Expression of IL-33 Receptor Is Significantly Up-Regulated in B Cells During Pregnancy and in the Acute Phase of Preterm Birth in Mice

Valeff, Natalin Jimena; Juriol, Lorena; Quadrana, Florencia; Muzzio, Damián Oscar; Zygmunt, Marek; Quiroga, María Florencia; Ventimiglia, Maria; Jensen, Federico

doi:10.3389/fimmu.2020.00446

Cited by 11 publications

(6 citation statements)

References 69 publications

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“…The spleen has a wide range of immunologic functions and plays key roles in the initiation of adaptive immunity [ 6 ]. Interleukin-33 (IL-33) participates in innate and adaptive immunity, and the IL-33 receptor is upregulated in splenic B cells during normal gestation in mice [ 7 ]. Our previous studies demonstrate that interferon-stimulated genes (ISGs), progesterone (P4) receptor, P4-induced blocking factor, tumor necrosis factor β, interleukin-2 (IL-2), IL-5, IL-6, IL-10, cyclooxygenase 2, aldo-keto reductase family 1, member B1, melatonin receptor 1 (MT1), gonadotropin-releasing hormone (GnRH) and its receptor are upregulated.…”

Section: Introductionmentioning

confidence: 99%

Changes in Expression of Complement Components in the Ovine Spleen during Early Pregnancy

Yang

Wang

et al. 2021

Animals

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During early gestation in humans, complement regulation is essential for normal fetal growth. It is supposed that a complement pathway participates in maternal splenic immune regulation at the early stage of gestation in ewes. The aim of this study was to analyze the effects of early pregnancy on the expression of complement components in the maternal spleen of ewes. In this study, ovine spleens were sampled on day 16 of nonpregnancy, and days 13, 16 and 25 of gestation. RT-qPCR, Western blot and immunohistochemical analysis were used to detect the changes in expression of complement components in the ovine maternal spleens. Our results reveal that C1q was upregulated during early gestation, C1r, C1s, C2, C3 and C5b increased at day 25 of gestation and C4a and C9 peaked at days 13 and 16 of gestation. In addition, C3 protein was located in the capsule, trabeculae and splenic cords. In conclusion, our results show for the first time that there was modification in the expression of complement components in the ovine spleen at the early stage of gestation, and complement pathways may participate in modulating splenic immune responses at the early stage of gestation.

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Section: Introductionmentioning

confidence: 99%

Changes in Expression of Complement Components in the Ovine Spleen during Early Pregnancy

Yang

Wang

et al. 2021

Animals

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“…To address the infection related PTL, several mouse models have been developed using bacteria directly ( E. coli ) or LPS, the toxic component on the surface of gram‐negative bacteria. LPS induces PTL and preterm birth (PTB) 41–48 …”

Section: Discussionmentioning

confidence: 99%

“…In particular, M1 macrophages produce proinflammatory cytokines LPS induces PTL and preterm birth (PTB). [41][42][43][44][45][46][47][48] Treatment of mice with LPS is widely used to mimic human PTL. Thus, in this study, we used bacterial LPS to induce PTL in an established model that mimics infection; whether this also replicates other inflammatory events that lead to PTL remains to be investigated.…”

Section: Smc-cm Induce Macrophage Function Through Cxcl12/cxcr4 Signa...mentioning

confidence: 99%

Myometrial‐derived CXCL12 promotes lipopolysaccharide induced preterm labour by regulating macrophage migration, polarization and function in mice

Zhang

Mamillapalli

Habata

et al. 2022

J Cellular Molecular Medi

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Preterm birth is a major contributor to neonatal mortality and morbidity. Infection results in elevation of inflammation‐related cytokines followed by infiltration of immune cells into gestational tissue. CXCL12 levels are elevated in preterm birth indicating it may have a role in preterm labour (PTL); however, the pathophysiological correlations between CXCL12/CXCR4 signalling and premature labour are poorly understood. In this study, PTL was induced using lipopolysaccharide (LPS) in a murine model. LPS induced CXCL12 RNA and protein levels significantly and specifically in myometrium compared with controls (3‐fold and 3.5‐fold respectively). Highest levels were found just before the start of labour. LPS also enhanced the infiltration of neutrophils, macrophages and T cells, and induced macrophage M1 polarization. In vitro studies showed that condition medium from LPS‐treated primary smooth muscle cells (SMC) induced macrophage migration, M1 polarization and upregulated inflammation‐related cytokines such as interleukin (IL)‐1, IL‐6 and tumor necrosis factor alpha (TNF‐α). AMD3100 treatment in pregnant mice led to a significant decrease in the rate of PTL (70%), prolonged pregnancy duration and suppressed macrophage infiltration into gestation tissue by 2.5‐fold. Further, in‐vitro treatment of SMC by AMD3100 suppressed the macrophage migration, decreased polarization and downregulated IL‐1, IL‐6 and TNF‐α expression. LPS treatment in pregnant mice induced PTL by increasing myometrial CXCL12, which recruits immune cells that in turn produce inflammation‐related cytokines. These effects stimulated by LPS were completely reversed by AMD3100 through blocking of CXCL12/CXCR4 signalling. Thus, the CXCL12/CXCR4 axis presents an excellent target for preventing infection and inflammation‐related PTL.

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“…When IL-33 is increased and released as a DAMP during pregnancy, ST2 + B1 B cells expand and play a significant role in maintaining a type 2 anti-inflammatory immune response. This prevents preterm birth, 60 potentially through secretion of the anti-inflammatory molecule active progesterone-induced blocking factor 1 (PIBF1). 61 These studies suggest that IL-33 targets ST2 + immune cell populations during pregnancy to promote tolerance and establish and maintain local homeostasis between the mother and fetus.…”

Section: Il-33 and Homeostasismentioning

confidence: 99%

The Reparative Roles of IL-33

Saba

Turnquist

2023

Transplantation

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When discovered in the early 2000s, interleukin-33 (IL-33) was characterized as a potent driver of type 2 immunity and implicated in parasite clearance, as well as asthma, allergy, and lung fibrosis. Yet research in other models has since revealed that IL-33 is a highly pleiotropic molecule with diverse functions. These activities are supported by elusive release mechanisms and diverse expression of the IL-33 receptor, STimulation 2 (ST2), on both immune and stromal cells. Interestingly, IL-33 also supports type 1 immune responses during viral and tumor immunity and after allogeneic hematopoietic stem cell transplantation. Yet the IL-33–ST2 axis is also critical to the establishment of systemic homeostasis and tissue repair and regeneration. Despite these recent findings, the mechanisms by which IL-33 governs the balance between immunity and homeostasis or can support both effective repair and pathogenic fibrosis are poorly understood. As such, ongoing research is trying to understand the potential reparative and regulatory versus pro-inflammatory and pro-fibrotic roles for IL-33 in transplantation. This review provides an overview of the emerging regenerative role of IL-33 in organ homeostasis and tissue repair as it relates to transplantation immunology. It also outlines the known impacts of IL-33 in commonly transplanted solid organs and covers the envisioned roles for IL-33 in ischemia-reperfusion injury, rejection, and tolerance. Finally, we give a comprehensive summary of its effects on different cell populations involved in these processes, including ST2+ regulatory T cells, innate lymphoid cell type 2, as well as significant myeloid cell populations.

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Expression of IL-33 Receptor Is Significantly Up-Regulated in B Cells During Pregnancy and in the Acute Phase of Preterm Birth in Mice

Cited by 11 publications

References 69 publications

Changes in Expression of Complement Components in the Ovine Spleen during Early Pregnancy

Changes in Expression of Complement Components in the Ovine Spleen during Early Pregnancy

Myometrial‐derived CXCL12 promotes lipopolysaccharide induced preterm labour by regulating macrophage migration, polarization and function in mice

The Reparative Roles of IL-33

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