Capítulo 32. Defensas Inespecíficas 21/11/2014. Mecanismos de Defensa del Huésped. Mecanismos Específicos. Mecanismos no Específicos

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1 Capítulo 32 Defensas Inespecíficas Mecanismos de Defensa del Huésped Mecanismos no Específicos Mecanismos Específicos Primera Línea de Defensa Segunda Línea de Defensa Tercera Línea de Defensa 1

2 Vistazo de los Mecanismos de Defensa La Piel 2

3 Piel Epidermis Queratina Dermis Hipodermis Panículo adiposo Nasal cavity Pharynx Tongue Epiglottis Larynx (voice box) Esophagus Trachea Bronchus Bronchioles 3

4 Figure 15.3 The lacrimal apparatus-overview 4

5 Segunda Línea de Defensa Segunda Línea de Defensa Transferrina Fiebre Interferón Complemento Inflamación Fagocitosis 5

6 Figure 15.4 A schematic representation of hematopoiesis Blood stem cell in bone marrow Erythroid stem cell Myeloid stem cell Lymphoid stem cell Erythrocyte Platelets Basophil Neutrophil Eosinophil Monocyte Lymphocyte Clotting, Inflammation inflammation Phagocytosis Gas transportation Innate immunity, second line of defense Leukocytes Adaptive immunity Red Blood Cells Transport O 2 and CO 2 White Blood Cells: Neutrophils Phagocytosis Basophiles Histamine Eosinophils Kill parasites 6

7 Monocytes Phagocytosis T cells Cell-mediated immunity Dendritic cells Phagocytosis B cells Produce antibodies Platelets Blood clotting Natural killer cells Destroy target cells Percentage of each type of white cell in a sample of 100 white blood cells Neutrophils 60 70% Basophils 0.5 1% Eosinophils 2 4% Monocytes 3 8% Lymphocytes 20 25% 7

8 Figure One theoretical explanation for the production of fever in response to infection Figure 15.7 The actions of alpha and beta interferons Virus infects cell. Hypothalamus Chemicals secreted by phagocytes travel in blood to hypothalamus. Wound Hypothalamus secretes prostaglandin, which resets hypothalamic thermostat. Nerve impulses cause shivering, higher metabolic rate, inhibition of sweating, and vasoconstriction. These processes increase body termperature to the point set by the hypothalamic thermostat. Viral replication in cell triggers transcription and translation of IFN- or IFN-, depending on type of host cell. Interferon is released, diffuses to neighboring uninfected cells, and binds to receptors. Binding triggers transcription and translation of inactive antiviral proteins (AVPs). Inactive AVPs Virus Doublestranded RNA IFN gene Nucleus mrna IFN Infected cell Interferon receptor AVP gene mrna Uninfected neighboring cell Time passes Meanwhile, the infected cell dies, releasing viruses. Infected cell at a later time When the second cell becomes infected Inactive AVP with viruses, doublestranded RNA of the Doublestranded virus activates AVP. viral RNA Active AVPs Time passes Ribosome mrna Active AVPs degrade mrna and bind to ribosomes, Same which stops protein neighboring synthesis and viral cell now protected replication. at the later time Antiviral Actions of Interferons (IFNs) Fagocitosis Fago: Del Griego, significa comer Cito: Del griego, significa célula Ingestión de microbios o partículas por la célula, llevada a cabo por fagocitos 8

9 Fagocitosis 9

10 Sistema de Complemento Figure 15.8 Pathways by which complement is activated Classical pathway Alternative pathway Lectin pathway Antigen C3b Mannose La Vía Clásica de la Activación del Complemento C3b opsonin Membrane attack complexes Cytoplasmic membrane Endotoxin and glycoproteins Lectins Complement proteins 1, 2, 4 Antibody C3b Complement cascade Factors B, D, and P C1 becomes an active enzyme when it binds to antibody-antigen complexes. Pathogen Antigen Antibody Enzymatic C1 Causes chemotaxis of phagocytes and inflammation Acts as opsonin C5b combines with C6, C7, C8, and several molecules of C9 to form a membrane attack complex (MAC). A MAC drills a circular hole in the pathogen s cytoplasmic membrane, leading to lysis of the cell. This enzyme cleaves C5 into C5a and C5b. Activation (C3 C3a C3b) C5 convertases C5 C5a C5b Opsonization Inflammation Inflammation Enzyme C1 splits molecules of C2 and of C4. Fragments of C2 and C4 combine to form a third enzyme that splits C3 into C3a and C3b. Enzyme Enzyme C3b combines with the remaining fragments of C2 and C4 to form a third enzyme. Membrane attack complex and cell lysis Causes chemotaxis of phagocytes and inflammation Acts as opsonin 10

11 Vía Clásica de la Activación del Complemento Respuesta Inflamatoria Propósitos de la Inflamación 11

12 Estimulación de la Inflamación por el Complemento Estimulación de la Inflamación por el Complemento Granule containing chemicals Inflammatory mediators Proceso de la Inflamación 12

13 Capillaries Mediator Dilated capillaries Blood flow Venule Blood flow Arteriole Before After Au8mento de la Permeabilidad Capilar durante la Inflamación Venule wall Normal permeability of venule Small amount of fluid Interstitial spaces Increased permeability of venule during inflammation More fluid and antimicrobial chemicals Monocyte Small amount of fluid Monocyte squeezing through interstitial space (diapedesis) More fluid 13

14 Emigración de los Fagocitos & Fagocitosis [Insert Animation Inflammation: Overview, Steps.] An overview of the events of inflammation 14