Inflamation Flashcards
What are the symptoms of acute inflammation?
- swelling and redness
- heat and fever
- pain
- loss of function
What are the major cell mediators of acute inflammation?
- Neutrophils
- Macrophages
- Mast cells
- Endothelial cells
What are the major secreted mediators of inflammation?
-TNF -a
- IL-6
- IL-1
- Acute phase proteins
What prostaglandins are important with acute inflammatory?
- PGE2 (can sensitise nerves to pain)
- PGE2PGI2 (involved in vasodilation)
- PGE2 (involved in fever)
What PAMP/PRRs are involved as apart of recognition?
- innate cell recognition of pathogens
-macrophages and neutrophils
-mast cells
-TLRs and other PRRS
What do DAMPS do at recognition?
- innate cell recognition of damage
- damage associated molecular protein
- immune system should only see them when damage has occurred
How does redness and heat occur?
- IL-1 and TNF-a
- capillaries closer to the surface ( increase in redness and heat)
How does swelling occur?
- chemokines
-cellular infiltration of infection/damage - upregulation of adhesion molecules on endothelia (IL-4)
What happens at the acute phase response of acute inflamation?
- pro-inflammatory cytokines (IL-6) lead to downregulation and upregulation of hundreds of proteins
- release of acute-phase protiens from liver
How does complement effect inflamation?
- C3a (mast cell activation/degranulation)
- C4a (mast cell activation)
- C5 a (chemotaxis/ vasodilation/ neutrophil and mast cell activation/degranulation)
What acute phase proteins are released during inflamation?
- haptoglobin (binds to haemoglobin/ prevents bacteria requiring iron from gaining it)
- fibrinogen (potential damage to tissues/ generates fibrin threads/ clot can block pathogen)
How is pain caused during inflamation?
- serotonin and bradykinin stimulate nerve endings causing pain
What does the hypersecretion of cytokines during sepsis and toxic shock create?
positive feedback loop
What causes chronic inflammation?
- T cells important
- Pathogens or non-pathogens
- can be Th1/ Th2/Th17
How is acute inflammation resolved?
- short-half life proinflammatory mediatory
- production of pro-inflammatory prostaglandin and chemokines stops
-stops neutrophil migration - existing neutrophils are phagocytosed by macrophages
- major change in cell types (Tregs - CD4+ produce anti-inflammatory cytokines)