Acute and Chronic inflammation Flashcards
mediator of acute inflammation
TLRs Arachidonic acid metabolites Mast cells complement Hageman Factor (factor XII)
acute inflammation is characterized by
presence of edema and neutrophils
arises in response to infection or tissue necrosis
immediate response with limited specificity (innate immunity)
Role of TLRs in acute inflammation
on cells of innate immune system - Macs and DCs
activated by PAMPs
TLR activation leads to upregulation of NFkB that activates immune response genes and leads to production of immune mediators
TLR also on cells of adaptive immunity - lymphocytes
CD14
TLR on macrophages
recognizes LPS on gram neg bacteria
Role of Arachidonic acid in Acute inflammation
converted to prostanglandins and Leukotrienes
prostaglandins - mediate vasodilation and increase vascular permeability
LTB attracts and activates neutrophils
LTC, LTD and LTE - slow reacting substances of anaphylaxis - mediates vasoconstriction, bronchospasm, and increased vascular permeability
Role of Mast cells in Acute inflammation
in connective tissue
activated by trauma, complement, cross linking by IgE
immediate response - releases histamine which mediates vasodilation of arterioles and increases vascular permeability
delayed response involves production of arachidonic acid metabolites particularly leukotrienes
Role of complement in acute inflammation
all pathways result in C3 convertase C3a and C5a - anaphylatoxins - trigger mast cells C5a - chemotactic for neutrophils C3b - opsonin for phagocytosis MAC - lysis microbes
role of Hageman factor in acute inflammation
produced by liver activated by exposure to subendothelial or tissue collagen which activates coagulation and fibrnolytic systems complement Kinin system
Kinin system
cleaves high molecular weight kininogen to bradykinin, which mediates vasodilation and increased vascular permeability (similar to histamine) as well as pain
Rubor and Calor
due to vasodilation leads to increased blood flow
occurs via relaxation of arteriolar smooth muscle, key mediators are histamine, prostaglandins and bradykinin
Tumor
due to leakage of fluid from postcapillary venules intto interstitial space - called exudate
key mediators - histamine, causes endothelial cell contraction and tissue damage resulting in endothelial cell disruption
Dolor
Bradykinin and PGE sensitizes sensory nerve endings
Fever
pyrogens - LPS from bacteria- cause macs to release IL-1 and TNF which increase cyclooxygenase activity in perivascular cells of the hypothalmus
Increased PGE raises temperature set point
when do Macrophages predominate?
after neutrophils and peak around 2-3 days after inflammation begins
from monocytes in the blood
Manage resolution and healing (IL10 and TGfb), continued acute inflammation (seen as pus formation, IL-8 from macs attract more neutrophils), abcess (acute inflammation surrounded by fibrosis) and chronic inflammation (macs present antigen to CD4 T cells)
Chronic inflammation
characterized by presence of lymphocytes and plasma cells
delayed response but more specific (adaptive immunity)
stimuli include - persistent infection, infection with viruses, mycobacteria, parasites and fungi, autoimmune dis, foreign material and some cancers