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Immunity

Immunity. References: Roitt’s Essential Immunology, 11 th edition, 2006 Robbins Basic Pathology 7 th edition. Kumar, Cotran, Robbins editors. 2003. External barriers against infection a. Skin – impermeable to most infectious agents

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Immunity

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  1. Immunity References: Roitt’s Essential Immunology, 11th edition, 2006 Robbins Basic Pathology 7th edition. Kumar, Cotran, Robbins editors. 2003.

  2. External barriers against infection a • Skin – impermeable to most infectious agents • Sweat and sebaceous secretions - inhibitory effects of lactic acids and fatty acids • Membranes – mucus: adhesive • Ciliary movement • Coughing and sneezing • Secreted body fluids – bactericidal • Gastric juice – acid • Semen – spermine and zinc • Milk - lactoperoxidase • Tears, nasal secretions, saliva – lysozyme

  3. External barriers against infection a • Normal bacterial flora – microbial antagonism • Suppresses growth of many pathogenic bacteria • Competition for essential nutrients • Production of inhibitory substances • Colicins – a class of bactericidins • Antibiotics effects: disturbs protective commensals

  4. Once entry through external barriers occurs a • Two main defensive operations • Bactericidal enzymes – destructive effects of soluble chemical factors • Phagocytosis • Neutrophils and macrophages are dedicated “professional” phagocytes • Complement facilitates phagocytosis • Complement can mediate an acute inflammatory reaction • Humoral mechanisms provide a second defensive strategy • Extracellular killing

  5. PRR: Pattern Recognition Receptor Phagocyte Pathogen TLR 1) Recognizes the PAMP • 2) Produces Transcription Factors • IRF (Interferon Regulatory Factor • NFқB • Cell membrane – PAMP • Gram(+)ve peptidoglycan • Mycobacterial lipoarabinomannan • Lipoproteins • Yeast zymosan • Gram(-)ve LPS • Flagellin • Others • 3) Synthesis of: • Inflammatory Cytokines • Interferon ß PAMP = Pathogen Associated Molecular Pattern TLR = Toll Like Receptor Phagocytosis: recognition of pathogen a

  6. Phagocyte Phagocyte Phagocyte 1. Chemotaxis 2. Adherence through PAMP recognition 3. Membrane activation through “danger” signal Duration: 1 minute Phagocyte Phagocyte 8. Release of degradation products Phagocyte 4. Initiation of phagocytosis 5. Phagosome formation 6. Fusion 7. Killing and digestion Phagocytic process a

  7. Phagocyte killing mechanisms a • Oxygen intermediates: reactive oxygen • Respiratory burst phenomenon • Nitrogen intermediates: nitric oxide • Oxygen independent mechanisms: preformed antimicrobials • Cathepsin G, low molecular wt defensins, high molecular wt cationic proteins, bactericidal permeability increasing protein (BPI) – cause damage to microbial membranes • Lysozyme – splits mucopeptide in bacterial cell wall • Lactoferrin – complex with iron • Proteolytic enzymes, variety of other hydrolytic enzymes – digestion of killed organisms

  8. 1. Complement facilitates phagocytosis Complement system a,b

  9. 2. Complement can mediate an acute inflammatory reaction Complement system a,b

  10. Mast Cell Complement activation Ca 2+ Phospholipase A2 Arachidonic Acid • Granule release: • Histamine – vasodilation,  capillary permeability, chemokinesis, bronchconstriction • Proteoglycan – binds granule proteases • Neutral proteases, ß glucosamidase – activates C3, splits off glucosamine • ECF, NCF – Eosinophil chemotaxis, Neutrophil chemotaxis • Platelet Activating Factor – mediator release • IL3, IL4, IL5, IL6 / GM-CSF / TNF – multiple including macrophage activation, trigger acute phase proteins, etc. • Lipoxygenase Pathway • LTC4, LTD4 (SRS-A), LTB4 – vasoactive, bronchoconstriction, chemotaxis • Cyclo-oxygenase Pathway • Prostaglandins, Thromboxanes – affect bronchial muscle, platelet aggregation, and vasodilation Complement & inflammation: role of mast cell a

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