#Inflammation

#Recognition of tissue damage

Typically caused by tissue injury or infection.

• tissue injury → blood vessel disruption → mast cell degranulation and platelet activation
• infection
  • macrophages and granulocytes identify an invader leading to:
    • phagocytosis
    • macrophage cytokine release (e.g. IL-6, TNF-α)
    • mast cell and granulocyte degranulation with release of inflammatory mediators (more cytokines, ECFA, NCF, histamine, prostaglandin, leukotrienes)
  • activation of complement
• NK cells detect abnormal cells (e.g. absence of MHC), inducing apoptosis and secreting cytokines

#Local inflammatory response

Release of inflammatory mediators causes:

• vasodilation and increased vascular permeability
  • increases blood supply, which delivers oxygen, nutrients, leucocytes, plasma proteins, and heat
  • proteins include complement, lysozymes, antibodies, procoagulants, and anticoagulants
• endothelial expression of cell-surface adhesion molecules
  • leads to ‘transmigration’ of leucocytes towards site of injury/infection, enhancing the immune response
• activation of complement
  • results in MAC formation, opsonisation of pathogens, chemotaxis, and mast cell and basophil degranulation

#Systemic inflammatory response

In severe inflammation, pro-inflammatory cytokines escape into systemic circulation with multiple effects:

• fever augments phagocytosis and inhibits bacterial multiplication
• cytokines stimulate neutrophil release from bone marrow
• cytokines also stimulate the release of acute phase proteins from the liver, which are involved in opsonisation and augmentation of leucocyte functions

#Chronic inflammation

Antigen presentation leads to the activation of the acquired immune system, which predominates in chronic inflammation.