ORIGINAL ARTICLE: Effect of Progesterone on Proinflammatory Cytokine Production by Monocytes Stimulated with Pathogens Associated with Preterm birth
Article first published online: 5 SEP 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Munksgaard
American Journal of Reproductive Immunology
Volume 60, Issue 4, pages 346–353, October 2008
How to Cite
Peltier, M. R., Tee, S. C. and Smulian, J. C. (2008), ORIGINAL ARTICLE: Effect of Progesterone on Proinflammatory Cytokine Production by Monocytes Stimulated with Pathogens Associated with Preterm birth. American Journal of Reproductive Immunology, 60: 346–353. doi: 10.1111/j.1600-0897.2008.00633.x
- Issue published online: 5 SEP 2008
- Article first published online: 5 SEP 2008
- Submitted March 27, 2008; accepted May 27, 2008.
- innate immunity;
- preterm birth;
- Ureaplasma urealyticum
Problem A number of clinical trials have demonstrated that supplemental progesterone (P4) can prevent preterm birth. Although P4 can decrease the production of mediators of inflammation by lipopolysaccharide (LPS)-stimulated macrophages, a majority of infections associated with preterm birth are due to Ureaplasma urealyticum, which does not contain LPS. Therefore, we studied whether P4 could lower the production of proinflammatory cytokines by monocytes stimulated with U. urealyticum.
Method of study Human monocytes (THP-1 cells) were treated with P4 and then stimulated with heat-killed Escherichia coli or U. urealyticum. Cytokine concentrations in the conditioned medium were then measured by ELISA and relative viability of the cells was assessed colorimetrically. The impact of P4 on interleukin (IL)-1β, tumor necrosis factor-α (TNF-α) and IL-8 production was assessed by comparing levels across different P4 dosages and organism concentrations.
Results Both organisms increased IL-1β, TNF-α and IL-8 production in a dose-dependent manner. P4 enhanced the production of IL-1β and IL-8, but inhibited TNF-α production by monocytes stimulated with either organism.
Conclusion P4 modulates cytokine production by E. coli and U. urealyticum-stimulated monocytes in a similar manner and is not strictly immunosuppressive. This suggests that P4 does not prevent preterm birth by simply suppressing bacteria-stimulated cytokine production.