Abstract
Parturition is associated with a leukocyte influx into the intrauterine tissues; however, the exact role these leukocytes play in the onset of labor remains unclear. Neutrophil infiltration of the uteroplacental tissues has been particularly associated with infection-associated preterm labor (PTL) in both women and mouse models. In this study, we investigated the role of neutrophils in a mouse model of infection-induced PTL. Intrauterine administration of LPS on day 17 of gestation resulted in a 7-fold increase in the number of decidual neutrophils compared with control mice receiving PBS (p < 0.01; n = 8–11). We hypothesized that neutrophil influx is necessary for PTL and that neutrophil depletion would abolish preterm birth. To test this hypothesis, mice were depleted of neutrophils by treatment with anti–Gr-1, anti–Ly-6G, or the appropriate IgG control Ab on day 16 of gestation prior to LPS on day 17 (n = 6–7). Successful neutrophil depletion was confirmed by flow cytometry and immunohistochemistry. Neutrophil depletion with Gr-1 resulted in reduced uterine and placental Il-1β expression (p < 0.05). Neutrophil depletion with Ly-6G reduced uterine Il-1β and Tnf-α expression (p < 0.05). However, neutrophil depletion with either Ab did not delay LPS-induced preterm birth. Collectively, these data show that decidual neutrophil infiltration is not essential for the induction of infection-induced PTL in the mouse, but that neutrophils contribute to the LPS-induced inflammatory response of the uteroplacental tissues.
Highlights
Neutrophil depletion with either Ab did not delay LPS-induced preterm birth. These data show that decidual neutrophil infiltration is not essential for the induction of infection-induced preterm labor (PTL) in the mouse, but that neutrophils contribute to the LPS-induced inflammatory response of the uteroplacental tissues
Leukocyte infiltration into the uteroplacental tissues is known to occur in association with the onset of parturition, the precise role these immune cells play, and the role they play in infection-induced preterm labor, remains unclear
We have shown that the presence of bacterial LPS, as a model of intrauterine infection, induces increased expression of the neutrophil chemokines Cxcl1, Cxcl2, and Cxcl5 in the uteroplacental tissues and a neutrophil influx into the decidua
Summary
In experiments to investigate the role of neutrophils in the induction of infection-induced PTL, Ab-based depletion was performed using either an anti–Gr-1 Ab or anti–Ly-6G Ab prior to intrauterine LPS administration. To confirm that the LPS-induced increased chemokine and Ngp expression was due to neutrophil influx into the uterus and to determine the site of recruitment of neutrophils in the uterus, we performed immunohistochemistry with an anti–Gr-1 Ab on uterine tissue collected 6 h postsurgery from mice who had received either PBS or LPS or from untreated mice on day 17 of gestation, as a comparator.
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