This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Amarante-Paffaro, A Articles by Bevilacqua, E Search for Related Content PubMed PubMed Citation Articles by Amarante-Paffaro, A Articles by Bevilacqua, E

Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells

Department of Histology and Embryology and ¹ Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

Correspondence should be addressed to E Bevilacqua; Email: bevilacq{at}usp.br

Trophoblast giant cells are active phagocytes during implantation and post-implantation. Phagocytosis decreases during placental maturation as the phagocytic function of nutrition is gradually replaced by the direct uptake of nutrients by the labyrinth zone trophoblast. We hypothesize that, after placental maturation, trophoblast cells maintain phagocytic functions for purposes other than nutrition. This study employs histological techniques to examine the ability of trophoblast cells to phagocytose microorganisms (yeast or bacteria)–in vivo in females receiving thioglycolate to activate macrophages and in vitro in the presence of phagocytic promoters such as interferon- and complement component C3. Placental trophoblast cells from the second half of gestation show basal phagocytosis that can be dramatically up-regulated by these promoters when microorganisms are inoculated into pregnant animals or introduced into culture systems. Stimulated trophoblast cells phagocytosed organisms more rapidly and in greater numbers than non-stimulated trophoblast exposed to the same numbers of organisms. Taken together, our results indicate that trophoblast cells do not lose their ability to phagocytose during the placentation process, which may imply that trophoblast cells participate in embryonic and fetal innate immune defense through elimination of microorganisms present at the maternal–fetal interface.

This article has been cited by other articles:

				J. Zhu, X. Wu, S. Goel, N. M. Gowda, S. Kumar, G. Krishnegowda, G. Mishra, R. Weinberg, G. Li, M. Gaestel, et al. MAPK-activated Protein Kinase 2 Differentially Regulates Plasmodium falciparum Glycosylphosphatidylinositol-induced Production of Tumor Necrosis Factor-{alpha} and Interleukin-12 in Macrophages J. Biol. Chem., June 5, 2009; 284(23): 15750 - 15761. [Abstract] [Full Text] [PDF]

				N. Liu, A.T. Kaplan, J. Low, L. Nguyen, G.Y. Liu, O. Equils, and M. Hewison Vitamin D Induces Innate Antibacterial Responses in Human Trophoblasts via an Intracrine Pathway Biol Reprod, March 1, 2009; 80(3): 398 - 406. [Abstract] [Full Text] [PDF]

				A. Le Monnier, N. Autret, O. F. Join-Lambert, F. Jaubert, A. Charbit, P. Berche, and S. Kayal ActA Is Required for Crossing of the Fetoplacental Barrier by Listeria monocytogenes Infect. Immun., February 1, 2007; 75(2): 950 - 957. [Abstract] [Full Text] [PDF]

				H. R. Petty, A. L. Kindzelskii, J. Espinoza, and R. Romero Trophoblast contact deactivates human neutrophils. J. Immunol., March 1, 2006; 176(5): 3205 - 3214. [Abstract] [Full Text] [PDF]

				A. Le Monnier, O. F. Join-Lambert, F. Jaubert, P. Berche, and S. Kayal Invasion of the Placenta during Murine Listeriosis Infect. Immun., January 1, 2006; 74(1): 663 - 672. [Abstract] [Full Text] [PDF]

				J. Zhu, G. Krishnegowda, and D. C. Gowda Induction of Proinflammatory Responses in Macrophages by the Glycosylphosphatidylinositols of Plasmodium falciparum: THE REQUIREMENT OF EXTRACELLULAR SIGNAL-REGULATED KINASE, p38, c-Jun N-TERMINAL KINASE AND NF-{kappa}B PATHWAYS FOR THE EXPRESSION OF PROINFLAMMATORY CYTOKINES AND NITRIC OXIDE J. Biol. Chem., March 4, 2005; 280(9): 8617 - 8627. [Abstract] [Full Text] [PDF]