capítulo 32€¦ · fagocitosis. 21/11/2014 10 sistema de complemento figure 15.8 pathways by...
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21/11/2014
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Capítulo 32
Defensas Inespecíficas
Mecanismos de Defensa del Huésped
Mecanismos no Específicos
Primera Línea de Defensa
Segunda Línea de Defensa
Mecanismos Específicos
Tercera Línea de Defensa
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Vistazo de los Mecanismos de Defensa
La Piel
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Piel• Epidermis Queratina
• DermisHipodermis
• Panículo adiposo
Nasal cavity
Pharynx
Tongue
Epiglottis
Larynx(voice box)
EsophagusTrachea
Bronchus
Bronchioles
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Figure 15.3 The lacrimal apparatus-overview
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Segunda Línea de Defensa
Segunda Línea de Defensa
Transferrina Fiebre Interferón Complemento Inflamación Fagocitosis
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Figure 15.4 A schematic representation of hematopoiesis
Blood stem cell in bone marrow
Erythroidstem cell
Myeloidstem cell
Lymphoidstem cell
Erythrocyte Platelets Basophil Neutrophil Eosinophil Monocyte Lymphocyte
Clotting,inflammation
Inflammation Phagocytosis
Gastransportation
Innate immunity, second line of defense Adaptive immunity
Leukocytes
Red Blood Cells Transport O2 and CO2
White Blood Cells:
Neutrophils Phagocytosis
Basophiles Histamine
Eosinophils Kill parasites
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Monocytes Phagocytosis
Dendritic cells Phagocytosis
Natural killer cells Destroy target cells
T cells Cell-mediated immunity
B cells Produce antibodies
Platelets Blood clotting
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%
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Figure 15.15 One theoretical explanation for the production of fever in response to infection
Hypothalamus
Chemicals secretedby phagocytestravel in blood tohypothalamus.
Wound
Hypothalamussecretes prostaglandin,which resetshypothalamicthermostat.
Nerve impulsescause shivering,higher metabolic rate,inhibition of sweating,and vasoconstriction.
These processes increase bodytermperature to the point set bythe hypothalamic thermostat.
Figure 15.7 The actions of alpha and beta interferonsVirus infects cell.
Virus
Double-strandedRNA
IFNgene
mRNA
IFN
Infected cell
Viral replicationin cell triggerstranscription andtranslation of IFN- or IFN-,depending ontype of host cell.
Nucleus
Interferon is released,diffuses to neighboringuninfected cells, andbinds to receptors.
Timepasses Meanwhile, the
infected cell dies,releasing viruses.
Infected cellat a later time
Inactive AVP
Double-strandedviral RNA
Active AVPsTimepasses
Ribosome
mRNA
When the secondcell becomes infectedwith viruses, double-stranded RNA of thevirus activates AVP.
Active AVPs degrade mRNAand bind to ribosomes,which stops proteinsynthesis and viralreplication.
Sameneighboringcell now protectedat the later time
Binding triggerstranscriptionand translation ofinactive antiviralproteins (AVPs).
Interferon receptor
AVPgene
mRNA
Uninfectedneighboring cell
Inactive AVPs
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
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Fagocitosis
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Sistema de Complemento
Figure 15.8 Pathways by which complement is activatedClassical pathway Alternative pathway Lectin pathway
Antigen
Antibody
Complementproteins1, 2, 4
C3b
C3b
Endotoxin andglycoproteins
Factors B,D, and P
Mannose
Lectins
Complement cascade
OpsonizationInflammation
Inflammation
Membrane attackcomplex and cell lysis
Activation(C3 C3a C3b)
C5 convertasesC5 C5a C5b
La Vía Clásica de la Activación del Complemento
C3b opsoninMembraneattackcomplexes
Pathogen
Antigen
Antibody
Enzymatic C1
C1 becomesan active enzymewhen it binds toantibody-antigencomplexes.
Acts as opsonin
Causes chemotaxisof phagocytesand inflammation
Cytoplasmic membrane
C5b combines with C6, C7, C8,and several molecules of C9to form a membrane attackcomplex (MAC). A MAC drills acircular hole in the pathogen’s cytoplasmic membrane,leading to lysis ofthe cell.
This enzyme cleavesC5 into C5a and C5b.
Enzyme
C3b combineswith the remainingfragments of C2and C4 to form athird enzyme.
Acts as opsonin
Causes chemotaxisof phagocytesand inflammation
Enzyme
Fragments of C2and C4 combineto form a thirdenzyme thatsplits C3 intoC3a and C3b.
Enzyme C1splits moleculesof C2 and of C4.
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Vía Clásica de la Activación del Complemento
Respuesta Inflamatoria
Propósitos de la Inflamación
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Estimulación de la Inflamación por el Complemento
Estimulación de la Inflamación por el Complemento
Inflammatory mediators
Granulecontainingchemicals
Proceso de la Inflamación
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Capillaries
Bloodflow
Arteriole Before
Venule
Bloodflow
Dilatedcapillaries
Mediator
After
Au8mento de la Permeabilidad Capilar durante la Inflamación
Venule wallSmall amount of fluid
Small amount of fluid
Monocyte
Normal permeabilityof venule
Increased permeability of venuleduring inflammation
Interstitialspaces
More fluidand antimicrobialchemicals
Monocyte squeezingthrough interstitial space(diapedesis)
More fluid
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Emigración de los Fagocitos & Fagocitosis
[Insert Animation Inflammation: Overview, Steps.]
An overview of the events of inflammation
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