Acute Inflammation

Acute inflammation is the rapid, short-lived response of vascularised tissue to injury or infection. Within minutes to hours it brings plasma proteins and neutrophils to the affected site, producing the classic signs of redness, heat, swelling, pain, and loss of function. It is the body's first line of defence and, when the inciting stimulus is removed, is normally resolved within days.

Definition

Acute inflammation is the immediate and early response to an injurious agent, characterised by increased blood flow, increased vascular permeability with exudation of plasma proteins, and the emigration of neutrophils into the affected tissue.

Scope

The entry describes the vascular and cellular events of the acute inflammatory response, its principal mediators, its morphologic patterns, and the possible outcomes — resolution, progression to chronic inflammation, abscess formation, or healing by scar. It treats acute inflammation as a general-pathology mechanism rather than as guidance on any particular infection or injury.

Core questions

• What triggers the vascular and cellular changes of acute inflammation?
• How are neutrophils recruited from blood into injured tissue?
• What determines whether acute inflammation resolves or persists?

Key concepts

• Vascular phase: vasodilation and increased permeability
• Exudate and oedema
• Neutrophil recruitment and the leukocyte adhesion cascade
• Chemical mediators (histamine, prostaglandins, cytokines)
• Phagocytosis
• Resolution and pro-resolving mediators
• Cardinal signs: rubor, calor, tumor, dolor, functio laesa

Mechanisms

Injury and microbial products trigger resident cells to release mediators that dilate arterioles and increase venular permeability, allowing protein-rich fluid to leave the vasculature as an exudate. Circulating neutrophils then roll, adhere, and transmigrate across the endothelium in response to chemotactic signals, accumulating at the injury site where they phagocytose pathogens and debris. The reaction is normally self-limiting: once the stimulus is cleared, a coordinated resolution program — driven in part by specialised pro-resolving lipid mediators — halts leukocyte recruitment and restores tissue homeostasis. Failure of this program contributes to non-resolving, chronic inflammation (Medzhitov, 2008; Serhan, 2014; Nathan, 2010).

Clinical relevance

Acute inflammation underlies common signs and laboratory findings encountered across infection and injury, and recognising its features is part of understanding tissue pathology. The entry explains these mechanisms for reference and education and does not provide diagnostic criteria or treatment advice for any condition.

Evidence & guidelines

The description draws on experimental immunology and on standard pathology references such as Robbins & Cotran Pathologic Basis of Disease (Kumar, Abbas, & Aster, 2021). As a basic mechanism, acute inflammation is not the subject of clinical practice guidelines; any management belongs to the specific diseases in which it occurs.

History

Aulus Cornelius Celsus recorded four cardinal signs of inflammation (redness, heat, swelling, pain) in the first century, and Galen later added loss of function. Nineteenth-century pathologists, notably Julius Cohnheim, described the vascular events under the microscope, while Élie Metchnikoff established the central role of phagocytosis. Modern work has detailed the mediators and the active resolution program that brings the response to a close (Serhan, 2014; Medzhitov, 2008).

Key figures

• Ruslan Medzhitov
• Charles N. Serhan
• Carl Nathan

Seminal works

• medzhitov-2008
• serhan-2014
• nathan-2010

Frequently asked questions

What are the cardinal signs of acute inflammation?

Redness (rubor), heat (calor), swelling (tumor), and pain (dolor), with loss of function (functio laesa) added later; they follow from vasodilation, increased vascular permeability, and the accumulation of fluid and cells.

Which cell predominates in acute inflammation?

The neutrophil is the characteristic cell of acute inflammation, rapidly recruited from the blood to phagocytose pathogens and debris, in contrast to the mononuclear cells that dominate chronic inflammation.