The Basic Inflammatory Response

Inflammation is a vital innate defense against microbial invaders. Microorganisms trigger inflammation by growing and damaging host cells. Resident immune cells called macrophages engulf and digest these invaders, cleaning up the infection.

In response to infection, macrophages release cytokines, small proteins regulating the immune response. Cytokines stimulate endothelial cells to express selectins, which bind to carbohydrates on neutrophils, causing them to slow down and roll along the endothelium. Inflammatory signals then trigger neutrophils to express integrins, which lock onto adhesion molecules (ICAM-1 and VCAM-1) on endothelial cells, halting their movement.

Damaged tissue cells release bradykinin, a polypeptide that loosens tight junctions between endothelial cells. This allows neutrophils to extravasate, squeezing through the loosened wall into tissues to help macrophages attack microbes.

Bradykinin also binds to mast cells, causing them to release histamine, which further loosens endothelial junctions, allowing more fluid and cells to exit capillaries. Bradykinin also induces capillary cells to synthesize prostaglandins, which stimulate nerve endings, causing pain. The five cardinal signs of inflammation are redness, warmth, pain, swelling, and altered function at the affected site.