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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