NOD1 expression elicited by iE-DAP in first trimester human trophoblast cells and its potential role in infection-associated inflammation

Zhou, Shengtao; Yu, Ping; Guan, Li-li; Xing, Aiyun; Liu, S.; Xiong, Q.; Peng, Bo

doi:10.1016/j.ejogrb.2013.04.011

Cited by 8 publications

(3 citation statements)

References 24 publications

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“…A dipeptide present in the cell wall of gram-negative bacteria (Chamaillard et al, 2003), iE-DAP can activate NOD1 receptors in the cell membrane of first-trimester human trophoblast cells to cause inflammation and oxidative stress (Zhou et al, 2013). Our results revealed the optimal iE-DAP concentration (10 μg/L) and incubation time (2 and 8 h) for inducing inflammation and oxidative stress, respectively.…”

Section: Discussionmentioning

confidence: 72%

“…Glutamine is an important amino acid in the body: studies have shown that GLN can alleviate inflammation by inhibiting the activation of NF-κB in lung epithelial cells and first-trimester human trophoblast cells (Hou et al, 2012;Zhou et al, 2013). Early studies have proven that iE-DAP can promote the secretion of maternal-fetal proinflammatory cytokines such as IL-6 and TNF-α (Cardenas et al, 2011) and chemokines such as IL-8 in bovine hepatocytes (Xu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

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Glutamine pretreatment protects bovine mammary epithelial cells from inflammation and oxidative stress induced by γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP)

Cheng

Aabdin

Wang

et al. 2021

Journal of Dairy Science

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Glutamine (GLN) has many types of biological activity in rats, including anti-inflammatory, antioxidative stress, and anti-apoptosis effects. However, little is known about the effects of GLN on bovine mammary epithelial cells (BMEC). γ-d-Glutamyl-mesodiaminopimelic acid (iE-DAP) is a cell wall peptidoglycan component of gram-negative bacteria that can be recognized by the intracellular receptor nucleotidebinding oligomerization domain-containing protein 1 (NOD1) and can cause bovine mastitis. The goal of the present study was to investigate whether GLN protects BMEC from iE-DAP-induced inflammation, oxidative stress, and apoptosis. We cultured BMEC in a GLNfree medium for 24 h and then separated them into 4 groups: cells treated with 1× PBS for 26 or 32 h (control); cells stimulated by 10 μg/mL iE-DAP for 2 or 8 h (2-or 8-h iE-DAP); cells pretreated with 8 or 4 mM GLN for 24 h followed by 2 or 8 h of 1× PBS treatment (8 or 4 mM GLN); and cells pretreated with 8 or 4 mM GLN for 24 h followed by 2 or 8 h of iE-DAP treatment (DG). In the 2-h iE-DAP group, when levels of inflammation peaked, iE-DAP treatment increased both the mRNA and protein expression of NOD1, inhibitor of nuclear factor-κB (NFKBIA, IκB), and nuclear factor-κB subunit p65 (RELA, NF-κB p65), as well as the mRNA expression of IL6 and IL8 and levels of IL-6 and tumor necrosis factor-α in cell culture supernatants. In contrast, 8 mM GLN pretreatment inhibited the mRNA and protein expression of inflammatory-related factors by suppressing the NOD1/NF-κB pathway. In the 8-h iE-DAP group, iE-DAP treatment decreased the mRNA and protein expression of extracellular regu-lated kinase (Erk, ERK) and nuclear factor erythroid 2-associated factor2 (NFE2L2, Nrf2), as well as the mRNA expression of superoxide dismutase 1 (SOD1), catalase (CAT), coenzyme II oxidoreductase 1 (NQO1), and heme oxygenase 1 (HMOX1, HO1). In addition, iE-DAP treatment increased the expression of malondialdehyde in BMEC when oxidative stress levels peaked. Interestingly, 4 mM GLN pretreatment induced the mRNA and protein expression of antioxidative stressrelated factors and inhibited the expression of reactive oxygen species in BMEC by promoting the ERK/Nrf2 pathway. Moreover, GLN reduced apoptosis caused by inflammation and oxidative stress in BMEC. This is the first report showing that GLN protects against iE-DAP-induced inflammation and oxidative stress via the NOD1/NF-κB and ERK/Nrf2 pathways in BMEC.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Glutamine pretreatment protects bovine mammary epithelial cells from inflammation and oxidative stress induced by γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP)

Cheng

Aabdin

Wang

et al. 2021

Journal of Dairy Science

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“…NOD1 binding and downstream signaling elicits an inflammatory reaction, inducing the production of cytokines, chemokines and antimicrobial peptides. Among these products, some are pro-inflammatory, such as interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α and human beta defensin (hBD)-2, while others have immuno-regulatory or antimicrobial properties, such as interferon (IFN)-γ and human β-defensin-1 (hBD-1).The effects of iE-DAP on cytokine production have also been investigated with conflicting results: while it was reported that iE-DAP stimulated various human epithelial cells to produce anti-microbial peptides, but not pro-inflammatory cytokines like IL-6 and IL-8 (127, 129, 131, 145), it was also shown in human intestinal epithelial cells and dental pulp fibroblasts that NOD1 activation induces the production of pro-inflammatory cytokines (127, 142, 146–148).…”

Section: Cellular Receptorsmentioning

confidence: 99%

Oral Mucosal Epithelial Cells

2019

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Cellular Phenotype and Apoptosis: The function of epithelial tissues is the protection of the organism from chemical, microbial, and physical challenges which is indispensable for viability. To fulfill this task, oral epithelial cells follow a strongly regulated scheme of differentiation that results in the formation of structural proteins that manage the integrity of epithelial tissues and operate as a barrier. Oral epithelial cells are connected by various transmembrane proteins with specialized structures and functions. Keratin filaments adhere to the plasma membrane by desmosomes building a three-dimensional matrix. Cell-Cell Contacts and Bacterial Influence: It is known that pathogenic oral bacteria are able to affect the expression and configuration of cell-cell junctions. Human keratinocytes up-regulate immune-modulatory receptors upon stimulation with bacterial components. Periodontal pathogens including P. gingivalis are able to inhibit oral epithelial innate immune responses through various mechanisms and to escape from host immune reaction, which supports the persistence of periodontitis and furthermore is able to affect the epithelial barrier function by altering expression and distribution of cell-cell interactions including tight junctions (TJs) and adherens junctions (AJs). In the pathogenesis of periodontitis a highly organized biofilm community shifts from symbiosis to dysbiosis which results in destructive local inflammatory reactions. Cellular Receptors: Cell-surface located toll like receptors (TLRs) and cytoplasmatic nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) belong to the pattern recognition receptors (PRRs). PRRs recognize microbial parts that represent pathogen-associated molecular patterns (PAMPs). A multimeric complex of proteins known as inflammasome, which is a subset of NLRs, assembles after activation and proceeds to pro-inflammatory cytokine release. Cytokine Production and Release: Cytokines and bacterial products may lead to host cell mediated tissue destruction. Keratinocytes are able to produce diverse pro-inflammatory cytokines and chemokines, including interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor (TNF)-α. Infection by pathogenic bacteria such as Porphyromonas gingivalis ( P. gingivalis ) and Aggregatibacter actinomycetemcomitans ( A. actinomycetemcomitans ) can induce a differentiated production of these cytokines. Immuno-modulation, Bacterial Infection, and Cancer Cells: There is a known association between bacterial infection and cancer. Bacterial components are able to up-regulate immune-modulatory receptors on cancer cells. Interactions of bacteria with tumor cells could support malignant transformation an environment with deficient immune regulation. The aim of this review is...

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Impact of Progesterone on Molecular Mechanisms of Preterm Premature Rupture of Membranes

et al. 2021

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NOD1 expression elicited by iE-DAP in first trimester human trophoblast cells and its potential role in infection-associated inflammation

Cited by 8 publications

References 24 publications

Glutamine pretreatment protects bovine mammary epithelial cells from inflammation and oxidative stress induced by γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP)

Glutamine pretreatment protects bovine mammary epithelial cells from inflammation and oxidative stress induced by γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP)

Oral Mucosal Epithelial Cells

Impact of Progesterone on Molecular Mechanisms of Preterm Premature Rupture of Membranes

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