TNF-α release:
A Can be effectively blocked by anti–TNF-α antibodies to halt systemic inflammatory response syndrome (SIRS)
B Does not have any beneficial effects in the early phases of the inflammatory response
C Is primarily from leukocytes
D Promotes polymorphonuclear (PMN) cell adherence and further cytokine release
E Is always deleterious
Comments
Tumor necrosis factor-α is a vital component of the early response, especially locally at the site of injury; it is released when the biologically active anaphylatoxins C3a and C5a are stimulated by the humoral system. Infusion of low doses of TNF-α in rats simulates the septic response with resulting fever, hypotension, fatigue, and anorexia. TNF-α promotes adherence of PMN cells to endothelium, production of prostaglandins by fibroblasts, and neutrophil activation and stimulates the release of multiple other cytokines from lymphocytes. TNF-α becomes deleterious when the proinflammatory
stimuli become unchecked and leads to cellular damage and multi–organ system failure. TNF-α is released by macrophages and natural killer cells, not leukocytes. Trials involving anti–TNF-α
antibodies (NORASEPT, INTERSEPT) have not shown statistically significant improvement in patient outcomes
Answer-D
A Can be effectively blocked by anti–TNF-α antibodies to halt systemic inflammatory response syndrome (SIRS)
B Does not have any beneficial effects in the early phases of the inflammatory response
C Is primarily from leukocytes
D Promotes polymorphonuclear (PMN) cell adherence and further cytokine release
E Is always deleterious
Comments
Tumor necrosis factor-α is a vital component of the early response, especially locally at the site of injury; it is released when the biologically active anaphylatoxins C3a and C5a are stimulated by the humoral system. Infusion of low doses of TNF-α in rats simulates the septic response with resulting fever, hypotension, fatigue, and anorexia. TNF-α promotes adherence of PMN cells to endothelium, production of prostaglandins by fibroblasts, and neutrophil activation and stimulates the release of multiple other cytokines from lymphocytes. TNF-α becomes deleterious when the proinflammatory
stimuli become unchecked and leads to cellular damage and multi–organ system failure. TNF-α is released by macrophages and natural killer cells, not leukocytes. Trials involving anti–TNF-α
antibodies (NORASEPT, INTERSEPT) have not shown statistically significant improvement in patient outcomes
Answer-D
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