IL-2 regulates SEB induced toxic shock syndrome in BALB/c mice.

IL-2 regulates SEB induced toxic shock syndrome in BALB/c mice.

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BACKGROUND:Toxic Shock Cyclist Accessories - Triathlon - Accessories Syndrome (TSS) is characterized by fever, rash, hypotension, constitutional symptoms, and multi-organ involvement and is caused by Staphylococcus aureus enterotoxins such as Staphylococcal Enterotoxin B (SEB).SEB binds to the MHC-IIalpha chain and is recognized by the TCRbeta chain of the Vbeta8 TCR(+) T cells.The binding of SEB to Vbeta chain results in rapid activation of T cells and production of inflammatory cytokines, such as Interleukin-2 (IL-2), Interferon-gamma and Tumor Necrosis Factor-alpha which mediate TSS.Although IL2 was originally identified as the T cell growth factor and was proposed to contribute to T cell differentiation, its role in TSS remains unexplored.

METHODOLOGY/PRINCIPAL FINDINGS:Mice were injected with D-Gal (25 mg/mouse).One hour after D-Galactosamine (D-Gal) injection each mouse was injected with SEB (20 microg/mouse.Mice were then observed for 72 hrs and death was recorded at different times.We tested Interleukin-12, IFNgamma, and IL-2 deficient mice (IL-2(-/-)), but only the IL-2 deficient mice were resistant to SEB induced toxic shock syndrome.

More importantly reconstitution of IL-2 in IL-2 deficient mice restored the shock.Interestingly, SEB induced IL-2 production from T cells was dependent on p38MAPK activation in macrophages as Dip Set inhibition of it in macrophages significantly inhibited IL-2 production from T cells.CONCLUSION:This study shows the importance of IL -2 in TSS which has not been previously explored and it also shows that regulating macrophages function can regulate T cells and TSS.