to support this high pressure and prevent cell from bursting BACTERIAL CELLWALL- keeps cell from burstin • Semi-rigid structure permeable, gives cell its shape • Protects cell from rupture due to osmotic pressure – cell pressure =2atm • Composed of peptidoglycan (PG): teichoic acids • Peptide composition and thickness varies among species 4 • Based on cell wall composition the cell is gram positive or negative • THE CELLWALL OF BACTERIA: PEPTIDIDOGLYCAN o Rigid layer provides strength to cell wall o Polysaccharide composed of repeating of n-acetylglucosamine (NAG) and n- acetylmuramic acid (NAM) linked but peptide bridges o Amino acids o lysine or diaminopimelic acid (DAP) – anAAanallog o these all form a tetrapeptidethat repeats many times in the PG (peptidoglycan) layers. – formd long chains linked to each other to form sheets on the cell wall o cross-linked differently gram- and gram+ bacteria – the 2 types • PEPTIDOGLYCAN IN E. COLI AND S. AUREUS o E. coli: gram-negative  glycan backbone made of n-acetylglucosamin (NAG) and n- acetylmuramic acid (NAM)  Has glycan/sugar backbone andAA o Staphylococcus aureus: gram positive  glycogen backbone and interbridges forms fromAA- in this case, lysine. o Antibiotics act on production of PG layer, inhibiting crosslinking. Acts only on newly formed bacterial cell walls, not on dormant bacteria that already have cell wall formed o Long chains of glycan (NAG & NAM) formed by glycosidic bonds. Crosslinking between chains is done through peptide bonds = gives stability to structure CELLWALL OF GRAM POSTIVE BACTERIA • Peptidoglycan is found in a thick layer on top of cell membrane • The cytoplasmic membrane is thin. The cell wall is thick • Smooth appearance…____________________ • Ribitol – other components made of lipidophosphate of glycerol phosphates attaches to the PG layer___________ • Contains up to 90% peptidoglycan = stability • Common to have teichoic acid (acidic substances “-“ charged attracts Na+, Ca , Mg ) embedded in their cell wall. Only in PG layer o Lipoteichoic acids: teichoic acids covalently bound to membrane lipids. – goes across the thick PG layer into the lipid bilayer o Provides rigidity to the cell-wall by attracting cations and a role in biofilm formation CELLWALL OF GRAM NEGATIVE BACTERIA • First has outer membrane (lipopolysaccharide and protein) • Followed by in middle by a periplasm layer with a thin PG layer in its middle • This periplasm layer is on top of cytoplasmic membrane – lots of proteins • Rough, not smooth appearance…___________ • More complex: the cell wall is composed of the outer membranes, which consists of the cell wall, and the periplast that contains a thin PG layer within • Membranes has channels, porins, pores allow molecules from one side of outer membrane of the other________ • Composed of 10% pertidoglycan • Most of cell wall composed of outer membrane aka LPS -- • The top lipid layer of the outer membrane is called the lipopolysaccharide (LPS) layer– important for chemical recognition. Vs PG layer in gram + 5 o LPS contains core polysaccharides with O polysaccharides attached  O comes from type of O linked antigen to antibody o LPS replaces most of the phospholipids in outer half of outer membrane o Endotoxin  the toxic component of LPS. It’s released into the blood after destruction of bacterial wall. Bacteria is lysed • Porins: channels for movement of hydrophilic low molecular substances o Non-specific for water. Specific porins for special molecules • Periplasm: space located between cytoplasmic and outer membrane- gel-like. Protein important for function o Kept there for outer membrane that had little permeability. Outter membrane prevents proteins from diffusing away  15nm wide, houses many proteins GRAM +/- CELLWALLS SUMMARY GRAM + GRAM – • thick PG (10-100nm) • Thin PG (2nm) • Teichoic acid (TA) linked to PG • No TAor LTA • Single membrane • Inner membrane and outer membrane • Lipoteichoic acid (LTA) anchored to separated by the periplasmic space mebrane • Lipopolysaccharide (LPS) on surface STRUCTURES EXTERNALTO THE CELLWALL – various appendages • Capsule and slime layers o Stick to cell wall of bacteria. If loosely attached = slime layer o Polysaccharide layers- help retain water, especially in slime layers o Assist in attachment to surfaces – capsule to cell wall of bacteria o Aid in evasion of immune system – increase bacterial survival o Resist desiccation – protects against phagocytosis so hard for body to get rid of encapsulated bacteria • Flagella – motility o Structure assists in swimming – long and thin o Helical in shape – can have more than one flagella on surface; chape and number used in classification; has base embedded in cell wall where motor is, and hs filament that moves o Consist s of many components – flagella proteins present in the filament o Moves by rotation – CW or CCW or by pushing/pulling o Translocation of virulence factors into host cell o Modulates immune system – presence of flagellum = inflammatory response • Fimbriae- smaller and more appendages – for motility and attachment to various substrates o Filamentous protein structures o Enables organisms to stick to surfaces or form pellicles  Stick to host cell they invasde  Helps bacteria form pellicles- like biofilms but on water & very thin and loose • *pili – very few that are present in bacteria o filamentous protein structures o longer than fimbriae – very few. o Help bacteria attach to surfaces o facilitate genetic exchange between cells (conjugation) – closest to sexual reproduction. Allows communication b/w bacteria. 6 o Abridge b/w 2 bacterial cells o Type IV pili involved in twitch motility GRAM STAIN • Structural differences in cell walls of gram+ and gram- bacteria are responsivle for differences in Gram stain reaction o Gram+ cell wall has PG thick layers with several components and cytoplasmic membrane- stains purple? S. aureus o Gram – has a little permeable outer membrane lipid bilayer, thin PG layer. Periplasmic and cytoplasmic layers – the stain is difficult to get inside so no colour? • Developed by Hans Christian gram in Denmark 1844 1. Bacterial suspension dried on glass slide – by flame or air 2. Crystal violet 1 min. wash off. (1 dye) 3. Iodine 1 min. wash off. – decolourizing agent: fixes the first dye. 4. 95% alcohol 10sec. wash off. – red dye 5. Safranin 30 sec • 2 dyes are added separately • gram + = blue/violet; gram- = red • timing is important! If left too long gram+ will loose dye and end up looking like gram- • crystal violet + iodine = dy2-I complexes in cytoplasm2( I stabilizes crystal violet). The bacterial cell wall can retain crystal violet. Iodine fixes it so it can’t be removed • in Gram-, de-colourizer dissolves thick lipid bilayer, diffuses through cell wall and ecolourizes crystal violet. 2 stain taken up. • In Gram+, wall is too thick to allow uptake of de-colourizing agent and remains violet • The addition of the second dye (red) – it can get into Gram - • repeat: first fix bacteria = both black. Crystal violet =both violet; iodine = both same colour. De-colourize (acetone-alcohol) = gram+ violet; gram- black. Safranin = gram+ violet; gram- red PATOGENIC GRAM+AND GRAM- BACTERIA • gram+ cocci: Staphylococcus  aureus, pyogenes, agalactiae, pneumonia; Enterococcus species • gram + rods: Corynebacterium diphtheria; Listeria monocytogenes; Clostridium tetani • gram- cocci: Neisseria species; Moraxella catarrhalis, Branhamella catarrhalis • gram- rods: Escherichia coli; Campylobacter species; Salmonella species; Shingella species; Shigella species; Yersinia species; Vibrio cholera; Bordetella pertussis; Legionella species; Pseudomonas aeruginosa LEC 3 – IMMUNITYAND INFLAMMATION Look at readings and go back to first slides and fill in info IMMUNITY • Collections of mechanisms that defend the body against disease. Many organs involved • Lymph and blood help the immune system by producing and transporting immune soldiers • 2 branches: o innate immune system: bult-in, fast, generic. Short-term protection for a wide range of pathogens 7 o adaptive immune system: acquired, slower, specific, long-term. Acquired over lifetime; lasts long and is very specific IMMUNITY FORMS 3 LINES OF DEFENSE • 1 line (non-specific, part of innate immunity) – several barriers o physical barriers, chemical barriers, resident bioflora: ciochemical or biological barriers nd • 2 line (part of non-specific, innate immunity) – built-in, natural o non-specific immune cells o chemical mediators  produced by previous cells o fever  response to infection o inflammation o phagocytosis  cells injesting and breaking down pathogens rd • 3 line ( part of specific, adaptive immunity)- specific immunity o T cells, B cells, antibodies 1 LINE OF DEFENCE: • Physical barriers: provide resistance against colonization and invasion by pathogens o Intact skin – provides structural support for tissues. o Sloughing of Dead skin – old skin shed away with microbes that live on it. Washing sheets, towels and other personal item important b/c microbes on those objest are still capable of causing infection o Mucous membranes & cilia (line the respiratory, urinal, gastrointestinal, and reproductive tracts) – pathogens trapped on mucus membrane and swept out of body by cilia (coughing, sneezing, swallowing) o Tears, saliva, urine, sweat …- flush out pathogens and debris. Some of these secretions will chemically disrupt the pathogens before removing them • Chemical barriers: o Skin secretions: fatty acids and lactic acid (lower the pH) – a decrease in pH helps destroy pathogens; products that destroy bacteria (shampoo) might destroy beneficial bacteria o Lysozymes (saliva, sweat, sebum, tears): destroy PG (peptidoglycan layer) in bacterial cell wall o Salt (in sweat) –hypertonic medium  dehydrates bacteria o Stomach acid & digestive enzymes: HCl, pepsin (kill most ingested bacteria) –not many bacteria can survie this hostile environment. Exception Helicobacter pylori o Vaginal & prostrate secretions: lactoferrin (binds iron prevents microbes from attaching, and slows their metabolism). • Resident microflora: they help with digestion and absorption of food; they get rid of pathogens by killing pathogen attachment site (body cells) o Beneficial microbes living in and on our bodies; o Competes with pathogens for nutrients and attachment sites - pathogens have to attach to body cells before they are able to multiply and attack o Secret toxins Kill some pathogens. • Sometimes these barriers fail! 2NDAND 3 RDLINE OF DEFENCE: • Innate and adaptive immunity: if pathogens get into body, the 2 and 3 line of defence kicks in to counter the attack • Consist of a network of cells, tissues, and organs with a wide distribution: 8 o Cells: leukocytes (WBC= immune cells) o Tissues (diffuse): lymph nodes and cell patches o Organs: bone marrow  produces and stored RBCs and WBCs. Spleen, thymus (lymphoid organs) • Rely on 2 systems for transport of immune cells and proteins: circulatory & lymphatic system-------- BLOODAND LYMPH SYSTEMS • Blood and immune cells –transported quickly through the cirvulatory system (pumping by heart) • Lymph: o Similar to blood, but contains only leukocytes/WBC, which can go from blood stream to lymph stream and vice vera (via spleen) o Moved back slowly to heart via contraction of skeletal muscles – why wheel-chair ppl experience swelling in legs b/c lymph can’t leave up to heart b/c no muscle contraction. Circulates in 1 direction ONLY o Functions in reabsorbtion o Filtered in nodes LEUKOCYTES = IMMUNE CELLS • Develop from multipotent stem cells from bone marrow throufh hematopoiesis (together with RBCs and platelets) • RBCs and leukocytes have same origin • All lymphocytes, erythrocytes, and platelets via erythropoiesis • Leukocytes move through blood, lymph, tissue. Many types of WBCs- very differentiated – only 0.1% found in lymph and tissue. Act as soldiers TYPESAND ROLES OF LEUKOCYTES • Found in blood (0.1%) and lymph • Are microscopic immune warriors that protect us from injury & infection • Have specialized recptors on their surface that enable them to determine what is “self” and what is “non-self” • Can be non-specific: recognize many pathogens, innate; or specific: one cell type only recognizes one type of pathogen, acquired • 2 groups based on appearance under microscope o granulocyte- visible large granules that store enzymes and toxins. 75%. Most WBCs are granules  include: eosinophils, neutrophils, basophils and mast cells o agranulocytes –no easily visible granules  include: monocytes, macrophages, T- & B- lymphocytes NON-SPECIFIC LEUKOCYTES: • Granykocytes o Eosinophils (2-4%= small) –in blood or tissue.Attach to surface and secrete enzymes that that breaks down parasite into smaller pieces  Elimination of allergens and parasites  Eosinophilia = hig level of eosinophils in the blood, indicates infection 9 o Neutrophils (55-65% = most of WBC) – non-specific immune cells; in blood or tissue. Don’t care what pathogens they kill  Aka PMN (polymorphonuclear) leukocytes – their nuclei have different shapes – not always round  Lookout for forgeign invaders  1 to arrive at site of injury/nfeciton - secrete chemicals to attract other immune cells to the site of infection  eat and digest invading microbes by phagocytosis  short-lived (3-8days); when dying form pus o basophils (0.5-1%) – non-specific immune cells in blood. Important for allergies  release histamine in response to injury, infection, or allergic response  vasodilation increased blood flow  inflammation  recruitment of WBCs into the infected/injured tissue o Mast cells –similar to basophils; in tissues near the point of entry (mouth, eyes, ancus, etc.)  Release histamine in response to injury, infection and allergens in tissues • Agranulocytes o Macrophages – non-specific immune cells – monocytes leave blood and migrate to tissues, where they mature into macrophages  Eat and digest pathogens & cellular debris (phagocytosis)  Secrete chemicals singles to stimulate other immune cells/macrophages (chemical messengers)  Present info about antigen to T cells – they have antigen recognition complexes/proteins on their surface  Are named for their location in the body (alveolar=lungs, kuppfer= kidney, microglia = brain) o Dendritic cells- relatives of macrophages- from monocytes; in tissues & move to lymph nodes o Process foreign matter/pathogens & present it to T cells – have antigen recognition complexes on surface that are non-specific - adaptive immunity SPECIFIC LEUKOCYTES-LYMPHOCYTES- from lymphoid progenitor • T lymphocytes = T cells – specialized immune cells o Produced in bone marrow, but matured in thymus o All have the T cell receptor (TCR) on their surface; used to bind and recognize specific antigens o Some have CD4 cell surface receptor  CD4+ T cells = helper T cells - help direct the immune response o Some have the CD8 cell surface receptor  CD8+ T cells= cytotoxic T cells – kill infected or tumour cells o Some cytotoxic T cels become memory cells – memory of that pathogen = adaptive immunity • B lymphocytes = B cells – specialized immune cells o Produced and matured in the bone marrow o All have B cell receptor (BCR) and major histocompatibility complex II (MHCII) on their surface – used to recognize and bind specific antigens o Activated by helped T cells – helper II T cells. After activation become.. o plasma cells- Produce antibodies against the extracellular invader 10 o Some activated B cells become memory cells – recognize invader and have a faster response FUNCTION TYPES OF LEUKOCYTES • Phagocyte – injest invading organisms (neutrophils, monocytes, mast cells, dendritic cells, macrophages) • Lymphocytes – allow the body to remember and recognize previous invaders and help body destroy them ( B & T cells) • Natural killer cells – ability to recognize stressed cells in the absence of antibodies and MHC (faster immune response); kill tumour cells & viruses by inducing apoptosis (contain perforin & granzymes) LYMPHATIC SYSTEM • Responsible for the immunological defense of the body o Self/non-self recognition o Protection from foreign invaders (antigens) o Initiate and participate in the immune response (B-cells, T-cells and antigen presenting cells-APC) • Component organs: bone marrow, thymus, lymph nodes, spleen, liver & diffuse lymphoid tissue LYMPHATIC ORGANS • Primary (central) lymphoid organs –trained to distinguish b/w cell and non-cell bodies o Thymus- where lymphoid stem cells are, fetal liver, pre-& post- natal bone marrow o Development and maturation of lymphocytes  immunocompetent cells • Secondary (peripheral) lymphatic organs – o Lymph nodes, spleen, diffuse lymphoid tissue and post-natal bone marrow o Provide the proper environment for immunocompetent cells to react, their work area o Anitgens interact with other antigen presenting lymphocytes/phagocytes? For and immune response PRIMARY LYMPHATIC ORGANS • Bone marrow – site of hematopoiesis and T & B cell production; maturation of B cells • Thymus – no nodules o Located in the central compartment of the thoracic cavity o Larges & most active gland in neonatal and pre-puberty stages o Originates early in embryogenesis and continues to grow until puberty o Removal of thymes in early development may cause irreversible damage to the immune system o During embryogenesis, T-cells migrate to the thymes to become immunocompetent (stock fo T cells early in life) used up as body ages ­ structure o encapsulated organ with 2 identical lobes:  covered by an irregular connective tissue capsule  lobes separated by thin septa (trabeculae) into lobules o each lobules has a core- central medulla – surrounded by and outer cortex o lacks afferent lymphatics - no lymph in thymus – stuff leaves the thymus! Efferent lymphatics o No lymph nodules present o Blood-thymus barrier present ­ Thymus cortex 11 o Dense population of T cells (stains darker) – more t cells! o Few macrophages o Contains mainly stellate epithelial reticular cells (ERC): 3 types in cortex: V ­ Thymus medulla o Fewer T-cells (stains lighter) o Contains stellate epithelial reticular cells (ERC): Type IV-VI o Contains Hassall’s corpuscules (thymic corpuscules) – made of larger ERCs  corpuscules– site where T-lymphocytes that are not good enough will die ­ ERCs o Type I  Surround the vascular elements of the cortex  Form the blood- thymus barrier- separate septa and thymes from blood. Seperates capsules from the septa  Isolate (via occluding junctions) the thymus cortex from the rest o Type II  Compartmentalize the thymus into lobule (have long wide processed that form desmosomal junctions with each other  subdivides that cortex into small T-cell compartments: provides environment for T cells to be trained – don’t come into contact with antigens and can become immune-competent o Type III- corticomedullary junction – separates cortex from medulla  Deep in the cortex near the medulla – corticomedullary junctions  Long wide processes similar to type I – more T-cell compartments o Type IV-VI  Type IV form thymus corpuscles – site of T-cell death ­ Thymus structure in child o Thin outer capsule sends thin connective tissue trabeculae into the lobe to form lobules. Dark cortex= more t cells, light medulla. Medullary areas of adjacent lobules look confluent. Blood vessel travel in trabeculae to the interior. Lacks lymphatic nodules! o Highle active thymus! ­ Thymus of adult - starts involution after puberty o Adipose connective tissue made mostly of fat cells, predominates at this stage b/c of gradual loss of lymphocytes with age. Remenents of lymphoid parenchyma have round irregular shape. The boundary b/w the cortex and medulla fades. Blood vessels in connective tissue  Few t cells, adiposcytes present, lacks compartmentalization, SUMMARY OF THYMUS  T-cell factory; highly compartmentalizes to prevent t cells from getiing into contact with any foreign antigen  Is the training-academy for t-cells -> become immunocompetent  Has cells with roles in “education” of T-cells, presenting self-antigens and MHC I and II molecules to developing T-cellls (ERCs II & III are teachers!)  T-cells (competent but naïve_ enter the medulla of the thymus where they further differentiate.  Only 5-10% of T-cells graduate and get out of thymus  Damage to thymes in early development  immunodeficient  Involution of thymus in adults – responsible for decrease in cells with aging 12  They learn self and non-self, ERC II ans III are teacher, mature and develop in thymus – all in the cortex SECONDAY LYMPAHTIC ORGANS SPLEEN  Function o Primary function- blood filter o immunity roles: o considered a large lymph node; where immune rxns are initiated o synthesizes antibodies (in the white pulp); o removes antibody-coated bacteria and antibody-coated blood cells through blood and lymph o macrophage factory (contains ½ the body’s monocytes, in red pulp) o removes RBCs from circulation; holds a blood reserve and recycles hemoglobin and blood and iron  structure o highly organized lymphoid compartment. Encapsulated organ o thick connective-tissue capsule o 2 types of splenic tissue:  white pulp: lymphoid tissue contains mainly lymphocytes. Surrounds the blood vessels  red pulp: - lighter colour. a network of channel (sinuses) filled with blood- contains RBCs and macrophages. Antibodies produced here and blood is filtered here o has only efferent lymphatics LYMPH NODES  function: o filter lymph fluid before returning it to blood o assist the immune system in building an immune response o release lymphocytes into the blood strem in infection o contain B-cells (make antibodies) & T-cells (cellular immunity)– killer T-cells o filter out cellular waste, dead and cancerous tumour cells o maintain normal blood volume and pressure in the body o have clinical significance (staging diseases) – lymph nodes become enlarged if infection occurs (inflamed) used to stage cancers – important for treatment  structure o situated deep within tissue or near the surface o oval and bean-shaped o surrounded by thick capsule made of connective tissue o highly compartmentalized cortex o nodules – storage for B- & T- cells; have cortices and medullae o central medulla – storage of macrophages o afferent & efferent lymphatics  cross section of tonsil that’s infected – oval structures inside are nodules. DIFFUSE LYMPHATIC TISSUE – named by region  Mucosa-associated lymphoid tissue (MALT) – several types: nose, genitals 13 o Gut-associated lymphatic tissue (GALT) go to next page!  Peyer’s patch found in small intestine*** o Bronchus-associated lymphatic tissue (BALT)  Located in the wall of bronchi  Skin associated lymphoid tissue (SALT) o Associated with the dermis of the skin  Appendix, anal, and genital area  Contains lymphocytes and phagocytes  Interact with antigens and microbes  Wide-spread through the body, common in mucus membranes  Ciliated epithelial cells that live in the small intestine. Have nodules  Lymphatic nodules – localized in the lamina propria of the tissue  Rod dots on pic – lymphocytes  Organize in lymph nodes?  ***Peyer’s patch common in the gut. Line the epithelium. When stimulated by pathogens, they start to change ­darker structures: primary nodules; haven't had T­ cells activated yet lighter region in the middle: secondary nodules –  have when T/B­cells activated due to action of  pathogens  2ND LINE OF DEFENCE – jumps into actions when barriers are breached INNATE IMMUNITY  built in (natural) immunity; always present. At birth  activated really fast after contact with pathogen  confers general protection (many pathogen; common general features of pathogens)  does not require previous exposure to pathogen or its products  important in 1 4 days after infection  includes o non-specific immune cells o chemical mediators o fever o inflammation o phagocytosis – phagocytes are the cells that eat pathogens  the cells involved: o Mast cells: release bioactive chemical. Respond early b/c Found in tissue close to entry points 14 o Neutrophils (PMN) (phagocytes) – signal other cells, ingest & digest pathogen – some of the 1 to arrive too. Large in numbers. o Macrophages (phagocytes) – stimulate other immune cells & eat & digest pathogens & cellular debris. Also ignal other cells and stimulate T and B cells for adaptive immunity later  How it works o Mediated by phagocytes – recognize a pathogen using pattern recognition receptors (PRRs) – PRR proteins recognize similar genetic sequences in the pathogen o PRRs – membrane bound phagocyte proteins that recognize common pathogen- associated molecular patterns (PAMPs)  Ex) bacterial LPS = lipopolysaccharides on the outer membrane of gram- bacteria. Immunity associated with inflammation  Innate response mechanism: inflammation o Inflammation is a nonspecific reaction to injury or infection o Reaction of vascularized tissue to local injury o Mediators of inflammation  Distress signals – histamine= vasodilation  Macrophages secrete cytokines and chemokines – attract immune cells o Signs of inflammation: redness- increased blood flow, swelling, pain – sensory neurons activated to send pain sensors to brain, heat o Effective inflammatory response isolates and limits tissue damage, destroying damaged cells and pathogens o If prolonged, Inflammation cen result in considerable damage to healthy tissue 1. Bacteria and other pathogens enter wound 2. Platelets from blood release blood-clotting proteins to ate wound site 3. Mast cells secrete factors that cause vasodialation and vascular constriction. Delivery of blood, plasma, and cells to injured cite inc. 4. Neutrophils secrete factors aht killa dn degrade pathogens 5. Neutrophils and macrophages remove pathogens by phagocytosis 6. Macrophages secrete hormones called cytokines that attract immune system cells to the site and activate cells involved in tissue repair 7. Inflammatory response continues until the foreign material is eliminated and the wound is repaired  Innate immunity fails b/c… o Some pathogens have developed mechanisms for neutralizing toxic phagocytic products  Staphylococcus aureus & Mycobacterium TB o Some intracellular pathogens produce leukocidins that kills phagocytes  Streptococcus pyogenes & S. aureus o Some bacteria produce a capsule resistant to phagocytosis  Streptococcus pneumonia RD 3 LINE OF DEFENCE Adaptive Immunity  Acquired ability to recognize & destroy a particular pathogen or its product  Dependent on previous exposure to the pathogen or its products  Directed toward an individual molecular component of the pathogen (antigen)  target specific strains 15  Takes time to be andivated  slower b/c only a few cells in the body can recognize specific strain of bacteria pathogen- 2 response is faster  Cellulite immunity and humoral immunity – 2 types of response  The cells involved: o Macrophages – engulf foreign bodies/ pathogens o Helper T-cells – boost immune response through cytokines o Cytotoxic T-cells –Eliminate infected or tumour cells o B-cells (plasma cells) – produce antibodies  How it works: st o After 1 antigen exposure – a primary immune response occurs o Stimulation of specialized antigen-reactive immune leukocytes (lymphocytes : T & B cells) o Each lymphocyte produces a unique protein that interacts with a single antigen- specific protein for specific antigen  T cells: T cell receptors (TCRs)  B cells: antibodies or immunoglobulins (igs) o Begins with interaction of T cells with antigens on infect cells o T cells can recognize antigen only when present on self protein called major histocompatibility complex- MHC- proteins  2 exposure to same antigen = faster and stronger response – immune memory ANTIGENSANDANTIBODIES  antigen - antibody generator o foreign body, epitope –region that reacts with an antibody TCR, SIGs  antibodies (immunogloculin – Ig) o soluble proteins madde by B cells & plasma cells o mark antigens for elimination o antibodies provide targets for interaction, by binding, with proteins of the complement system – read textbook! – resulting in destruction of antigens through lysis or opsonization =protein coating B lymphocytes turn to plasma cells and secret antiboies o 5 classes based onAAsequences in the heavy chain =  IgG – most common circulating antibody. In blood stream – transferred acriss placenta from mother to bab  IgM – immunoglobin. 1 type of antibody to be secreted in response to new antgen. Good at causing atigen clumping and activating complement  IgA– crosses epithelial cells. Protects epithelial surfaces and present in breast milk  IgD – no known function  IgE – - fights parasites. Eosinophils have receptors for the IgE. Release histamine= toxic to parasites  Cellular immunity = T cell immunity o Macrophage ingests and digests pathogen through phagocytosis; pieces moved out to cell surface and expressed on MHCII complex (antigen presentor) – this will bind to a TCR on a helper T cells = antigen presentation.  Phagocytosis, pathogen destruction, antigen processing o Helper TI cell = T-cell immunity. Release cytokines = inflammation. Cytokine also increases B cell activation 16 o Helper TII cell= activates B cells. Release perforin & granzyme –target cell lysis o MHCI also binds antigens and presents them to cytotoxic T cells o Antigen presentation: --- 1. Antigen enters dendritic cell 2. Enzymes inside cell breaks antigen into pieces 3. Antigen pieces bind to MHC protein inside ER 4. The MHC-antigen complex is transported to the cell surface via the Golgi apparatus 5. The MHC protein presents the antigen on the surface of the cell membrane – different types of T cells attracted to cell surface o All host cells have MHC I o APCs (macrophages, dendritic cells, B cells) – have also MHC II • H
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