Chapter 6: Innate Immunity

The first line of defense comprises physical, mechanical, and biochemical barriers that prevent pathogen entry, including the skin, mucous membranes, cilia, and secreted antimicrobial substances such as defensins and collectins. The normal microbiome contributes to immunity by synthesizing essential vitamins, facilitating digestion, and outcompeting pathogenic organisms, though these resident microorganisms can become problematic when barrier integrity is compromised. The second line of defense involves the acute inflammatory response, which is initiated by tissue damage or infection and generates the characteristic signs of inflammation: erythema, warmth, edema, pain, and functional impairment. Three plasma protein systems are central to inflammation: the complement cascade promotes opsonization and bacterial lysis through complement fragments and the membrane attack complex; the coagulation cascade produces fibrin to arrest bleeding and contain infection; and the kinin system generates bradykinin, which mediates vasodilation and pain perception. Cellular participants in inflammation include mast cells that release histamine and inflammatory mediators, neutrophils and macrophages that phagocytose pathogens, dendritic cells that bridge innate and adaptive immunity, natural killer cells that destroy infected cells, and platelets that promote clotting and inflammation. Pattern recognition receptors on immune cells detect pathogen-associated molecular patterns and damage-associated molecular patterns, triggering the release of proinflammatory cytokines such as tumor necrosis factor alpha, interleukin-1, and interleukin-6, which collectively induce fever and increase circulating white blood cells. Antiinflammatory cytokines and interferons subsequently limit and resolve the inflammatory response. Acute inflammation is typically self-limiting within days, whereas chronic inflammation from persistent stimuli leads to granulomatous inflammation, exemplified by tuberculosis. The chapter then addresses wound healing across four sequential phases: hemostasis and clot formation, inflammatory cell infiltration, proliferative activity involving angiogenesis and collagen deposition, and tissue remodeling that produces mature scar tissue. Healing by primary intention occurs in sutured wounds with minimal tissue loss, while healing by secondary intention occurs in large or open wounds. Complications including wound dehiscence, aberrant scarring, and impaired healing are influenced by age, nutritional status, infection, and metabolic factors, with specific considerations for pediatric and geriatric populations.