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Infection and Immunity, April 2004, p. 1866-1873, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.1866-1873.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Effect of Escherichia coli and Lactobacillus rhamnosus on Macrophage Inflammatory Protein 3{alpha}, Tumor Necrosis Factor Alpha, and Transforming Growth Factor ß Release by Polarized Rat Uterine Epithelial Cells in Culture

Mardi A. Crane-Godreau* and Charles R. Wira

Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire, 03756-0001

Received 19 May 2003/ Returned for modification 9 July 2003/ Accepted 12 January 2004

Entry of bacteria from the vagina into the uterus raises the question of uterine epithelial cell (UEC) signaling in response to the presence of bacteria. Our model system helps to define microbially elicited UEC basolateral cytokine release, important in regulating underlying stromal immune cell protection. UECs from adult rats were grown in cell culture inserts to establish a confluent polarized monolayer as was determined by transepithelial resistance (TER). Polarized epithelial cell cultures were treated apically with live or heat-killed Escherichia coli or Lactobacillus rhamnosus prior to collection of basolateral media after 24 h of incubation. Coculture of polarized UECs with live E. coli had no effect on epithelial cell TER. In response to exposure to live E. coli, epithelial cell basolateral release of macrophage inflammatory protein 3{alpha} (MIP3{alpha}) and tumor necrosis factor alpha (TNF-{alpha}) increased at a time when basolateral release of biologically active transforming growth factor ß (TGF-ß) decreased. Incubation of UECs with heat-killed E. coli resulted in an increased basolateral release of MIP3{alpha} and TNF-{alpha}, without affecting TER or TGF-ß. In contrast to E. coli, live or heat-killed L. rhamnosus had no effect on TER or cytokine release. These studies indicate that polarized rat UECs respond to gram-negative E. coli by releasing the cytokines MIP3{alpha} and TNF-{alpha}, signals important to both the innate and adaptive immune systems. These findings suggest that UEC responses to bacteria are selective and important in initiating and regulating immune protection in the female reproductive tract.

* Corresponding author. Mailing address: Department of Physiology, Dartmouth Medical School, Borwell Building, 1 Medical Center Dr., Lebanon, NH 03756. Phone: (603) 650-7733. Fax: (603) 650-6130. E-mail: Mardi.A.Crane{at}Dartmouth.edu.

Editor: S. H. E. Kaufmann

Infection and Immunity, April 2004, p. 1866-1873, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.1866-1873.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Soboll, G., Shen, L., Wira, C. R. (2006). Expression of Toll-Like Receptors (TLR) and Responsiveness to TLR Agonists by Polarized Mouse Uterine Epithelial Cells in Culture. Biol. Reprod. 75: 131-139 [Abstract] [Full Text]  
  • Crane-Godreau, M. A., Wira, C. R. (2005). Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture. Infect. Immun. 73: 4231-4237 [Abstract] [Full Text]  
  • Crane-Godreau, M. A., Wira, C. R. (2005). CCL20/Macrophage Inflammatory Protein 3{alpha} and Tumor Necrosis Factor Alpha Production by Primary Uterine Epithelial Cells in Response to Treatment with Lipopolysaccharide or Pam3Cys. Infect. Immun. 73: 476-484 [Abstract] [Full Text]  


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