Endometriosis, Prostaglandins & Bacterial Growth

by endosolu

It has been a long term view of mine that bacteria has a role to play endometriosis… the following study although difficult to read if you are not into science suggests that higher bacteria counts in menstrual blood of those with endometriosis stimulates growth of endometrial cells… this is one of the reasons as part of our endometriosis treatment program we cleanse the gut and bowel.

Results

The clinical profiles of women with and without endometriosis are shown in Table I. There were no significant differences in the mean age or other clinical characteristics between women with and without endometriosis. The distribution of peritoneal lesions in women with revised-ASRM stage I–II endometriosis and stage III–IV endometriosis are shown in Table I. We found a predominance of mixed peritoneal lesions in both stage I–II and stage III–IV endometriosis. Two cases in stage III–IV endometriosis had a chocolate cyst only without any coexistent peritoneal lesions.

Extract

Our findings have some clinical and biological implications. First, higher PGE2 levels in PF after menstrual reflux may be involved in the growth of endometriosis, because PGE2 acts as a regulator of COX2/P450 aromatase activation resulting in tissue accumulation of estrogen (Attar and Bulun, 2006; Bulun, 2009). As a master molecule, PGE2 has a multi-functional role including the regulation of cell proliferation, anti-apoptosis, immune suppression and angiogenesis during the development of endometriosis (Wu et al., 2010). Second, the role of PGE2 in bacterial growth such as E. coli by its direct and indirect effect may partly explain the mechanistic basis of E. coli contamination of menstrual blood in women with endometriosis as we reported recently (Khan et al., 2010).

In fact, we demonstrated that a higher colony formation of E. coli in menstrual blood with consequent higher endotoxin (LPS) levels in MF and PF of women with endometriosis significantly stimulated the growth of eutopic and ectopic endometrial cells via LPS/TLR 4 cascade (Khan et al., 2010). When we tried to link our current findings with our previous experiment on LPS/TLR 4 system, we found a parallel increase of both LPS and PGE2 in the menstrual blood collected from women with endometriosis. LPS is one of the mediators stimulating overexpression of COX2 with consequent production of different PGs including PGE2. LPS-mediated COX2 expression and PGE2 production have already been reported (Takenaka et al., 2010; Liu et al., 2011). If we consider the inflammatory condition of the intrauterine or pelvic environment, we can collectively make an association between LPS/TLR 4/COX2 and PGE2 with the growth of endometrial cells as well as growth of bacteria.

After similar ascending migration of bacteria from the vaginal cavity into the uterine cavity of all women, differences in PGE2 levels of MF between women with and without endometriosis may be involved in higher colony formation of E. coli in the menstrual blood of women with endometriosis. Further studies are needed to investigate sub-clinical infection within the vaginal cavity and to clarify our current findings.

for more info…

http://www.medscape.com/viewarticle/775401_3

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