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January 21 lecture.docx

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Paul W Andrews

3F03 January 21, 2014 Adaptation, disorder, and the febrile system Wakefield/Andrews recap Andrews: Evolved function is identified by deconstructing the trait’s structure and figuring out how the components work together *Missing Medical perspective on fever • Harrison’s principles of internal medicine o No significant evidence that antipyretics (fever suppressant drug) delay the resolution of viral or bacterial infections, nor is there evidence that fever facilitates recovery from infection or acts as an adjuvant to the immune system o Routine treatment of fever and its symptoms does no harm and does not slow the resolution of common viral and bacterial infections (this is wrong) Components of the febrile system • Preoptic area of the anterior hypothalamus o Sensory and regulator of temperature o Homeostatic control • Cytokines o Chemical messengers of the immune system  Trigger fever  Regulated by fever • Innate immune system o General defences (macrophages, white blood cells) • Adaptive immune system o Pathogen specific defences (antibodies, slower acting) Types of immune cells *check slides *no focus Normal febrile range • Normal body temps for modern animals o Human 36-37.8, 37.9-41 (fever) o Horse 38-38.4, 38.3-39.3 (fever) There are benefits of heat/fever on the immune system • Neutrophil and monocyte motility and emigration • Enhanced phagocytosis and pinocytosis (engulfing bacteria and removing it) • Etc. o Is this enough evidence to demonstrate that the febrile system was shaped/modified by natural selection to coordinate various components of the immune response Temperature-dependent phagocytosis • Ingested bacteria per leukocite increase as temperatures fall in the fever range Cytokines important in bacterial immune response TNF-a • Triggers migration of neutrophils o Phagocytosis o Cytotoxic proteins o Dna webs that trap microbes IL-1B • Activation of lymphocytes o Natural killer cells  Cytotoxic proteins o T cells *missing Both important but if they are co-expressed—it can lead to shock, organ failure, and death Ie. Mice • Fever staggers cytokine expression—produces them at the same time Febrile temperatures promote migration of lymphocytes to peripheral lymph nodes (PLN) • Pa
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