BackInnate Immunity: Nonspecific Defenses of the Host (Chapter 16) – Study Notes
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Innate Immunity: Nonspecific Defenses of the Host
Overview of Innate vs. Adaptive Immunity
The immune system protects the body from pathogens through two main strategies: innate (nonspecific) and adaptive (specific) immunity. Innate immunity provides immediate, general defense mechanisms, while adaptive immunity develops more slowly and targets specific pathogens.
Innate Immunity: Present from birth, responds rapidly to a broad range of pathogens, does not confer long-lasting immunity.
Adaptive Immunity: Develops after exposure to specific antigens, involves B and T lymphocytes, provides memory for faster future responses.
Example: Skin and mucous membranes are part of innate immunity, while antibody production is part of adaptive immunity.
First Line of Defense: Physical, Chemical, and Biological Barriers
Physical Barriers
Physical barriers prevent the entry of pathogens into the body.
Skin: Acts as a tough, impermeable barrier; shedding of skin removes microbes.
Mucous Membranes: Line the respiratory, gastrointestinal, and genitourinary tracts; mucus traps microbes.
Mechanical Actions: Cilia in the respiratory tract move mucus and trapped particles out; tears, saliva, and urine flush out microbes.
Chemical Barriers
Chemical factors inhibit or destroy pathogens.
Lysozyme: Enzyme found in tears, saliva, and mucus; breaks down bacterial cell walls.
Lactoferrin & Transferrin: Proteins that bind iron, making it unavailable to microbes.
Defensins: Small antimicrobial peptides that disrupt microbial membranes.
Acidity: Low pH of stomach (gastric juice) and skin inhibits microbial growth.
Normal Flora (Microbiota)
Normal flora are non-pathogenic microorganisms that reside on body surfaces and provide protection.
Competitive Exclusion: Normal flora outcompete pathogens for nutrients and attachment sites.
Production of Inhibitory Substances: Some normal flora produce bacteriocins or acids that inhibit pathogens.
Example: Lactobacillus in the vagina produces lactic acid, lowering pH and preventing pathogen growth.
Second Line of Defense: Cellular Components of Blood
Blood Components and Their Roles
Erythrocytes (Red Blood Cells): Transport oxygen; do not play a direct role in immunity.
Platelets: Involved in blood clotting; help prevent pathogen entry through wounds.
Leukocytes (White Blood Cells): Main cells of the immune system; some are phagocytic.
Types of Leukocytes
Neutrophils (PMNs): Most abundant; highly phagocytic; first responders to infection.
Basophils: Release histamine; involved in inflammation and allergic responses.
Eosinophils: Combat parasites; involved in allergic reactions.
Monocytes/Macrophages: Monocytes circulate in blood; become macrophages in tissues; professional phagocytes.
Dendritic Cells: Phagocytic; bridge innate and adaptive immunity by presenting antigens.
B and T Lymphocytes: Key cells of adaptive immunity; do not participate in innate immunity.
Natural Killer (NK) Cells: Destroy infected or abnormal cells by releasing cytotoxic granules.
Professional Phagocytes: Neutrophils, macrophages, and dendritic cells.
Pattern Recognition and Signaling Molecules
Toll-Like Receptors (TLRs)
Toll-like receptors are proteins on immune cells that recognize pathogen-associated molecular patterns (PAMPs) such as bacterial lipopolysaccharide or viral RNA.
Function: Detect conserved microbial structures and trigger immune responses.
Cytokines
Cytokines are small proteins released by cells that regulate immune responses.
Roles: Mediate communication between cells, promote inflammation, recruit immune cells, and regulate cell growth.
Example: Interleukin-1 (IL-1) induces fever and inflammation.
Phagocytosis
Process and Stages of Phagocytosis
Phagocytosis is the process by which certain cells ingest and destroy microbes and debris.
Chemotaxis: Phagocytes are attracted to infection sites by chemical signals.
Adherence: Phagocyte attaches to the microbe (often enhanced by opsonins such as C3b).
Ingestion: Microbe is engulfed into a phagosome.
Digestion: Phagosome fuses with lysosome to form a phagolysosome; enzymes digest the microbe.
Exocytosis: Indigestible material is expelled from the cell.
Cells Involved in Phagocytosis
Neutrophils
Macrophages
Dendritic cells
Microbial Evasion of Phagocytosis
Capsules: Streptococcus pneumoniae uses a capsule to avoid phagocytosis.
Inhibition of Phagolysosome Fusion: Mycobacterium tuberculosis prevents fusion, surviving inside phagocytes.
Survival in Phagolysosome: Some bacteria resist digestion.
Opsonization: The process by which opsonins (e.g., C3b) coat microbes, enhancing phagocytosis.
Inflammatory Response
Signs and Causes of Inflammation
Inflammation is a localized response to infection or injury, aiming to contain and eliminate pathogens and initiate tissue repair.
Signs: Redness, heat, swelling, pain, and sometimes loss of function.
Causes: Infection, tissue injury, or immune reactions.
Triggers and Steps of Inflammation
Tissue Damage: Releases chemical mediators (e.g., histamine, cytokines).
Vasodilation: Blood vessels widen, increasing blood flow (redness, heat).
Increased Vascular Permeability: Fluid and immune cells leave blood vessels (swelling).
Phagocyte Migration (Diapedesis): Neutrophils and monocytes move through vessel walls to the site (chemotaxis).
Pus Formation: Accumulation of dead cells and microbes.
Tissue Repair: Damaged tissue is replaced or healed.
Cells Involved: Neutrophils arrive first, followed by monocytes/macrophages.
Key Terms: Vasodilation (widening of blood vessels), Diapedesis (movement of cells out of blood vessels).
Fever
Fever is a systemic increase in body temperature, often in response to infection.
Mechanism: Pyrogens (e.g., IL-1) are released by phagocytes, signaling the hypothalamus to raise body temperature.
Benefits: Inhibits growth of some microbes, enhances immune responses, speeds up tissue repair.
Chemical Responses to Invading Organisms
Interferons
Interferons are cytokines produced by virus-infected cells that help protect neighboring cells from viral infection.
Types: Alpha, beta, and gamma interferons.
Induction: Produced in response to viral infection.
Effectiveness: Limit viral spread, activate immune cells.
Complement System
The complement system is a group of plasma proteins that enhance immune responses through a cascade of activation.
Activation Pathways:
Classical pathway
Alternative pathway
Lectin pathway
Consequences/Functions of Complement Activation
Function | Description | Key Complement Proteins |
|---|---|---|
Opsonization | Coating of microbes to enhance phagocytosis | C3b |
Inflammation | Attraction and activation of immune cells | C3a, C5a |
Cytolysis (Membrane Attack Complex) | Formation of pores in microbial membranes, leading to cell lysis | C5b, C6, C7, C8, C9 |
Example: C3b acts as an opsonin, C5a is a chemoattractant, and the membrane attack complex (C5b-C9) lyses bacteria.
Additional info: The complement system bridges innate and adaptive immunity and is tightly regulated to prevent host damage.