Inflammation

Tissue injury and infection are the primary triggers of acute inflammation. Mast cells, located in areas contacting the exterior like skin and airways, are the first to respond. They detect stimuli including microbial antigens, complement activation products, and damage-associated molecular patterns. Upon activation, mast cells release chemical signals that initiate the inflammatory cascade and attract immune cells to the affected site.

Mast cells release histamine and prostaglandins that increase capillary permeability through vasodilation, expanding local blood vessels. This allows increased blood flow to injured tissue, causing redness and warmth. Mast cells also release chemical signals that attract phagocytic neutrophils and other immune cells via chemotaxis. These chemicals create a bidirectional communication network with macrophages, dendritic cells, and lymphocytes to coordinate the immune response.

Neutrophils are phagocytic white blood cells that exit the bloodstream through diapedesis, squeezing through widened capillary junctions. They follow chemical trails to infection sites and capture pathogens using neutrophil extracellular traps made of DNA fibers and proteins. Neutrophils engulf invaders through phagocytosis or release antimicrobial components via degranulation. Though short-lived, they are later replaced by macrophages and lymphocytes in later inflammatory phases.

Increased vascular permeability occurs when mast cell chemicals cause endothelial cells to contract, creating gaps in capillary walls. Protein-rich fluid called exudate leaks into affected tissue, producing swelling and pain. This fluid also contains clotting proteins that form a fibrin mesh, isolating the injury site and providing a scaffold for tissue repair. The combination of increased blood flow and fluid accumulation creates the characteristic redness, warmth, and swelling of inflammation.

Improper regulation of inflammation can lead to chronic inflammatory diseases such as atherosclerosis, stroke, heart disorders, and diabetes. In atherosclerosis, initial vessel injury triggers acute inflammation that becomes chronic, recruiting excessive immune cells. Foam cells accumulate, forming fatty streaks and hardened plaques that narrow arteries and reduce blood flow. Chronic inflammation accounts for three of five deaths worldwide, making proper immune regulation crucial for bodily function.

Platelets, cell fragments derived from bone marrow megakaryocytes, follow mast cell chemical signals to injured tissue. They aggregate in response to blood vessel damage, patching disrupted areas and sealing wounds. Platelets release growth factors that induce wound healing and can engulf pathogens directly. Along with the fibrin mesh formed by leaked clotting proteins, platelets create a protective barrier that initiates tissue repair and prevents further infection.

Atherosclerosis begins with small vessel injury that triggers acute inflammation and vasodilation. Neutrophils and monocytes move beneath the vessel lining via diapedesis. Monocytes differentiate into macrophages that engulf low-density lipoprotein through phagocytosis, becoming foam cells. When inflammatory signals persist instead of resolving, chronic inflammation develops, accumulating foam cells into fatty streaks and eventually hardened plaques that narrow arteries and impair blood flow.