The inflammatory response is a fundamental biological process initiated by the body in response to harmful stimuli, such as pathogens, damaged cells, or irritants. This protective mechanism serves to localize and eliminate the injurious agent, clear out damaged tissue components, and begin the process of repair. It is a non-specific and immediate defense system, forming a part of the innate immune response.
The Visible Signs of Inflammation
Inflammation presents with several recognizable signs. Redness (rubor) is caused by the dilation of small blood vessels in the injured area, increasing blood flow to the site. This increased blood flow also leads to heat (calor), most noticeable in peripheral body parts like the skin.
Swelling (tumor or edema) results from fluid accumulation outside blood vessels in the affected tissue. Pain (dolor) is experienced due to tissue distortion from swelling and the release of chemical mediators that stimulate nerve endings. Loss of function (functio laesa) can occur due to pain inhibiting movement or severe swelling.
The Body’s Immediate Internal Changes
Following tissue injury or infection, rapid vascular changes initiate the inflammatory response. Small blood vessels, particularly arterioles, undergo vasodilation (widening). This widening increases blood flow to the injured site, contributing to the visible signs of redness and heat.
Simultaneously, venule permeability increases significantly. This increased vascular permeability makes blood vessels “leaky,” allowing fluid, plasma proteins, and immune cells to exit the bloodstream and accumulate in the injured tissue, causing swelling. This fluid accumulation is known as exudation.
Damaged cells and resident immune cells, like mast cells, release chemical mediators that orchestrate these vascular changes. Histamine, released by mast cells, causes blood vessels to dilate and capillaries to become more permeable. Prostaglandins, synthesized at the site of tissue damage, also contribute to vasodilation and increase pain sensitivity. Other mediators like bradykinin and leukotrienes further enhance vascular permeability and smooth muscle contraction.
How Immune Cells Act During Inflammation
Following initial vascular changes, immune cells (primarily neutrophils and later macrophages) are recruited to the injury site. This movement from the bloodstream to the affected tissue is a multi-step process called leukocyte extravasation or diapedesis:
Margination: Leukocytes move closer to vessel walls as blood flow slows.
Rolling: Leukocytes transiently attach to the endothelial lining of blood vessels and then detach, appearing to “roll” along the surface. This loose attachment is mediated by selectins.
Tight Adhesion: Chemokines activate rolling leukocytes, causing integrin molecules to firmly bind to complementary receptors on endothelial cells.
Diapedesis (Transmigration): Leukocytes squeeze through vessel walls into the injured tissue.
Neutrophils are the first responders, arriving within hours. They perform phagocytosis, engulfing pathogens and cellular debris. Macrophages, differentiating from later-arriving monocytes, continue phagocytosis, clearing cellular debris and initiating tissue repair.
From Inflammation to Healing
Inflammation is a transient process facilitating the body’s healing. As the injurious agent is eliminated and debris cleared, the inflammatory response enters a resolution phase. During this phase, inflammatory mediators are neutralized or degraded, vascular permeability normalizes, and leukocyte emigration ceases. Remaining neutrophils undergo programmed cell death (apoptosis) and are cleared by macrophages.
Tissue repair has two main outcomes: regeneration or fibrosis. Regeneration involves replacing damaged tissue with new cells of the original type, restoring normal structure and function. This outcome is possible when the tissue framework remains intact and cells can divide.
Alternatively, if tissue damage is extensive or the original tissue cannot regenerate, repair occurs through fibrosis (scarring). This involves replacing damaged tissue with connective tissue, forming a scar. While functional capabilities may be reduced, this process provides structural integrity. If acute inflammation fails to resolve, it can become chronic, leading to persistent immune cell activation and potential ongoing tissue damage.