Placental inflammasome signaling: Protection for mother and baby

Burgener, Sabrina Sofia; Schroder, Kate

doi:10.1084/jem.20201738

Cited by 5 publications

(8 citation statements)

References 15 publications

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“…This complex catalyzes a cellular reaction that leads to the processing and maturation of two proinflammatory cytokines, the interleukin (IL)-1β and IL-18 [3,5]. Beside its proinflammatory role against immediate dangers [6], NLRP7 overexpression has been reported to function in an inflammasome-independent manner and exhibit antiinflammatory role by inhibiting IL-1β production [7,8].…”

Section: Introductionmentioning

confidence: 99%

NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Reynaud

Nahed

Lemaître

et al. 2021

Cancers

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The inflammatory gene NLRP7 is the major gene responsible for recurrent complete hydatidiform moles (CHM), an abnormal pregnancy that can develop into gestational choriocarcinoma (CC). However, the role of NLRP7 in the development and immune tolerance of CC has not been investigated. Three approaches were employed to define the role of NLRP7 in CC development: (i) a clinical study that analyzed human placenta and sera collected from women with normal pregnancies, CHM or CC; (ii) an in vitro study that investigated the impact of NLRP7 knockdown on tumor growth and organization; and (iii) an in vivo study that used two CC mouse models, including an orthotopic model. NLRP7 and circulating inflammatory cytokines were upregulated in tumor cells and in CHM and CC. In tumor cells, NLRP7 functions in an inflammasome-independent manner and promoted their proliferation and 3D organization. Gravid mice placentas injected with CC cells invalidated for NLRP7, exhibited higher maternal immune response, developed smaller tumors, and displayed less metastases. Our data characterized the critical role of NLRP7 in CC and provided evidence of its contribution to the development of an immunosuppressive maternal microenvironment that not only downregulates the maternal immune response but also fosters the growth and progression of CC.

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Section: Introductionmentioning

confidence: 99%

NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Reynaud

Nahed

Lemaître

et al. 2021

Cancers

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“…The first and third trimesters of human pregnancy are known to induce a strong physiological inflammation status (42). Recent studies showed that the second trimester of pregnancy also induces inflammasome signaling in placental trophoblasts to promote fetal and maternal antimicrobial defenses (43).…”

Section: Pregnancy/gestation Placental and Neonatal Inflammasomes During T Cruzi Infectionmentioning

confidence: 99%

Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?

2021

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The newborns of women infected with the parasite Trypanosoma cruzi (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route). Congenital Chagas disease can induce high levels of neonatal morbidity and mortality. Parasite-infected pregnant women transmit antibodies to their fetus. Antibodies, by opsonizing parasites, can promote phagocytosis and killing of T. cruzi by cells expressing FcγR, on the mandatory condition that such cells are sufficiently activated in an inflammatory context. Antibody-dependent enhancement (ADE) is a mechanism well described in viral infections, by which antibodies enhance entry of infectious agents into host cells by exploiting the phagocytic FcγR pathway. Previously reported Chagas disease studies highlighted a severe reduction of the maternal-fetal/neonatal inflammatory context in parasite-transmitting pregnant women and their congenitally infected newborns. Otherwise, experimental observations brought to light ADE of T. cruzi infection (involving FcγR) in mouse pups displaying maternally transferred antibodies, out of an inflammatory context. Herein, based on such data, we discuss the previously unconsidered possibility of a role of ADE in the trans-placental parasite transmission, and/or the development of severe and mortal clinical forms of congenital/neonatal Chagas disease in newborns of T. cruzi-infected mothers.

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“…Under certain conditions, the extrusion can occurs with neutrophil survival, a process termed as "vital NETosis". (Burgener & Schroder, 2020).…”

Section: Other Forms Of Programmed Necrosismentioning

confidence: 99%

“…These extracellular traps also contain antimicrobial proteins such as, MPO, NE, Proteinase 3 (PR3), Cathepsin G, Lysozyme and α-defensins representing a non-phagocytic mode of neutralize and degrade invading pathogens (Branzk & Papayannopoulos, 2013;Urban et al, 2009) and are able to stimulate the production of Interferon-α (IFN-α), a strong antiviral cytokine (Garcia-Romo et al, 2011). In the past 10 years, this form of PCD has been extensively studied to elucidate the sequence of its molecular events and its role in immune response, demonstrating that is actually one of the most specialized immune mechanism, which can be activated depending on microbe size and location, and as a strategy to control pathogens which are able to escape from neutrophil phagocytosis (reviewed in (Burgener & Schroder, 2020)). The effectiveness of this antimicrobial defense is evident in some pathogens such as Group A Streptococcus and Staphylococcus aureus , that produce nucleases and DNA binding proteins to impair NET formation and block NETosis as an active evasion mechanism (Storisteanu et al, 2017).…”

Section: Regulated Necrosis and Innate Immunitymentioning

confidence: 99%

“…It is part of various innate and adaptive immune mechanisms/processes such as antiviral defense, killing of intracellular pathogens, inflammation, chemoattraction, lymphocyte selection and immune tolerance (Miao, Rajan, & Aderem, 2011;Zhou & Fang, 2019). Increasing evidence is revealing novel functions of different cell death types in innate immunity, including the regulation and/or amplification of the inflammatory response, the modulation of cytokine production and release, as well as diverse microbekilling strategies in specialized immune cells (Andrade & Darrah, 2013;Burgener & Schroder, 2020;H. Chen, Ning, & Jiang, 2017;Humphries, Yang, Wang, & Moynagh, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Cell death as part of Innate Immunity: cause or consequence?

Riera‐Romo¹

2020

Preprint

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Regulated or programmed cell death play a critical role in development and tissue organization and function. In addition, it is intrinsically connected with immunity and host defense. Increasing cellular and molecular findings are changing the concept of cell death, revealing an expanding network of regulated cell death modalities and their biochemical programs. Likewise, recent evidences are demonstrating the interconnection between cell death pathways and how they are involved in different immune mechanisms. This work provides an overview of the main cell death programs and their implication in innate immunity not only as an immunogenic/inflammatory process, but also as an active defense strategy during immune response and at the same time, as a regulatory mechanism.

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Placental inflammasome signaling: Protection for mother and baby

Cited by 5 publications

References 15 publications

NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Is Antibody-Dependent Enhancement of Trypanosoma cruzi Infection Contributing to Congenital/Neonatal Chagas Disease?

Cell death as part of Innate Immunity: cause or consequence?

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