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Acute Immune Response, Inflammatory Cells migrate into tissues -thru venules mostly (PMNs early-6-24 hrs-neutrophils) (mononuclear after 24-48hr-monocytes) ->release inflam. mediators->DOLOR(pain) Leukocyte activation Activation Causes-microbes, cytokines from WBCs, antigen-AB complexes, cell necrosis products Pathways-DAG->inc. cytosolic Ca++->active Phospholipase A2 Response-arachidonic acid metabolites -activate oxidative burst (DAG-stimulated) -degranulation, secretion of lysosomal enzs (DAG-stimulated) -secretion of cytokines -modulate leukocyte adh. molecs.-increase LFA-1 affinity -priming, MB-Lectin (MBL) binds to mannose- containing carbs on bacs/viruses MBL in complex w/ MASP-1, MASP-2 (like C1 complex)-serine proteases MBL binds to pathogen surface-> ->MASP-2 activated, cleaves C4, C2 like classical C3 convertase Cleave C3 C3b-coat antigen surface-opsonin bind B, D cleaves to C3bBb->make more C3b -amplifies C3b on surface (like alt. pathway) C3b bound by CR1 on phagos (still need C5a to ingest) C3b+C3b convertase=C5 convertase C2b or Bb part converts C5 to C5a, C5b C3a, C4a, C5a-local inflamm. response, inc. vasc. perm->leakage of Igs, complements -inc PMN, macs, and lymphocyte migration C5a->mast cells->histamine, Inflammatory Cells migrate into tissues -thru venules mostly (PMNs early-6-24 hrs-neutrophils) (mononuclear after 24-48hr-monocytes) ->release inflam. mediators->DOLOR(pain) Leukocyte activation Phagocytosis 1. Recognition/Attachment- -mannose, scavenger receptors -enhance by opsonization (C3b) 2. Engulfment-enhanced by complements 3. Killing and Degradation -O2-dependent mechs mostly -HMP shunt increases->inc. NADPH -NADPH oxidase->superoxide (chronic granulomatous dz-NADPH oxidase def) -Myeloperoxidase (in neutro. granules) -MPO+H2O2+Cl-=>bactericidal -O2-independent-elastase release- -contain inflammation -Bactericidal Perm. Increasing protein (BPI), Macrophages release Cytokines, Chemokines Include Lipid Mediators - PGs, LTs, PAF Then Cytokines, Chemokines, CD59(protectin)-prevents MAC complex from forming at the C8 to C9 stage -on host cell membranes Paroxysmal Nocturnal Hemoglobinuria Cd59 and DAF fail to function -DAF not linked to memb by GPI ->intravascular RBC lysis by C, Vasodilation, Inc. vasc. perm. in venules mostly ->RUBOR, CALOR, TUMOR(edema) Cellular Rxn Inflammatory Cells migrate into tissues -thru venules mostly (PMNs early-6-24 hrs-neutrophils) (mononuclear after 24-48hr-monocytes) ->release inflam. mediators->DOLOR(pain) Leukocyte activation, Inflammatory Cells migrate into tissues -thru venules mostly (PMNs early-6-24 hrs-neutrophils) (mononuclear after 24-48hr-monocytes) ->release inflam. mediators->DOLOR(pain) Leukocyte activation Due to Upregulation of adhesion molecules WBC adheres to endoth, extravasation Exudation steps: Margination-line up on endoth Transmigration across endoth (diapedesis) Migration-up chemotactic gradient, Eventual Outcome of Acute Inflammation: Complete resolution Abscess formation Scar-heal w/ fibrous tissue replacement Chronic Inflammation -usually a mixture of acute, chronic, healing Histopathology Acute-short duration -edema, more PMNs, margination Chronic-longer duration, mononuc cells -proliferation of small blood vessels, Macrophages release Cytokines, Chemokines To Vessel Vasodilation, Inc. vasc. perm. in venules mostly ->RUBOR, CALOR, TUMOR(edema), Increase vasc perm, chemotaxis, opsonization 3 pathways to cleave C3:Classical, Alt, MB-lectin -Vasc-C3a, C5a->anaphylatoxins -WBC adhesion-C5a -Phagocytosis-C3b-great opsonin -Membrane attack complex (MAC) C5-9 -drill holes in bac. walls -Larger chunk of zymogen is serine protease Classical Pathway C1q binds to pathogen surface via: 1. C1q binds to surface of some bacs 2. C1q binds to C-reactive protein -CRP binds to bac. polysacchs 3. C1q binds to antigen-AB complexes ->Conform change in C1r ->cleave/activate C1s C1s cleaves C4 then C2 (C4b, C2b made) -C4b attaches to pathogen surface -binds C2, which is cleaved by C1s C4b2b=C3 convertase