Please enable JavaScript.
Coggle requires JavaScript to display documents.
INFLAMMATION (Adaptive response (Th 1 develop into cell that release…
INFLAMMATION
Adaptive response
-
Th2 control antibody mediate responses by stimulating B cells to proliferate into antibody-secreting plasma and memory cells
CD4 bearing T helper/Th cells are stimulated by different cytokines to develop into Th1/2/17 or Treg cells
-
-
induction phase= naive T cells bearing CD4/CD8 co-receptors are presented with antigen- trigger prolliferation
-
-
Acute inflammation
anaphylatoxins released at site of inflammation stimulate mast cells to release histamine, serotonin and prostaglandins- blood vessels expand and become more permeable
-
mediated by immune cells, cytokines and small molecules
-
induced by tissue damage due to trauma,noxious stimuli, microbial invasion
-
injuries includes infarction, bacterial infections, toxins and trauma
-
CELLULAR COMPONENTS
Mast cells
-
activared by IgE and complement release histamine,leukotrienes, PAF and IL-4,5,6
Neutrophils
-
release leukotrienes, prostaglandins free radicalsm IL-1, TNFL
-
Macrophages
antigen presentation, microbe killing
granuloma formation, innate inflammation, angiogensis and wound healing
-
-
antigents interact with IgE already bound to Fc receptors on surface of mast cell to induce degranulation via activation of tyrosine kinase inside the cell
-
Eosinophils
-
-
release leukotrenes, prostaglandins and interleukins
Neurons
neurogenic inflammation, release neuropeptides
-
-
IL-1
-
-
-
-
-
promotes muscle degradation, bone reasorption and cartillage degradation
-
-
Mechanism of initiation
-
-
cardinal signs include heat, redness, swelling, pain and loss of function
-
LEUKOCYTES EXTRAVASATION
Chemoattraction
IL-1, TNFL and C5a cause endothelial cells of blood vessels near site of infection to express cellular adhesion molecules
-
upon recognition and activation by pathogens, resident macrophages (affect tissue) release cytokines
Rolling adhesion
-
-
-
-
binding of PSGL-1 on leukocytes to P selectin on endothelial cells-leukocytes roll along endothelial surface
Tight adhesion
-
-
done by juxtacrine activation of integrins by chemokines and soluble factor released by endothelial cells
-
Transmigration
-
-
-
-
once in interstitial fluid leukocytes migrate along chemotactic gradient to site of injury/infection
HISTAMINE
Location
-
CNS: histamergic neurons in hypothalamus, projection into cortex, thalamus, striatum and hippocampus
-
-
Release
-
-
allergy determined by the capacity to bind IgE to specific receptor on mast cells/basophils and their capacity to release histamine in response
-
-
-
Chronic inflammation
primary immune cells are macrophage and T lymphocytes which produce cytokines, enzymes- cause damage to cells
angionesis, mononnuclear cell and fibrosis
injuries include viral infections,chronic infections, persisten injury and autoimmune diseases
-
COMPLEMENT PATHWAY
CLASSICAL PATHWAY
C1q2r2s complex splits C4 and then C2- produce C4a,C4b,C2a and C2b
-
occurs when C1q binds to IgM or IgG complexed with antigents or C1q binds directly to surface of pathogen-leads to activation of C1r
-
triggered by the activation of C1 complex: 1 molecule of C1q, 2 molecules of C1r and 2 molecules of C1s
-
-
ALTERNATIVE PATHWAY
when internal thioester of C3 reacts withOH/NH2 group - C3b is covalently bound to surface and protected from H inactuvation
-
-
-
continously activated at low levels due to spontaneous C3 hydrolysis due to breakage of internal thioester bond
complex is stabilized by factor P and then recruits more B,D and P
when alternative C3 convertase enzyme is formed on a pathogen it binds covalently to another C3bBbC3bP=C5 convertase
-
complex then recruits C6,C7,C8 and multiple C9 molecules to form membrane attack complex
-
-
VASCULAR RESPONSE
Mechanism of action
-
mediators vasodilatate and permeabilize blood veels- distribution of blood plasma from vessel into tissue space
upon contact with PAMPs. macrophages and mastocytes release vasoactive amines to remodel local vasculature
-
-
-
-
-
BRADYKININ
Synthesis
kalikrein is derived from inactive precursor prekallikrein by the action of Hageman factor (factor XII produced by liver)
kinin-kallikrein system makes bradykinin by cleavege of kininogen precurs, HMW kininogen by enzyme kallikrein
kininogen exists in high and low molecular form- produced by alteranative splicin and have no activity themselves
kinins are vasodilators, increase venular permeability
-
-