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Published ahead of print on October 1, 2004, doi:10.1164/rccm.200406-745OC
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American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 73-77, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200406-745OC

Original Article

Endotoxin-induced Chorioamnionitis Modulates Innate Immunity of Monocytes in Preterm Sheep

Boris W. Kramer, Machiko Ikegami, Timothy J. M. Moss, Ilias Nitsos, John P. Newnham and Alan H. Jobe

University Children's Hospital, Wuerzburg, Germany; Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio; and the School of Women's and Infants' Health, The University of Western Australia, Perth, Australia

Correspondence and requests for reprints should be addressed to Boris W. Kramer, M.D., University Children's Hospital, Josef-Schneider-Str. 2, 97080 Wuerzburg, Germany. E-mail: kramer_b{at}kinderklinik.uni-wuerzburg.de

The preterm fetus is immune naive and has immature innate immune function. Although the preterm fetus is frequently exposed to chorioamnionitis, the effects of exposure of the fetal lung to inflammation on innate immune responses are unknown. Using the fetal sheep model of chorioamnionitis, cord blood monocytes were isolated from preterm lambs 1 to 14 days after intra-amniotic endotoxin injection, cultured for approximately 16 hours, and challenged with endotoxin in vitro. Compared with monocytes from adult sheep, the preterm monocytes produced less H2O2 and interleukin-6, and toll-like receptor 4 expression was decreased. Three days after intra-amniotic endotoxin exposure, preterm monocyte responses to in vitro endotoxin challenge demonstrated decreased H2O2 and interleukin-6 production and decreased CD14 and major histocompatibility complex class II expression. Preterm monocyte responses 7 to 14 days after endotoxin tended to exceed those of adults and preterm control animals indicating augmented function. In contrast, a second intra-amniotic endotoxin injection 7 days after the initial endotoxin exposure suppressed monocyte function at 14 days. The fetal monocytes demonstrated patterns of responses consistent with endotoxin tolerance (immune paralysis) as well as maturation of function. Modulation of fetal innate immune responses by exposure to inflammation may alter subsequent immune adaptation after birth.

Key Words: endotoxin tolerance • fetal immunity • nosocomial infection • priming




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