Editing Inflammation (section)

==== Acute process ====
{{More medical citations needed|section|date=April 2023}}
[[File:Events in Acute Inflammation.pdf|thumb|569x569px|A flowchart depicting the events of acute inflammation.<ref>{{Cite book |title=Pathologic basis of disease |vauthors=Robbins S, Cotran R, Kumar V, Abbas A, Aster J |date=2020 |publisher=Saunders Elsevier |edition=10th |location=Philadelphia, PA}}</ref>]]
[[File:Granulation tissue low power.jpg|thumb|[[Micrograph]] showing granulation tissue. [[H&E stain]].]]
The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident [[macrophages]], [[dendritic cells]], [[histiocytes]], [[Kupffer cells]] and [[mast cell]]s. These cells possess surface receptors known as ''[[pattern recognition receptor]]s'' (PRRs), which recognize (i.e., bind) two subclasses of molecules: [[pathogen-associated molecular pattern]]s (PAMPs) and [[damage-associated molecular pattern]]s (DAMPs). PAMPs are compounds that are associated with various [[pathogen]]s, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related injury and cell damage.

At the onset of an infection, burn, or other injuries, these cells undergo activation (one of the PRRs recognize a PAMP or DAMP) and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes the redness (''rubor'') and increased heat (''calor''). Increased permeability of the blood vessels results in an exudation (leakage) of [[blood plasma|plasma]] proteins and fluid into the tissue ([[edema]]), which manifests itself as swelling (''tumor''). Some of the released mediators such as [[bradykinin]] increase the sensitivity to pain ([[hyperalgesia]], ''dolor''). The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly [[neutrophils]] and [[macrophages]], to flow out of the blood vessels (extravasation) and into the tissue. The neutrophils migrate along a [[chemotactic]] gradient created by the local cells to reach the site of injury.<ref name="robspath" /> The loss of function (''functio laesa'') is probably the result of a neurological reflex in response to pain.

In addition to cell-derived mediators, several acellular biochemical cascade systems—consisting of preformed plasma proteins—act in parallel to initiate and propagate the inflammatory response. These include the [[complement system]] activated by bacteria and the [[coagulation system|coagulation]] and [[fibrinolysis system]]s activated by [[necrosis]] (e.g., burn, trauma).<ref name="robspath" />

Acute inflammation may be regarded as the first line of defense against injury. Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed.<ref name="robspath" />