CXCR3 blockade protects against Listeria monocytogenes infection–induced fetal wastage

Chaturvedi, V. N.; Ertelt, James M.; Jiang, Tingting; Kinder, Jeremy M.; Luo, Xin; Owens, Kathryn; Jones, Helen; Way, Sing Sing

doi:10.1172/jci78578

Cited by 68 publications

(88 citation statements)

References 81 publications

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“…Interestingly, decidual stromal cells did not account for the increased production of the CXCR3 ligand CXCL9, supporting previous data where decidual stromal cells fail to upregulate CXCL9 and CXCL10 upon inflammatory stimuli (Nancy et al, 2012). In contrast, infiltrating macrophages and neutrophils were shown to be responsible for this inflammatory chemokine production (Chaturvedi et al, 2015). The observation that isolated human decidual macrophages fail to upregulate CXCL10 upon TLR-ligation in vitro (Duriez et al, 2014) supports the idea that newly recruited monocytes, rather than "resident" or differentiated decidual macrophages, may differentiate into Th1 chemokineproducing M1 macrophages.…”

Section: A Potential Role For Decidual Macrophages In Controlling Celsupporting

confidence: 81%

“…CXCR3 ligands have been of particular interest because of their involvement in Th1-associated responses, which are incompatible with normal fetal development. For instance, CXCR3-mediated recruitment of T cells during Listeria monocytogenes infection in mice resulted in fetal loss (Chaturvedi et al, 2015). Interestingly, decidual stromal cells did not account for the increased production of the CXCR3 ligand CXCL9, supporting previous data where decidual stromal cells fail to upregulate CXCL9 and CXCL10 upon inflammatory stimuli (Nancy et al, 2012).…”

Section: A Potential Role For Decidual Macrophages In Controlling Celsupporting

confidence: 57%

“…Although decidual macrophages have been proposed to be continuously recruited from blood monocytes (Tagliani et al, 2011) a recent report suggested that a subpopulation of uterine macrophages may be of fetal origin . In mice, infiltrating rather than tissue resident macrophages seem to account for the inflammatory response during infection in the uterus (Chaturvedi et al, 2015), but also in other conditions in other organs such as experimental autoimmune encephalomyelitis and colitis (Codarri et al, 2011;Bain et al, 2013). Thus, if decidual macrophages only derive from the continuous recruitment of monocytes, a pro-inflammatory milieu may cause the differentiation of M1 rather than M2 macrophages, quickly disrupting the homeostatic decidual environment.…”

Section: Future Perspectivesmentioning

confidence: 99%

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Immune regulation at the fetal‐maternal interface with focus on decidual macrophages

Svensson‐Arvelund¹

2015

Linköping University Medical Dissertations

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A successful pregnancy requires that the maternal immune system adapts to tolerate the semi-allogeneic fetal-placental unit. This adaptation mainly occurs locally, i.e. at the fetal-maternal interface, where fetal-derived tissues come into close contact with maternal cells in the uterine endometrium (called decidua during pregnancy). decidual macrophages preferentially secreted the monocyte-and Treg cell-associated chemokines CCL2 and CCL18, while Th1-, Th2-and Th17-related chemokines were produced at low levels. These results suggest that decidual macrophages contribute to create the unique decidual cell composition and a tolerogenic immune environment that is compatible with fetal development. Further, by comparing decidual macrophages with different in vitro macrophage subsets, we showed that M-CSF and

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Section: A Potential Role For Decidual Macrophages In Controlling Celsupporting

confidence: 81%

Section: A Potential Role For Decidual Macrophages In Controlling Celsupporting

confidence: 57%

Section: Future Perspectivesmentioning

confidence: 99%

See 1 more Smart Citation

Immune regulation at the fetal‐maternal interface with focus on decidual macrophages

Svensson‐Arvelund¹

2015

Linköping University Medical Dissertations

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“…It has been reported that the activation of CXCR3 signaling may impair maternal-fetal tolerance and predispose to spontaneous preterm labor [64] and Listeria monocytogenes-induced fetal death [120]. Also, there is an association between a fetal CXCR3 polymorphism (rs2280964) and spontaneous preterm birth [odds ratio: 0.52; 95% confidence interval (CI): 0.32-0.86] [64].…”

Section: A Role For Cxcr3 Cxcl9 and Cxcl10 In Preterm Labormentioning

confidence: 99%

“…In an intra-peritoneal lipopolysaccharide model of spontaneous preterm birth, CXCR3-deficient mice have shown a decrease in interleukin (IL)-6 and CCL2 (also known as MCP-1) concentrations in the amniotic fluid compared to wild-type mice [64]. In addition, mice that receive a CXCR3 blocking agent or are CXCR3-deficient were protected against Listeria monocytogenes-induced fetal death [120]. This effect is potentially mediated by a reduction in the expression of CXCL9 by innate immune cells and/or a diminished influx of fetal-specific CD8 + T cells into the maternal-fetal interface [120,121].…”

Section: A Role For Cxcr3 Cxcl9 and Cxcl10 In Preterm Labormentioning

confidence: 99%

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

Maymon

Romero

Bhatti

et al. 2018

Journal of Perinatal Medicine

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Objective: The objective of this study is to determine whether the amniotic fluid (AF) concentration of soluble CXCR3 and its ligands CXCL9 and CXCL10 changes in patients whose placentas show evidence of chronic chorioamnionitis or other placental lesions consistent with maternal anti-fetal rejection. Methods: This retrospective case-control study included 425 women with (1) preterm delivery (n = 92); (2) term in labor (n = 68); and (3) term not in labor (n = 265). Amniotic fluid CXCR3, CXCL9 and CXCL10 concentrations were determined by ELISA. Results: (1) Amniotic fluid concentrations of CXCR3 and its ligands CXCL9 and CXCL10 are higher in patients with preterm labor and maternal anti-fetal rejection lesions than in those without these lesions [CXCR3: preterm labor and delivery with maternal anti-fetal rejection placental lesions (median, 17.24 ng/mL; IQR, 6.79-26.68) vs. preterm labor and delivery without these placental lesions (median 8.79 ng/mL; IQR, 4.98-14.7; P = 0.028)]; (2) patients with preterm labor and chronic chorioamnionitis had higher AF concentrations of CXCL9 and CXCL10, but not CXCR3, than those without this lesion [CXCR3: preterm labor with chronic chorioamnionitis (median, 17.02 ng/mL; IQR, 5.57-26.68) vs. preterm labor without chronic chorioamnionitis (median, 10.37 ng/mL; IQR 5.01-17.81; P = 0.283)]; (3) patients with preterm labor had a significantly higher AF concentration of CXCR3 than those in labor at term regardless of the presence or absence of placental lesions. Conclusion: Our findings support a role for maternal antifetal rejection in a subset of patients with preterm labor.

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BCG-trained innate immunity leads to fetal growth restriction by altering immune cell profile in the mouse developing placenta

Dang

Souchet

Moresi

et al. 2021

Journal of Leukocyte Biology

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Trained immunity is a new concept illustrating that innate immune cells are able to undergo a long‐term metabolic and epigenetic reprogramming after infection or vaccination, thus displaying either a pro‐ or an anti‐inflammatory phenotype during a sequential unrelated challenge. Innate immune cells such as natural killer (NK) cells and macrophages constitute a large part of the decidual leukocyte population at the maternal–fetal interface, playing an important role in placental development and as such in fetal growth and development. In this study, we hypothesized that training the innate immune cells before pregnancy could have an impact on pregnancy. To test this hypothesis, we used CBA/J x DBA/2 mouse model to investigate pregnancy outcomes and leukocyte population at the maternal–fetal interface. Although we were not able to show a beneficial effect of LPS‐tolerogenic training on fetal resorption, Bacillus Calmette–Guérin (BCG) training, known to prime innate immune cells to be proinflammatory, led to fetal growth restriction, without aggravating the fetal resorption rate. We also found that BCG training led to less NK cells and macrophages at the maternal–fetal interface at the early stage of placentation (E9.5), associated with a down‐regulation of Ccr3 and Lif mRNA expression. This induced altered leucocyte population profile can be an explanation for the subsequent fetal growth restriction. These data suggest that preconceptional infections‐induced trained immunity could influence pregnancy outcomes.

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CXCR3 blockade protects against Listeria monocytogenes infection–induced fetal wastage

Cited by 68 publications

References 81 publications

Immune regulation at the fetal‐maternal interface with focus on decidual macrophages

Immune regulation at the fetal‐maternal interface with focus on decidual macrophages

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

BCG-trained innate immunity leads to fetal growth restriction by altering immune cell profile in the mouse developing placenta

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