> <marlac...@hotmail.com> wrote in message
>
[quoted text clipped - 4 lines]
> > drip mucus?
> > -Marla Comm
Rhinosinusitis derived Staphylococcal enterotoxin B possibly
associates with pathogenesis of ulcerative colitis.
Yang PC, Liu T, Wang BQ, Zhang TY, An ZY, Zheng PY, Tian DF.
Department of Pathology and Molecular Medicine, McMaster University,
Hamilton, ON, Canada. yangp@mcmaster.ca
BACKGROUND: During clinical practice, we noticed that some patients
with both ulcerative colitis (UC) and chronic rhinosinusitis (CRS)
showed amelioration of UC after treatment of CRS. This study was
designed to identify a possible association between CRS and UC.
METHODS: Thirty-two patients with both CRS and UC received treatment
with functional endoscopic sinus surgery (FESS) for CRS. Clinical
symptom scores for CRS and UC, as well as serum levels of anti-
Staphylococcal enterotoxin B (SEB) were evaluated at week 0 and week
12. Sinus wash fluid SEB content was measured with enzyme-linked
immunosorbent assay (ELISA). The surgically removed tissues were
cultured to identify growth of Staphylococcus. aureus (S. aureus).
Immunohistochemistry was employed to identify anti-SEB positive cells
in the colonic mucosa. Colonic biopsies were obtained and incubated
with SEB. Mast cell activation in the colonic mucosa in response to
incubation with SEB was observed with electron microscopy and
immunoassay. RESULTS: The clinical symptom scores of CRS and UC severe
scores (UCSS) were significantly reduced in the UC-CRS patients after
FESS. The number of cultured S. aureus colonies from the surgically
removed sinus mucosa significantly correlated with the decrease in
UCSS. High levels of SEB were detected in the sinus wash fluids of the
patients with UC-CRS. Histamine and tryptase release was significantly
higher in the culture supernate in the patients with UC-CRS than the
patients with UC-only and normal controls. Anti-SEB positive cells
were located in the colonic mucosa. CONCLUSION: The pathogenesis of UC
in some patients may be associated with their pre-existing CRS by a
mechanism of swallowing sinusitis-derived SEB. We speculate that SEB
initiates inappropriate immune reactions and inflammation in the
colonic mucosa that further progresses to UC.
PMID: 16144553 [PubMed - indexed for MEDLINE]
Michael - 04 Feb 2008 15:17 GMT
> > <marlac...@hotmail.com> wrote in message
>
[quoted text clipped - 4 lines]
> > > drip mucus?
> > > -Marla Comm
"Staphylococcal Enterotoxins
The SEs, SEA through SEI except SEF, are produced by various coagulase-
producing staphylococci. Although known for many years as the cause of
SFP, they have only recently been shown to be superantigenic, and in
particular SEB and SEC have been implicated in nonmenstrual TSS. All
SEs thus far characterized have the immunomodulatory properties of
superantigens, and several have been demonstrated to be lethal in the
rabbit model of TSS. Molecular studies of the SEs have shown that
superantigenicity and the capacity for causing SFP are determined by
separate parts of the protein (2, 67). Several reviews of SEs are
available, and other sections of this review provide background on
toxin genetics and TSS pathogenesis.
All toxins thus far identified share a number of important properties
(10, 12, 24, 26), including (i) an ability to cause emesis and
gastroenteritis in a primate model, (ii) superantigenicity, (iii)
intermediate resistance to heat and pepsin digestion, and (iv)
tertiary structural similarity (where known) including an
intramolecular disulfide bond. "
Note point (iii) intermediate resistance to ... pepsin digestion,
from:-
Exotoxins of Staphylococcus aureus
Martin M. Dinges, Paul M. Orwin, and Patrick M. Schlievert*
Department of Microbiology, University of Minnesota School of
Medicine, Minneapolis, Minnesota 55455
Clin Microbiol Rev. 2000 January; 13(1): 16-34.
Copyright (c) 2000, American Society for Microbiology
Full text at:-
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10627489