Tuesday 1 June 2004
Definition: Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defense-leukocytes and plasma proteins-to the site of injury.
It can be assessed by the presence of extravascular polymorphonuclear neutrophils in the absence of concurrent chronic inflammation.
Acute inflammation has three major components:
(1) alterations in vascular caliber that lead to an increase in blood flow;
(2) structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation;
(3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent. (Robbins, 7th ed.)
When a host encounters an injurious agent, such as an infectious microbe or dead cells, phagocytes that reside in all tissues try to get rid of these agents.
At the same time, phagocytes and other host cells react to the presence of the foreign or abnormal substance by liberating cytokines, lipid messengers, and the various other mediators of inflammation.
Some of these mediators act on endothelial cells in the vicinity and promote the efflux of plasma and the recruitment of circulating leukocytes to the site where the offending agent is located.
The recruited leukocytes are activated by the injurious agent and by locally produced mediators, and the activated leukocytes try to remove the offending agent by phagocytosis.
As the injurious agent is eliminated and anti-inflammatory mechanisms become active, the process subsides and the host returns to a normal state of health. If the injurious agent cannot be quickly eliminated, the result may be chronic inflammation.
The different components of the inflammatory response are mediated by different signals and serve distinct (and overlapping) functions.
The vascular phenomena of acute inflammation are characterized by increased blood flow to the injured area, resulting mainly from arteriolar dilation and opening of capillary beds induced by mediators such as histamine.
Increased vascular permeability results in the accumulation of protein-rich extravascular fluid, which forms the exudate.
Plasma proteins leave the vessels, most commonly through widened interendothelial cell junctions of the venules. The redness (rubor), warmth (calor), and swelling (tumor) of acute inflammation are caused by the increased blood flow and edema.
Circulating leukocytes, initially predominantly neutrophils, adhere to the endothelium via adhesion molecules, transmigrate across the endothelium, and migrate to the site of injury under the influence of chemotactic agents.
Leukocytes that are activated by the offending agent and by endogenous mediators may release toxic metabolites and proteases extracellularly, causing tissue damage.
During the damage, and in part as a result of the liberation of prostaglandins, neuropeptides, and cytokines, one of the local symptoms is pain (dolor).
Neutrophils going to the site of infection
- chronic inflammation