Superantigen antagonist peptides

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Superantigen antagonist peptides

The production of superantigenic exotoxins by Gram positive bacteria underlies the pathology of toxic shock syndrome. Future treatment strategies for superantigen-mediated diseases are likely to be directed at blocking the three-way interaction between superantigen, T cell receptor and major histocompatibility class II molecule, which inititates an excessive and disordered inflammatory response...

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Superantigen antagonist blocks Th1 cytokine gene induction and lethal shock.

Bacterial superantigens trigger an excessive, Th1-cytokine response leading to toxic shock. We designed a peptide antagonist that inhibits SEB-induced expression of human genes for IL-2, IFN-gamma, and TNF-beta, cytokines that mediate shock. The peptide antagonist shows homology to a beta-strand-hinge-alpha-helix domain that is conserved structurally in superantigens produced by Staphylococcus ...

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Ethanol antagonist peptides: structural specificity without stereospecificity.

Increasing evidence suggests that ethanol damages the developing nervous system partly by disrupting the L1 cell adhesion molecule. Ethanol inhibits L1-mediated cell adhesion, and compounds that antagonize this action also prevent ethanol-induced embryotoxicity. Two such compounds are the small peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL). We showed previously that NAP and SAL antagonize ethanol...

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Activity of antimicrobial peptides and conventional antibiotics against superantigen positive Staphylococcus aureus isolated from patients with atopic dermatitis

Introduction Staphylococcus aureus causes a diverse array of diseases, ranging from relatively harmless localized skin infections to life-threatening systemic conditions. It secretes toxins directly associated with particular disease symptoms. Aim To determine the prevalence of methicillin-resistant S. aureus (MRSA) and methicillin-susceptible S. aureus (MSSA) colonization among patients with...

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ژورنال

عنوان ژورنال: Critical Care

سال: 2001

ISSN: 1364-8535

DOI: 10.1186/cc986