Cortisol inhibits the Escherichia coli-induced endometrial inflammatory response through NF-κB and MAPK pathways in postpartum goats

Cui, Luying; Zheng, Yijing; Wang, Heng; Dong, Junsheng; Li, Jun; Song, Qingxu; Chen, Qian; Li, Jianji

doi:10.1016/j.anireprosci.2020.106333

Cited by 12 publications

(7 citation statements)

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“…Numerous reports have approved that multiple pathways were related to pathogenesis of endometrial injury, containing the mitogen-activated protein kinase (MAPK) signal pathway and NF-κB signal pathway [20,32]. NF-κB was first identified as a transcription factor in the B lymphocyte nucleus that mediates gene transcription by binding to specific sequences [33].…”

Section: Discussionmentioning

confidence: 99%

Oxycodone Alleviates Endometrial Injury via the TLR4/NF-κB Pathway

Yang

2022

Evidence-Based Complementary and Alternative Medicine

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Endometrial injury is a common female disease. This study was designed to illustrate the effects of oxycodone on mifepristone-induced human endometrial stromal cells (hEndoSCs) injury and delineate the underlying molecular mechanism. hEndoSCs were stimulated with mifepristone to generate the endometrial injury in vitro model. hEndoSCs viability, cytotoxicity, and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay, lactate dehydrogenase assay (LDH), and flow cytometry (FCM) analysis, respectively. Meanwhile, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot assay were conducted to evaluate gene and protein expressions. The secretions of inflammatory cytokines (TNF-α, IL-1β, and IL-6) were measured using enzyme-linked immunosorbent assay (ELISA). The data revealed that mifepristone exposure memorably inhibited hEndoSCs viability and promoted cell apoptosis and inflammatory cytokines secretion, and oxycodone had no cytotoxicity on hEndoSCs. Oxycodone increased hEndoSCs growth, blocked cell apoptosis, enhanced Bcl-2 expression, reduced Bax levels, and decreased the secretion of inflammatory cytokines in mifepristone-induced hEndoSCs, exhibiting the protective effects in endometrial injury. In addition, the TLR4/NF-κB pathway-related protein levels (TLR4 and p-p65) in mifepristone-treated hEndoSCs were enhanced, while these enhancements were inhibited by oxycodone treatment. In conclusion, oxycodone exhibited the protective role in mifepristone-triggered endometrial injury via inhibiting the TLR4/NF-κB signal pathway.

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Section: Discussionmentioning

confidence: 99%

Oxycodone Alleviates Endometrial Injury via the TLR4/NF-κB Pathway

Yang

2022

Evidence-Based Complementary and Alternative Medicine

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“…Cui et al . [ 55 ] reported that cortisol impairs E. coli -induced endometrial inflammatory response through NF-κB and MAPK pathways in postpartum goats.…”

Section: Role Of Hpa Axis In Innate Immunitymentioning

confidence: 99%

“…They found that cortisol had anti-inflammatory effects on LPS-or heat-killed E. coli-stimulated BEEC, but displayed pro-inflammatory action on live E. coli-induced BEEC. Cui et al [55] reported that cortisol impairs E. coli-induced endometrial inflammatory response through NF-κB and MAPK pathways in postpartum goats.…”

Section: Role Of Hpa Axis In Innate Immunitymentioning

confidence: 99%

Interaction between stress hormones and phagocytic cells and its effect on the health status of dairy cows: A review

Alhussien

Dang

2020

Vet World

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Dairy cows are exposed to various stressors during their production cycle that makes them more susceptible to various diseases. Phagocytes (neutrophils and macrophages) are important soldiers of the innate immune system. Neutrophils are the first responders to an inflammatory response and stress and kill pathogens by generating reactive oxygen species and by the release of various antimicrobial peptides, enzymes, neutrophil extracellular trap formation, etc. Macrophages, the other phagocytes, are also the cleanup crew for the innate immune system that removes debris, pathogens, and dead neutrophils later on after an inflammatory response. The neuroendocrine system along with phagocytes exhibits an immunomodulatory potential during stressful conditions. Neuroendocrine system directly affects the activity of phagocytes by communicating bidirectionally through shared receptors and messenger molecules such as hormones, neurotransmitters, or cytokines. Different immune cells may show variable responses to each hormone. Short time exposure to stress can be beneficial, but repeated or extended exposure to stress may be detrimental to the overall health and well-being of an animal. Although some stresses associated with farming practices in dairy cows are unavoidable, better understanding of the interactions occurring between various stress hormones and phagocytic cells can help to reduce stress, improve productivity and animal welfare. This review highlights the role played by various stress hormones in modulating phagocytic cell performance of dairy cattle under inflammatory conditions.

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“…These stimuli regulate immunoreaction, cell proliferation, cell survival, and apoptosis [ 31 , 32 ]. Numerous studies have shown that MAPKs can be activated by pathogens, and activated MAPKs phosphorylate various proteins, including transcription factors, leading to the regulation of inflammatory responses [ 33 ]. The inflammatory response is a major pathological feature of MG infection, causing chronic respiratory disease in chickens [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Low let-7d microRNA levels in chick embryos enhance innate immunity against Mycoplasma gallisepticum by suppressing the mitogen-activated protein kinase pathway

Wang

Sun

Zhao

et al. 2023

Vet Res

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Chick embryos are a valuable model for studying immunity and vaccines. Therefore, it is crucial to investigate the molecular mechanism of the Mycoplasma gallisepticum (MG)-induced immune response in chick embryos for the prevention and control of MG. In this study, we screened for downregulated let-7d microRNA in MG-infected chicken embryonic lungs to explore its involvement in the innate immune mechanism against MG. Here, we demonstrated that low levels of let-7d are a protective mechanism for chicken embryo primary type II pneumocytes (CP-II) in the presence of MG. Specifically, we found that depressed levels of let-7 in CP-II cells reduced the adhesion capacity of MG. This suppressive effect was achieved through the activated mitogen-activated protein kinase phosphatase 1 (MKP1) target gene and the inactivated mitogen-activated protein kinase (MAPK) pathway. Furthermore, MG-induced hyperinflammation and cell death were both alleviated by downregulation of let-7d. In conclusion, chick embryos protect themselves against MG infection through the innate immune molecule let-7d, which may result from its function as an inhibitor of the MAPK pathway to effectively mitigate MG adhesion, the inflammatory response and cell apoptosis. This study may provide new insight into the development of vaccines against MG.

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Cortisol inhibits the Escherichia coli-induced endometrial inflammatory response through NF-κB and MAPK pathways in postpartum goats

Cited by 12 publications

References 50 publications

Oxycodone Alleviates Endometrial Injury via the TLR4/NF-κB Pathway

Oxycodone Alleviates Endometrial Injury via the TLR4/NF-κB Pathway

Interaction between stress hormones and phagocytic cells and its effect on the health status of dairy cows: A review

Low let-7d microRNA levels in chick embryos enhance innate immunity against Mycoplasma gallisepticum by suppressing the mitogen-activated protein kinase pathway

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