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VCU BIOL 209 - Immunopathology; allergy, sepsis, autoimmunity
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BIOL 209 1st Edition Lecture 27 Outline of Last Lecture I. Question/Answer’sII. ELISA AssayA. IndirectOutline of Current LectureI. Question/Answer’sII. LymphocytesIII. InflammationIV. AllergyV. AdhesionVI. MultiplicationVII. ExozymesCurrent LectureI. Question/Answer’sA. Salmonella typhi is associated with intestinal disease. If S. typhi got into a cut, are you likely to get a wound infection? No – it doesn’t have the tools to handle the innate immune defenses in that environmentB. Why do you think ingested pathogens typically have a high infectious dose? The stomach is very acidic, so they have to be able to survive that to get into the lower intestinesII. LymphocytesA. Recognize carbs, nucleotides, etc. (biomacromolecules)B. Don’t recognize these structures on or in our cells because they (self-reactive T and B cells) are deleted, killed, or inactivated during development1. Molecular mimicrya. Pathogens take advantage of this and resemble our structures in order to not be recognized- Lymphocytes that recognize that mimicked structure(s) have been deletedb. Examples: diabetes (type 1) and rheumatic fever - Immunopathology associated with pathogen infectionIII. InflammationA. A localized eventThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.1. What if it wasn’t local, but systemic? Inflammatory cytokines act on blood vessels throughout the body, leading to loss of blood volume (septic shock)IV. AllergyA. Hypoimmune response, even though substances aren’t extremely harmful1. Histamine: alert system recruiting defenses to site of allergen2. Systemic response = anaphylaxis (loss of blood pressure, induced airway/muscle contraction), which is fatal3. Allergen might be systemic when you’re allergic to a drug (penicillin, venom, food)* Table 13.4 – factors that weaken host defenses and increase susceptibility to infectionV. AdhesionA. Non-specific adhesion of bacterial glycocalyx to host cell surfaceB. Specific bacterial fimbrae binding to host cell surfaceVI. MultiplicationA. Invasive and/or toxigenic processes promote growth and expand infectionB. Bacteria use a variety of mechanisms to secrete virulence factors1. Type III system can inject factors directly into host cells2. Injected factors can change host cell cytoskeleton, first enhancing adherence, then leading to internalizationa. This apparatus is a virulence factorVII. ExozymesA. Some pathogens secrete hyaluronidase, which breaks down hyaluronic acid, a component of the extracellular matrix, that forms part of the epithelial


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VCU BIOL 209 - Immunopathology; allergy, sepsis, autoimmunity

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