Summary
Highlights
Cytokines stimulate fibroblasts to proliferate and increase collagen synthesis, leading to tissue repair. Damaged blood vessels are repaired through the coagulation cascade, and chemotaxis also promotes tissue repair.
Cell-derived inflammatory mediators like cytokines and histamine recruit immune cells such as macrophages and neutrophils. These cells use special receptors to bind to and engulf pathogens, initiating the immune response.
Plasma-derived complement proteins, in conjunction with antibodies, can opsonize pathogens (coating them for easier detection by phagocytes) or create holes in bacteria, causing them to lyse. Complement proteins like C3a and C5a also act as chemoattractants and increase vascular permeability, further promoting inflammation and tissue repair.
Cell-derived arachidonic acid metabolites, such as prostaglandins (from endothelial cells, mast cells, and granulocytes) cause fever and pain, while leukotrienes (from mast cells and basophils) act as chemoattractants and increase vascular permeability, promoting inflammation.
Inflammation is characterized by five signs: rubor (redness) and calor (heat) due to dilating blood vessels, tumor (swelling) from plasma fluid and protein leakage, dolor (pain) caused by nerve firing and mechanical damage, and sometimes loss of function, especially in chronic inflammation.
If a pathogen causes an infection, the adaptive immune system is initiated. Antigen-presenting cells (like dendritic cells or macrophages) engulf pathogens, become activated, and travel to lymph nodes to activate naive B and T cells. B cells become plasma cells that secrete antibodies, and T cells become T helper or T killer cells.
Plasma cells secrete antibodies (IgM, IgG, IgA) which stimulate the inflammatory response to remove pathogens and restore the body to its normal state.