Inflammation is the body’s protective response to a perceived threat, such as an injury, infection, or exposure to irritants. This complex biological process is a fundamental part of the innate immune system, activating immediately following tissue damage. Its primary purpose is to localize and eliminate the damaging agent, preventing further harm. Successfully completing this defense sets the stage for tissue repair and healing.
The Initial Response and Vascular Changes
The initial phase begins with the rapid release of chemical messengers by damaged cells and resident immune cells, such as mast cells, present in the injured tissue. These messengers, including substances like histamine and prostaglandins, act directly on the local blood vessels surrounding the injury site. Histamine is one of the first mediators released, triggering changes in the microvasculature.
This chemical signaling causes the small arteries feeding the injured area to widen (vasodilation), which increases blood flow. This surge of warm blood produces the physical signs of redness (rubor) and heat (calor). Simultaneously, chemical mediators increase the permeability of the blood vessel walls by causing the lining cells to contract. This widening allows fluid, proteins, and immune cells to leak out of the bloodstream and into the surrounding tissue.
The leakage of protein-rich fluid (exudate) into the extravascular space results in noticeable swelling (tumor). This edema serves a functional purpose, as the fluid dilutes toxins or irritating substances present at the injury site. Furthermore, the fluid carries plasma proteins, such as components of the clotting and complement systems, which help wall off the area and flag pathogens for destruction.
Cellular Recruitment and Phagocytosis
Following the initial vascular response, the next stage involves the directed migration of specialized white blood cells from the bloodstream to the site of tissue damage. The chemical messengers released earlier create a concentration gradient that guides immune cells toward the injury through chemotaxis. The first line of cellular defense to arrive in large numbers, typically within the first few hours, is the neutrophil.
Neutrophils are highly mobile and immediately confront and destroy invading pathogens or cellular debris. They squeeze through the gaps in the blood vessel walls and actively engulf foreign material (phagocytosis). Once internalized, the neutrophil destroys the material by releasing potent enzymes and reactive oxygen species into a phagolysosome. Neutrophils are short-lived cells, often dying after a single act of destruction, and their accumulation forms the basis of pus found at an infected site.
As the response progresses, monocytes begin to arrive from the circulation, following the same chemotactic signals. Once they exit the bloodstream and enter the tissue, these monocytes transform into macrophages. Macrophages are slower to mobilize but are more robust and longer-lived than neutrophils, taking over the role of clearing the remains of the initial battle. They phagocytose dead neutrophils, damaged host cells, and remaining pathogens, ensuring the area is clean before healing can begin.
Resolution or Progression to Chronic State
The process of acute inflammation is designed to be self-limiting, moving toward a definitive conclusion once the threat has been neutralized. The ideal outcome is complete resolution, which occurs when the inciting agent is eliminated and the damaged tissue is capable of full repair. In this scenario, inflammatory chemical mediators are broken down or removed, the influx of immune cells ceases, and the fluid that caused swelling is drained away, often through the lymphatic system.
This phase requires a coordinated shutdown of defense mechanisms and the initiation of healing, returning the tissue to its normal structural and functional state. However, the inflammatory response may not always achieve swift resolution, particularly if the initial cause of the damage persists. The acute phase can progress into a prolonged, less intense, and more damaging state if the injurious agent cannot be cleared.
This failure of termination can occur if an infection is resistant, if the body is exposed to a foreign material it cannot degrade, or if there is an ongoing autoimmune reaction. When the defense mechanism fails to switch off and the inciting stimulus remains, the process transitions into a chronic inflammatory state. This shift moves the response from a protective, short-term state to a sustained condition that can lead to tissue pathology.
Characteristics of Chronic Inflammation
Chronic inflammation is defined by its duration, lasting for weeks, months, or even years, and is fundamentally different from the acute phase in its cellular composition and pathological processes. While acute inflammation is characterized by neutrophils, the chronic state involves a sustained infiltration of different cell types. The predominant cells are mononuclear cells, including lymphocytes, plasma cells, and macrophages.
Macrophages are the central players in chronic inflammation, persisting in the tissue where they attempt to clear the unresolved irritant while releasing chemical signals that sustain the response. Lymphocytes, including T and B cells, are also involved, indicating an overlap with the adaptive immune system in a prolonged defense effort. The constant activity of these cells leads to the simultaneous occurrence of tissue destruction and attempted repair.
Activated macrophages release enzymes and toxic molecules that can inadvertently destroy healthy surrounding tissue while trying to eliminate the threat. Simultaneously, the body attempts to heal the damage through processes like fibrosis (excessive formation of scar tissue) and angiogenesis (the growth of new blood vessels). This persistent cycle of injury, repair, and ongoing inflammation drives the tissue damage seen in many long-term health conditions.