24.8
Inflammation
Overview
In response to tissue injury and infection, mast cells initiate inflammation. Mast cells release chemicals that increase the permeability of…
Acute inflammation is the body's immune response to a potentially harmful situation, such as an infection.
At the site of injury, the initial stimulus triggers a complex cascade of numerous chemicals. For example, mast cells release histamines and generate prostaglandins to promote vasodilation.
The expansion of these local blood vessels allows more blood flow to the injured tissue, resulting in redness and warmth.
Vascular permeability also increases. Due to the contraction of endothelial cells, gaps form, causing exudate, protein rich fluid to leak into the affected area. That produces swelling and pain.
Concurrently, neutrophils, the phagocytic white blood cells, respond to chemicals called leucocytosis inducing factors by increasing their number in blood. In a process known as margination, they bind tightly at the gaps and then flatten out and squeeze through the capillaries during diapedesis.
The neutrophils follow the chemicals trail towards the site along with additional cells such as monocytes and lymphocytes that are also attracted via chemotaxis.
Some of the proteins that leaked out of the capillaries then help with clotting, forming a fibrin mesh that isolates the area and acts as a scaffold for repair to start the healing process.
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Q1: What triggers the inflammatory response in the body?
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.
Q2: How do mast cells initiate inflammation at an injury 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.
Q3: What is the role of neutrophils during acute inflammation?
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.
Q4: How does vascular permeability contribute to inflammation symptoms?
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.
Q5: What happens when inflammatory regulation fails?
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.
Q6: How do platelets support wound healing during inflammation?
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.
Q7: What is the relationship between inflammation and atherosclerosis development?
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.