Define and describe the general features of acute and chronic inflamma

Define and describe the general features of acute and chronic inflammation including stimuli, vascular and cellular enents

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acute chronic inflammation vascular cellular events pathology overview

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inflammation pathology

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https://www.ncbi.nlm.nih.gov/books/NBK534820

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Inflammation: definition

Inflammation is a protective response of vascularized living tissue to infection, tissue injury, or other harmful stimuli. Its purpose is to eliminate the cause of injury, remove dead cells and damaged tissue, and begin repair. The response can itself cause tissue damage if excessive or prolonged.

The classic local signs are:

Redness (rubor) and heat (calor): increased blood flow
Swelling (tumor): leakage of fluid and proteins into tissues
Pain (dolor): mediators such as bradykinin and prostaglandins, plus pressure from edema
Loss of function (functio laesa): pain, edema, and tissue injury

Acute inflammation

Definition and general features

Acute inflammation is a rapid, short-duration response, usually beginning within minutes to hours and lasting hours to days. It is characterized by vascular changes, exudation of protein-rich fluid (edema), and predominantly neutrophilic leukocyte infiltration.

Its possible outcomes are:

Complete resolution
Suppuration/abscess formation
Healing by fibrosis and scar formation
Progression to chronic inflammation if the insult persists.

Robbins & Kumar Basic Pathology, pp. 27, 39-41.

Stimuli causing acute inflammation

Category	Examples
Infections	Bacteria, viruses, fungi, parasites, and microbial toxins
Tissue necrosis	Ischemia/infarction, trauma, burns, frostbite
Physical and chemical agents	Radiation, heat, cold, corrosive chemicals
Foreign bodies	Splinters, sutures, crystals, dirt
Immune reactions	Allergic reactions and some autoimmune responses

Vascular events in acute inflammation

Most changes occur in postcapillary venules.

Brief vasoconstriction
- A transient reflex response immediately after injury.
Vasodilation
- Mainly affects arterioles.
- Mediated chiefly by histamine, also nitric oxide and prostaglandins.
- Causes increased blood flow, producing redness and warmth.
Increased vascular permeability
- Endothelial-cell contraction creates gaps between endothelial cells.
- Major mediators include histamine, bradykinin, leukotrienes, and others.
- Plasma proteins and fluid leave vessels, causing protein-rich exudate and edema.
Stasis of blood flow
- Loss of fluid from vessels concentrates red cells and increases blood viscosity.
- Flow slows, allowing leukocytes to move toward the endothelial surface.
Lymphatic drainage
- Lymph flow increases to drain edema fluid, proteins, cellular debris, and microbes.
- Draining lymph nodes may enlarge due to reactive lymphoid hyperplasia.

An exudate is inflammatory extravascular fluid rich in protein and cells. In contrast, a transudate is low-protein fluid caused by altered hydrostatic or osmotic pressure without primary vascular inflammation.
Robbins & Kumar Basic Pathology, pp. 27-28.

Cellular events in acute inflammation

The main cells are neutrophils, especially during the first 6-24 hours.

1. Leukocyte recruitment from blood to tissue

This occurs in a sequence:

Margination: leukocytes move from the central blood column toward the vessel wall due to stasis.
Rolling: weak, transient attachment mediated by endothelial and leukocyte selectins.
Firm adhesion: leukocyte integrins bind to endothelial ligands such as ICAM-1 and VCAM-1.
Transmigration (diapedesis): leukocytes pass between endothelial cells, mainly in postcapillary venules. PECAM-1/CD31 participates.
Chemotaxis: movement toward the inflammatory focus along a chemical gradient.

Important chemoattractants include bacterial products, C5a, LTB4, and chemokines such as IL-8/CXCL8.

2. Leukocyte activation and phagocytosis

Activated neutrophils and macrophages:

Recognize microbes and dead cells through pattern-recognition receptors and opsonin receptors.
Engulf material by phagocytosis.
Kill microbes using reactive oxygen species, nitric oxide, lysosomal enzymes, and antimicrobial proteins.

Although these mechanisms remove harmful material, released enzymes and oxidants can also injure normal host tissue.

3. Predominant cell pattern

Neutrophils predominate early.
Monocytes/macrophages usually replace neutrophils after 24-48 hours.
Eosinophils may predominate in allergies and parasitic infections.
Lymphocytes may be prominent in viral infections.

Robbins, Cotran & Kumar Pathologic Basis of Disease, pp. 84-90.

Chronic inflammation

Definition and general features

Chronic inflammation is prolonged inflammation, lasting weeks, months, or years. It occurs when the injurious agent persists or when immune responses become self-sustaining.

Unlike acute inflammation, chronic inflammation has three linked features:

Mononuclear-cell infiltration, particularly macrophages, lymphocytes, and plasma cells
Ongoing tissue destruction caused by the persistent stimulus and inflammatory cells
Attempts at repair, with angiogenesis, connective-tissue deposition, fibrosis, and eventual scar formation

Robbins & Kumar Basic Pathology, pp. 41-42.

Stimuli causing chronic inflammation

Category	Examples
Persistent infections	Tuberculosis and other mycobacterial infections, some viral, fungal, and parasitic infections
Immune-mediated diseases	Rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, autoimmune thyroid disease
Allergic disease	Bronchial asthma and persistent hypersensitivity reactions
Prolonged exposure to toxic material	Silica inhalation causing silicosis; foreign bodies
Endogenous substances	Cholesterol and lipid deposition in atherosclerosis
Unresolved acute inflammation	Chronic abscess or persistent infection after an acute inflammatory response

Robbins & Kumar Basic Pathology, p. 41.

Vascular events in chronic inflammation

Acute-type vascular permeability may continue, especially during exacerbations, but the more characteristic vascular changes are related to repair and tissue remodeling:

Persistent endothelial activation and continued leukocyte recruitment
Formation of new small vessels, called angiogenesis
Increased blood flow in new and remodeled vessels
Continued leakage of plasma proteins may contribute to edema
Fibroblast activation and collagen deposition around the inflammatory focus
Progressive fibrosis can distort normal tissue architecture and impair organ function

Thus, chronic inflammation often combines ongoing injury with ongoing healing.

Cellular events in chronic inflammation

1. Macrophages

Macrophages are the central cells in chronic inflammation. They arise mainly from circulating monocytes that enter tissues and differentiate into macrophages.

They have two broad functional patterns:

Classically activated macrophages (M1)
Activated by microbial products and cytokines such as IFN-gamma. They kill microbes and produce inflammatory mediators, reactive oxygen species, nitric oxide, proteases, TNF, IL-1, and chemokines. They can cause tissue injury.
Alternatively activated macrophages (M2)
Activated by IL-4 and IL-13. They promote repair by stimulating angiogenesis, fibroblast activation, collagen deposition, and fibrosis.

2. Lymphocytes

T lymphocytes and macrophages activate each other, sustaining chronic inflammation:

Th1 cells produce IFN-gamma, activating macrophages.
Th17 cells produce IL-17 and recruit additional leukocytes, especially neutrophils.
Macrophages produce cytokines such as TNF, IL-1, IL-6, and chemokines that recruit and activate more leukocytes.
B cells may differentiate into plasma cells that produce antibodies.

3. Plasma cells

Plasma cells secrete antibodies directed against persistent microbes, foreign antigens, or self-antigens in autoimmune disease.

4. Eosinophils and mast cells

Eosinophils are prominent in parasitic infections and IgE-mediated allergic disorders.
Mast cells release mediators such as histamine and cytokines and may contribute to persistent inflammation.

5. Granulomatous inflammation

A special form of chronic inflammation in which activated macrophages become epithelioid cells, often with multinucleated giant cells, and aggregate with lymphocytes to form a granuloma. It is typical of tuberculosis, some fungal infections, foreign-body reactions, and diseases such as sarcoidosis.

Acute versus chronic inflammation

Feature	Acute inflammation	Chronic inflammation
Onset	Rapid, minutes to hours	Slow or persistent
Duration	Hours to days	Weeks to years
Main stimuli	Infection, trauma, necrosis, acute immune reactions	Persistent infection, autoimmunity, prolonged toxic exposure, unresolved acute inflammation
Predominant cells	Neutrophils	Macrophages, lymphocytes, plasma cells
Main vascular response	Vasodilation, increased permeability, exudation, edema	Persistent endothelial activation, angiogenesis, remodeling
Tissue injury	Often limited and reversible	Often progressive due to persistent agent and inflammatory cells
Repair	Resolution is common if injury is removed	Fibrosis and scarring are common
Typical outcome	Resolution, abscess, scar, or chronicity	Fibrosis, tissue remodeling, organ dysfunction; sometimes granuloma formation

A recent pathology overview similarly describes acute inflammation as rapid and neutrophil-predominant, while chronic inflammation is longer-lasting and dominated by monocytes/macrophages and lymphocytes, as summarized in this NCBI inflammation review.

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