Textbook Notes (368,794)
Canada (162,165)
Biology (600)
BIO120H1 (305)
Chapter 2

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Department
Biology
Course
BIO120H1
Professor
Bebhinn Treanor
Semester
Winter

Description
Chapter 2  Extracellular infections-pathogens live and replicate in spaces btw human cells o Accessible to soluble molecules of immune system  Intracellular infections-pathogens replicate inside human cells o Not accessible to soluble molecules of immune system o Pathogens that live in nucleus or cytosol can be attacked by killing the infected cell o Pathogens that live in intracellular vesicles can be attacked by activating the infected cell to intensify its antimicrobial activity  Vast majority of human infections come from transmission of pathogen either direct or indirect from another person already infected  Anthrax is spread by spores that are resistant to heat and dessication so they can go long distances.  HIV is sensitive to enviro changes, passed btw ppl by intimidate contact  As soon as pathogen penetrates epithelial barrier and starts to live in human tissue, innate immunity starts. o Liver makes complement which coats the surface of bacteria and extracellular virus particles and makes it easier to phagocytosize  Many complement components are proteolytic enzymes, proteases that circulate in inactive forms=zymogens  Infection triggers complement activation o Each protease cleaves and activiates the next enzyme in path o Each protease is highly specific for complement component it cleaves and cleaves at signle site o Usually serine protease, involves digestive enzymes trypsin and chymotrypsin  C3 (complement component 3) is most important o Patients lacking C3 are prone to successive severe infections o When complement activated by infection, it cleaves C3 into small C3a and large C3b…some C3b covalently bonds to pathogen surface=complement fixation o Bound C3b tags pathogen for destruction by phagocytes and also organizes formation of protein complexes that damage the pathogens membrane o C3a acts as chemoattractant to recruit effector cells, including phagocytes form blood to infection  C3 has high energy thioester bond o C3 is made and enters circulation in inactive form, where the thioester is sequestered and stabilized within the hydrophobic interior of protein o When C3 is cleaved into C3a and C3b, the bond is exposed and is nucleophilic attacked by water or AA and hydroxyl groups of proteins and carbohydrates on pathogen surface. Results in some of C3b covalently bonding to pathogen  The pathway that works at the start of infection is the alternative pathway of complement activation  Second pathway, lectin pathway of complement activation is also part of innate immu
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