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Acute Inflammation

Injury or Infection

Endothelial Tissue damage and infection

Cells near damage site secrete IL-8

IL-8 activates other leukocytes

endothelial tissues also release NO and histamines

NO and histamines cause vasodilation

Vasodilation causes edema. Transudates escape

TNF and cytokines cause endothelial cells to express adhesion molecules

E selectin, L selectin expression increases

Neutrophils roll along vascular wall

IL-8 causes the leukocytes to stop at the damage site

Ca2+ helps polymerize actin for extravasation

Neutrophils follow chemoattractant cascade

anaphylatoxins from complement signal the location of infections

Simultaneously, Bradykinin and PGs cause more vasodilation and pain

Pyrogens particularly IL-1 and IL-6 cross blood brain barrier to cause fever

Fever causes more vasodilation, inhibits bacterial growth, and stimulates more leukocytes

At the damage site, TLRs, GPCRs, Opsonin receptors and Cytokine receptors help immune cells recognize the pathogen

Neutrophils and Macrophages engulf bacteria

Lysosomes fuse with the phagosome

ROS and RNOS in lysosome destroy bacteria

Macrophages phagocytose damaged or necrotic tissue to initiate repair process

Tissue Damage Activates Macrophages Infection

BK Complement activation (C3a, C4a, and C5a) Histamines, NO



1. 2. 3. 4. 5. 6.

Extravastion Migration to damage site Recognition (PRR; TLR; NOD etc) Ox. Burst in Neutrophils M activation Repaired tissue