jean robert
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A college freshman is scheduled for tonsilloadenoidectomy to manage chronic tonsillar abscesses that have been refractory to antibiotic therapy. The procedure is completed uneventfully and the area is packed with surgical gauze to minimize bleeding .The patient is discharged to recover as an outpatient, and intructed to return to the physician s office for removal of the surgical packing within week. The patient is brought to the emergency department of the hospital after 2 days, however, suffering from high fever,hypotension, and diffuse erythematous rash that is desquamating over the palms of his hands.The pathogenesis for the causative agent in this case is similar to the pathogenesis of gram negative sepsis. Which of the following mediators would be found in higher concentration in the serum of this patient than in one suffering from gram negative sepsis?
a) Interferon alpha
b) IL-1
c) IL-2
d) IL-4
e) IL-6
f) Tumor necrosis factor-alpha
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| lakshya_0_7
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TSST......IL-2
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| taipei817
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IL-1
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| Tiff
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B. IL-1
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| lakshya_0_7
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well they have asked which one will be higher in this case than in gram negative sepsis..IL-2 is unique to TSST.....so the ans should be IL-2.......IL-1 will be high in both TSST and sepsis......
whats the answer jean?
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| GoodGirl
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Which one would be higher ???  
TNF is has a key role in gram- sepsis... so NO for answer
IL 1 could be , but not sure. Has role in both, but in which one is higher.Don't know.
IL 2 , gosh, have no idea about this one, right now.
IL 4, NOT, bc class switches to IgE.
IL 6 , in G negative sepsis, LPS are poorly antigenic, they induce very little protective Ab. So that might mean little IL 6.
In G positive case, superantigens stimulates macrophages, resulting in outpour of cytokines like above mentioned IL1, TNF, and IL 6.
So going for answer : e, IL-6.
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| jean robert
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lakshya_0_7 wrote:
TSST......IL-2
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| GoodGirl
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Do you have an explanation?
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| lakshya_0_7
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the mechanism of TSST- being a superantigen it causes the variable region of TCR to interact directly with MHC-2 and stimulates the T- cells to release massive amounts of IL-2 and macrophages to release IL-1 n TNF...
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| jean robert
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EXPLANATION
This patient is suffering from Toxic Shock Syndrome, which resulted from growth of Staph. aureus in the surgical packing associated with his tonsilloadenoidectomy.
S. aureus produces an exotoxin, TSST-1, which acts as a superantigen, cross-linking the T cell receptors and MHC II antigens of unrelated T lymphocytes and Macrophages (in the absence of antigen recognition) causing their polyclonal stimulation and the production of dangerous amounts of their cytokines. The cytokines that are overproduced during superantigen pathogenesis are
(From Macrophages)
a) IL-1
b) IL-6 .
c) TNF alpha
(From T helper Lymphocyte )
d) IL-2
e) Interferon GAMMA
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| jean robert
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The pathogenesis of endotoxin shock (gram negative sepsis) results from the DIRECT stimulation of macrophages because of the binding of bacterial Lipopolysaccharide (endotoxin) to the endotoxin receptor (CD 14) and would only involve T helper lymphocyte stimulation as a SECONDARY effect.
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| jean robert
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Take home message:
A patient suffering from superantigen pathogenesis will have HIGHER levels of cytokines from T helper lymphocytes (IL-2 and Interferon Gamma) than will a patient suffering from gram negative sepsis.
Both forms of pathogenesis will cause elevation of the macrophage cytokines,IL-1,IL-6, and TNF-alpha.
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