What is the role of a Chemical Mediator within Inflammation?
what is the role of chemical mediators in the process of acute inflammation?
Answers:
LOL, i actually made a table of this for an exam this week. I did this on word - taken from Robbin's Basic Pathology. Effects are heading with the cytokines (chemical mediators) underneath as bullet points. These are released by the host cells in sundry stages of acute inflammation. If you actually want to properly understand it read Robbins. I also thought id copy and cement the flow diagram I made for acute inflammation.
Enjoy
Effects of inflammation and their major mediators
Vasodilation
Prostaglandins
Nitric oxide
↑ Vascular permeability (i.e. blood vessels walls become more permeable forming exudate hence the reddishness of inflammation)
Vasoactive amines (histamine, serotonin)
C3a and C5a (indirectly)
Bradykinin
Leukotrienes C4, D4 & E4
Platelet activating factor
Chemotaxis (of leukocytes) and leukocyte activation
C5a
Leukotriene B4
Bacterial products
Chemokines e.g. IL-8
Fever
IL-1, IL-6, TNF
Prostaglandins
Pain
Prostaglandins
Bradykinin
Tissue overexploit
Neutrophil and macrophage lysosomal enzymes
Oxygen metabolites
Nitric oxides
Events in acute inflammation
1.Inflammatory stimulus
2.Release of chemical mediators from plasma or connective tissue cells (table)
3.Vascular change: alterations in vessel calibre leading to increased blood flow (vasodilation) secondary to arteriolar and capillary bed dilation and structural change resulting that permit plasma proteins to leave the circulation i.e. increased vascular permeability resulting in exudate of protein rich extravascular fluid (tissue oedema)
4.Leukocyte extravasation from blood – margination (accumulation of leukocytes along vascular endothelial surface) → Endothelial activation, increasing the expression of selectins and selectin ligands → leukocyte rolling, facilitate by relatively loose selectin binding to carbohydrate ligands → firm adhesion to endothelium, facilitated by chemokine-induced changes in integrin affinity for endothelial ligands → transmigration between endothelial cell utilising PECAM-1 interactions → migrate toward chemoattractants released from a source of injury
5.Leukocyte activation – e.g. resulting in degranulation and secretion of lysosomal enzymes and generation of oxidative burst via DAG-induced activation of protein kinase C
6.Phagocytosis, killing and loss of face of offending agent. Source(s): I adapted it from Robbins basic pathology 7th edition (though there is an 8th edition out)
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Answers:
LOL, i actually made a table of this for an exam this week. I did this on word - taken from Robbin's Basic Pathology. Effects are heading with the cytokines (chemical mediators) underneath as bullet points. These are released by the host cells in sundry stages of acute inflammation. If you actually want to properly understand it read Robbins. I also thought id copy and cement the flow diagram I made for acute inflammation.
Enjoy
Effects of inflammation and their major mediators
Vasodilation
Prostaglandins
Nitric oxide
↑ Vascular permeability (i.e. blood vessels walls become more permeable forming exudate hence the reddishness of inflammation)
Vasoactive amines (histamine, serotonin)
C3a and C5a (indirectly)
Bradykinin
Leukotrienes C4, D4 & E4
Platelet activating factor
Chemotaxis (of leukocytes) and leukocyte activation
C5a
Leukotriene B4
Bacterial products
Chemokines e.g. IL-8
Fever
IL-1, IL-6, TNF
Prostaglandins
Pain
Prostaglandins
Bradykinin
Tissue overexploit
Neutrophil and macrophage lysosomal enzymes
Oxygen metabolites
Nitric oxides
Events in acute inflammation
1.Inflammatory stimulus
2.Release of chemical mediators from plasma or connective tissue cells (table)
3.Vascular change: alterations in vessel calibre leading to increased blood flow (vasodilation) secondary to arteriolar and capillary bed dilation and structural change resulting that permit plasma proteins to leave the circulation i.e. increased vascular permeability resulting in exudate of protein rich extravascular fluid (tissue oedema)
4.Leukocyte extravasation from blood – margination (accumulation of leukocytes along vascular endothelial surface) → Endothelial activation, increasing the expression of selectins and selectin ligands → leukocyte rolling, facilitate by relatively loose selectin binding to carbohydrate ligands → firm adhesion to endothelium, facilitated by chemokine-induced changes in integrin affinity for endothelial ligands → transmigration between endothelial cell utilising PECAM-1 interactions → migrate toward chemoattractants released from a source of injury
5.Leukocyte activation – e.g. resulting in degranulation and secretion of lysosomal enzymes and generation of oxidative burst via DAG-induced activation of protein kinase C
6.Phagocytosis, killing and loss of face of offending agent. Source(s): I adapted it from Robbins basic pathology 7th edition (though there is an 8th edition out)
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