Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF ) Freely available
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bailey, M. T.
Right arrow Articles by Coe, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bailey, M. T.
Right arrow Articles by Coe, C. L.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Reproduction, Vol. 17, No. 7, 1704-1708, July 2002
© 2002 European Society of Human Reproduction and Embryology

Endometriosis is associated with an altered profile of intestinal microflora in female rhesus monkeys

Michael T. Bailey,1 and Christopher L. Coe

University of Wisconsin, Harlow Center for Biological Psychology, 22 N. Charter St, Madison, WI 53715, USA

BACKGROUND: The intestinal microflora provide a strong defence against intestinal pathogens, and may be altered in inflammatory conditions that impact the gut, such as endometriosis. Therefore, intestinal bacteria shed from rhesus monkeys with endometriosis were compared with age-matched healthy controls. A second study assessed the prevalence of intestinal inflammation in female monkeys to determine whether endometriosis is associated with an increased likelihood of intestinal inflammation. METHODS: Differential and selective agars were used to enumerate total and Gram-negative aerobic and facultatively anaerobic bacteria, as well as Lactobacilli, from female monkeys with or without endometriosis. In addition, the prevalence of intestinal inflammation in monkeys with or without endometriosis was determined in a retrospective analysis of necropsy reports. RESULTS: Monkeys with endometriosis had a significantly different profile of shed microflora. Endometriosis was associated with lower Lactobacilli concentrations and higher Gram-negative bacteria concentrations. Moreover, there was a higher prevalence of intestinal inflammation in monkeys with endometriosis in comparison to healthy controls. CONCLUSIONS: Endometriosis is associated with an altered profile of intestinal microflora in rhesus monkeys. Although the exact mechanisms linking endometriosis and the microflora are unknown, it is possible that the microflora were affected by endometriosis-associated intestinal inflammation.

Key words: endometriosis/intestinal microflora/Lactobacillus/rhesus monkey

1 To whom correspondence should be addressed. E-mail: mtbailey{at}students.wisc.edu


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Toxicol PatholHome page
J. M. Cline, C. E. Wood, J. D. Vidal, R. P. Tarara, E. Buse, G. F. Weinbauer, E. P. C. T. de Rijk, and E. van Esch
Selected Background Findings and Interpretation of Common Lesions in the Female Reproductive System in Macaques
Toxicol Pathol, December 1, 2008; 36(7_suppl): 142S - 163S.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
C. B. Appleyard, M. L. Cruz, E. Rivera, G. A. Hernandez, and I. Flores
Experimental Endometriosis in the Rat Is Correlated With Colonic Motor Function Alterations but Not With Bacterial Load
Reproductive Sciences, December 1, 2007; 14(8): 815 - 824.
[Abstract] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.