- Published on
Pathology – Innate Immunity
innate immunity
Epithelial interfaces
Epithelial surfaces serve as the primary entry points for infections into the body. A continuous epithelial layer establishes a physical barrier to infection. The acidic pH of the skin and the presence of fatty acids in sebum suppress microbial proliferation.
The gastrointestinal system contains gastric acid, pancreatic enzymes, mucosal IgA, and normal colonic flora that function to inhibit the onset of infection. The respiratory tract produces mucus to capture organisms, while cilia facilitate their passage to the throat for swallowing. Continuous urination along the urinary system inhibits microbial adherence to the urothelium.
Phagocytes
Organisms penetrating epithelial surfaces meet tissue macrophages that identify infections and recruit neutrophils to the location
Macrophages and neutrophils are phagocytic cells that engulf bacteria through phagocytosis, forming a phagosome
The phagosome then merges with cytoplasmic lysosomes, which harbor enzymes and reactive oxygen species that eliminate the bacterium. Phagocytes identify species by pattern recognition receptors, such as mannose receptors, Toll-like receptors, and Nod-like receptors.
Acute-phase proteins
Cytokines generated by phagocytes prompt the liver to swiftly manufacture and discharge acute phase proteins. Mannose-binding lectin identifies microbial surface sugars and undergoes a conformational alteration, enabling it to attach to the protein MASP, thereby forming a complex that activates the complement system.
C-reactive protein attaches to the phosphorylcholine components of microbial lipopolysaccharides, facilitating their phagocytosis by macrophages.
Complement
• A assemblage of circulating proteins that aid the immune system in eliminating pathogens.
• Can be initiated by antibodies attached to a microbe (traditional pathway), automatically activated by bacteria devoid of a regulatory protein found on host cells (alternative pathway), or by mannose-binding protein (lectin pathway). A sequential cascade results in the formation of C3 convertase, an enzyme that cleaves many C3 molecules into C3b.
• Microbes coated with C3b are eliminated through phagocytosis or the membrane assault complex, a polymer of terminal complement components that creates pores in the microbial cell membrane.
• The complement system is stringently regulated to avert unregulated activation. Decay-accelerating factor impedes the binding of C3b to cellular surfaces, while membrane cofactor protein degrades C3b.
innate immunity
Epithelial interfaces
Epithelial surfaces serve as the primary entry points for infections into the body. A continuous epithelial layer establishes a physical barrier to infection. The acidic pH of the skin and the presence of fatty acids in sebum suppress microbial proliferation.
The gastrointestinal system contains gastric acid, pancreatic enzymes, mucosal IgA, and normal colonic flora that function to inhibit the onset of infection. The respiratory tract produces mucus to capture organisms, while cilia facilitate their passage to the throat for swallowing. Continuous urination along the urinary system inhibits microbial adherence to the urothelium.
Phagocytes
Organisms penetrating epithelial surfaces meet tissue macrophages that identify infections and recruit neutrophils to the location
Macrophages and neutrophils are phagocytic cells that engulf bacteria through phagocytosis, forming a phagosome
The phagosome then merges with cytoplasmic lysosomes, which harbor enzymes and reactive oxygen species that eliminate the bacterium. Phagocytes identify species by pattern recognition receptors, such as mannose receptors, Toll-like receptors, and Nod-like receptors.
Acute-phase proteins
Cytokines generated by phagocytes prompt the liver to swiftly manufacture and discharge acute phase proteins. Mannose-binding lectin identifies microbial surface sugars and undergoes a conformational alteration, enabling it to attach to the protein MASP, thereby forming a complex that activates the complement system.
C-reactive protein attaches to the phosphorylcholine components of microbial lipopolysaccharides, facilitating their phagocytosis by macrophages.
Complement
• A assemblage of circulating proteins that aid the immune system in eliminating pathogens.
• Can be initiated by antibodies attached to a microbe (traditional pathway), automatically activated by bacteria devoid of a regulatory protein found on host cells (alternative pathway), or by mannose-binding protein (lectin pathway). A sequential cascade results in the formation of C3 convertase, an enzyme that cleaves many C3 molecules into C3b.
• Microbes coated with C3b are eliminated through phagocytosis or the membrane assault complex, a polymer of terminal complement components that creates pores in the microbial cell membrane.
• The complement system is stringently regulated to avert unregulated activation. Decay-accelerating factor impedes the binding of C3b to cellular surfaces, while membrane cofactor protein degrades C3b.
0 Comments
