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Trophoblast Contact Deactivates Human Neutrophils¹

Howard R. Petty^2,*,, Andrei L. Kindzelskii^*, Jimmy Espinoza and Roberto Romero

^* Department of Ophthalmology and Visual Sciences and Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48105; Perinatology Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892; and Hutzel Hospital, Detroit, MI 48201

Trophoblasts are fetal epithelial cells that form an interface between mother and offspring. To evaluate their anti-inflammatory capacity, we tested the hypothesis that trophoblasts deactivate neutrophils using single-cell assays. Several biophysical (Ca²⁺ and NAD(P)H oscillation frequency) and physiological (oxidant production) markers of activated neutrophils revert to a nonactivated phenotype as activated cells make contact with trophoblasts. Indistinguishable results were obtained using syncytiotrophoblasts and in experiments using trophoblasts and neutrophils from the same mother to recapitulate the semiallogeneic system. These changes suggest reduced hexose monophosphate shunt (HMS) activity. We discovered that two metabolic regulatory points, glucose transport and HMS enzyme trafficking, are affected by trophoblasts. This restriction in HMS activity deactivates neutrophils, thereby limiting oxidative DNA damage within trophoblasts.

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The JI 2006 176: 2679-2680. [Full Text]  

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