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Flashcards in Innate immune response Deck (12)
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1

Describe the initial stages of the inflammatory response

Breaking open of the skin

  1. Pathogens entering
  2. Chemicals released- toll-like receptors can be involved with the release of chemicals
  3. Macrophages and dendritic cells phagocytose and produce cytokines
  4. Cytokines increase blood vessel permeability, and neutrophils come from the blood vessels to site of injury
  5. Neutrophils, through chemotaxis, are attracted to the pathogen
  6. Neutrophils and macrophages phagocytose pathogens and cell debris at the site

2

Provide 3 examples of complex innate immune chemicals which specifically directly target microbes

  • antimicrobial peptides
  • lyzozymes
  • type 1 interferon

3

antimicrobial peptides

  • e.g. defensins
  • Active against gram-positive and gram-negative bacteria
  • Disrupt bilayer
  • Disrupt membrane-bound machineries
  • Hydrophobic region targets non-polar membrane of plants and mammals
  • Electrostatic region targets zwitterionic phospholipids present in bacterial membrane

4

lysozymes

break bonds between glycopeptides (breaks NAM and NAG part) in polymer outer layer of bacteria (especially gram-positive), breaking cell wall

5

type 1 interferon

  • Cytokine produced by virus-infected cells 
  • Signals neighbouring uninfected cells to destroy RNA and reduce protein synthesis 
  • Signals neighbouring infected cells to undergo apoptosis (programmed cell death) 
  • Activates immune cells 
  • Side effects include muscle aches, chills, headache, and fever (all of which prevent further infection)

6

what causes a fever

  • when phagocytic cells phagocytose pyrogenic pathogens, they release cytokine called interleukin 1 ( and IL-6)
  • Travels to hypothalamic body temperature
  • Increased set point value causing fever
  • At the higher temperature, cells phagocytose more efficiently, and pathogens cannot ingest iron as well

7

Describe the process of phagocytosis, and how it kills and digests microbes

  1. Pseudopodia formation ("fake feet")
  2. Adherence of microbe to cell membrane
  3. Ingestion of microbe into phagocytic cell
  4. Vacuole/lysosome fusion
  5. Killing and digestion by lysosome
    • Lysosome - low pH acid environment, reactive oxygen and reactive nitrogen intermediates, and enzymes (proteases, lipases, nucleases)
  6. Elimination out of phagocytic cell

8

3 complement pathways

  1. classical - antibody bound to pathogen binds to complement
  2. alternative - complement binds directly to pathogen surface or to a pathogen component (e.g. endotoxin)
  3. lectin - carbohydrates on microbial bind to complement

9

toll-like receptors

  • Pattern recognition receptors (TLR 1-9) in or on innate cells
  • Bind to common features of pathogens (microbial molecular patterns)
  • TLR engagement leads to many innate immune mechanisms
    • Phagocytosis
    • Cytokine release
    • Interferon release

10

3 outcomes of complement cascade

Label - opsonisation

  • labels pathogens which bind to complement receptors on phagocytes)
  • C3a

Destroy

  • membrane attack complex formation pores in bacterial cells à Death
  • C9

Recruit

  • complement proteins act as peptide mediators of inflammation and recruit phagocytes
  • C3a and C5a

11

5 signs of inflammation

  1. heat (calor) - casued by increased blood flow (histamine)
  2. redness (rubor) - caused by increased blood flow (histamine)
  3. swelling (tumor) - caused by increased vascular permeability (prostaglandins and leukotrienes)
  4. pain (dolor) - caused by cytokine release
  5. loss of function (functio laesa) - damaged tissue 

12

steps of inflammation

  1. Damaged or infected tissue causes mast cells to release cytokines and other mediators (histamine, prostaglandins, leukotrienes)
  2. Macrophages in the damaged tissue start to phagocytose the pathogen. They also release cytokines
  3. Cytokines released from macrophages and mast cells attract phagocytic cells (macrophages, neutrophils etc.) into the site of infection. These cells are allowed to cross the blood barrier because it has been made leaky (more permeable) by mast cell cytokines.  
  4. Phagocytic cells phagocytose pathogens