自卫机制第1部分.pptVIP

MAST CELLS Most important activator of inflammatory response Releases biochemical mediators Histamine Chemotactic factors Synthesizes other mediators Prostaglandins Leukotrienes Platelet-Activating Factor (PAF) MAJOR VASOACTIVE AMINES OF INFLAMMATION Histamine serotonin Effects: Constricts vascular smooth muscles Dilation of capillaries Retraction of endothelial cells lining capillaries Increases vascular permeability ACUTE PHASE RESPONSE Systemic changes present if inflammation is severe enough May be transient, dissipating with recovery or persistent in chronic disease Mediated by inflammation-associated cytokines Changes in concentrations of large number of plasma proteins Fever Somnolence Anorexia Changes in plasma protein synthesis Altered synthesis of endocrine hormones Hormones effected: CRH Glucagon Insulin ACTH Cortisol Catecholamines Growth Hormones TSH, Thyrpxine Aldosterone AVP ACUTE PHASE RESPONSE Major acute phase proteins (APP) C-Reactive protein (CRP) Serum amyloid A (SAA) Negative APP Albumin Transthyretin Transferrin Other positive APP Complement proteins Ferritin ?-1- antitrypsin (antiprotease) Fibrinogen Fibronectin Hempexin Haptoglobin Ceruloplasmin ACUTE PHASE PROTEINS C-REACTIVE PROTEIN Influences inflammatory tissue repair processes Recognizes some foreign pathogens Activates complement system Bonds to phagocytic cells Induces production of inflammatory cytokines Main initiator of blood coagulation Net effect may be antiinflammatory PLASMA PROTEIN SYSTEM Inflammation is mediated by 3 key plasma proteins systems Complement system Clotting system Kinin system COMPLEMENT SYSTEM The “complement cascade” (Fig 7-7) Activated by antigen-antibody reactions (classic pathway) Activated by other products especially bacterial polysaccharides [alternate (nonantibody) pathway] Produces biologically active (anaphylactic or chemotactic) fragments Produces target cell lysis Phagocytosis Increases vascular permeability CLOTTING SYSTEM Extrinsic Intrin