Mol. Hum. Reprod. Advance Access originally published online on October 22, 2007
Molecular Human Reproduction 2007 13(12):863-868; doi:10.1093/molehr/gam074
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Regulation of surfactant protein D in the mouse female reproductive tract in vivo
1Department of Medicine, National Jewish Medical and Research Center, Denver, CO 80206, USA 2Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, IA 52242, USA 3Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA 30303, USA 4Department of Obstetrics and Gynecology, University of Iowa College of Medicine, Iowa City, IA 52242, USA 5Department of Microbiology and Immunology, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL 60515, USA
6 Correspondence address. Tel: +1-303-398-1749; Fax: +1-303-270-2249; E-mail: oberleyr{at}njc.org
Surfactant protein D (SP-D) plays a role in innate immunity in the lung and is expressed at many other mucosal surfaces throughout the human body. In this study, we show that SP-D mRNA and protein are present in the murine female reproductive tract; i.e. in the vagina, cervix, uterus and oviduct. SP-D protein is primarily localized to epithelial cells lining the genital tract and is also present in secretory material within the lumen of the uterus and cervix. The levels of SP-D mRNA in the uterus vary by a factor of 10 during the estrous cycle with peak levels present at estrus and the lowest levels at diestrus. In contrast, SP-D mRNA levels in the lung do not change during the estrous cycle. Since SP-D is an innate host defense protein present in the mouse reproductive tract, we studied the influence of infection on SP-D levels in vivo. We found that Chlamydia muridarum infection caused an increase in the SP-D protein content of reproductive tract epithelial cells. These data are suggestive that SP-D may play a role in innate immunity in the female reproductive tract in vivo.
Key words: female reproductive tract/infection/mouse/regulation/SP-D
Submitted on September 13, 2007; accepted on September 21, 2007.