Different effects of cortisol on pro-inflammatory gene expressions in LPS-, heat-killed E.coli-, or live E.coli-stimulated bovine endometrial epithelial cells

Cui, Luying; Wang, Yali; Wang, Heng; Dong, Junsheng; Li, Zixiang; Li, Jun; Chen, Qian; Li, Jianji

doi:10.1186/s12917-020-2231-z

Cited by 12 publications

(9 citation statements)

References 35 publications

(54 reference statements)

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“…Dong et al [42] demonstrated that high cortisol concentrations attenuate LPS-induced inflammatory responses in the RAW264.7 macrophage cell line by regulating the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPK) signaling pathways. Cui et al [54] demonstrated a two-side effect of cortisol in bovine endometrial epithelial cells (BEECs) stimulated with LPS, heat-killed Escherichia coli or live E. coli. 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.…”

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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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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“…This glucocorticoid regulates inflammation and immune function and its anti-inflammatory effects occur from the downregulation of several pro-inflammatory transcription factors, which then suppress synthesis of inflammatory mediators such as cytokines and prostaglandins. [43][44][45] Cortisol is produced by the adrenal glands and is controlled by adrenocorticotropic hormone (ACTH), a hormone made by the adrenal gland, and corticosteroids are known to decrease secretion of ACTH through the suppression of the hypothalamic-pituitary-adrenal axis. 46 In this study, when comparing the corticosteroid-only treatments to each other, triamcinolone suppressed cortisol levels for a significantly longer period of time compared with betamethasone.…”

Section: Discussionmentioning

confidence: 99%

Residual effects of intra‐articular betamethasone and triamcinolone acetonide in an equine acute synovitis model

Partridge

Adam

Wood

et al. 2022

Equine Veterinary Journal

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BackgroundIntra‐articular (IA) corticosteroids are regularly used in equine athletes for the control of joint inflammation.ObjectivesThe goal of this study was to use an acute synovitis inflammation model to determine the residual effects of IA betamethasone and triamcinolone acetonide on various inflammatory parameters and lameness.Study designCrossover randomised trial.MethodsFive mixed‐breed, 2‐year‐old horses were randomly allocated to an IA treatment of the radiocarpal joint with 9 mg of either betamethasone or triamcinolone acetonide. Two weeks following treatment, horses were injected with 1 μg of lipopolysaccharide (LPS) diluted in 1 ml of saline. Following LPS injection, horses were crossed‐over and both sets of injections were repeated after a washout period. Blood samples were collected at multiple time points for mRNA analysis, as well as serum amyloid A (SAA) and cortisol determination. At each time point, lameness was also subjectively scored. Additional injections with saline‐only or LPS‐only (twice) were conducted as negative and positive controls, respectively. Two‐way repeated measures analysis of variance was used to analyse all data.ResultsCorticosteroid‐only treatments result in significant mRNA expression differences, as well as significant and prolonged cortisol suppression. Following LPS injection, there was a residual treatment effect with triamcinolone evidenced by a significant treatment effect on IL‐6 and PTGS1 (cyclooxygenase‐1), lameness, SAA and cortisol concentrations, while only IL‐6 expression was affected by betamethasone.Main limitationsThe acute synovitis model used here results in significant inflammation and is not representative of the low‐grade inflammation seen with typical joint disease and residual anti‐inflammatory effects may be more profound in naturally occurring joint disease.ConclusionsCurrent regulatory guidelines may be insufficient if the concern is residual anti‐inflammatory effects. Additionally, intra‐articular corticosteroid administration is not without risk, as evidenced by a significant suppression of serum cortisol concentration and, as such, the benefits of their administration should be weighed against those risks.

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“…Thus, it is particular important to identify the underlying mechanism of S. aureus mastitis. A number of studies have performed to explore the host/pathogen interactions in the mammary gland by using animal model [25,26]. However, the experimental infections are costly furthermore the interactions between host defense and bacterial virulence factors are complex which make it di cult to analysis.…”

Section: Discussionmentioning

confidence: 99%

S. Aureus Lipoteichoic Acid Failed to Activate NLRP3, but Downregulated the Transduction of NLRP3/MAPK and NF-κB Signaling Pathway in Mouse Mastitis Induced by S. Aureus

Shen

et al. 2020

Preprint

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Background It was confirmed that S. aureus infection activated the expression of NLRP3. As a major component of S. aureus cell wall, what about LTA? Firstly, in this study a mouse model was built following LTA intramammary infection for 0, 12, 24, 48 and 72 h, the characterization of mammary inflammatory response induced by LTA was observed. Subsequently, mouse mammary preconditioned with LTA was modelling. The effect of LTA treatment on the activation of NLRP3/ MAPK and NF-κB signaling pathways induced by S. aureus were detected.Results Results shown that the LTA intramammary infection induce mild but rapid recovery inflammation in mammary gland whereas failed to stimulate NLRP3. LTA treatment protected mammary gland against S. aureus infection by suppressed the activation of NLRP3/ MAPK and NF-κB signaling pathways. Meanwhile it is noteworthy that the expression of NLRP3/MAPK JNK induced by S. aureus was not regulated by LTA treatment.Conclusions These results suggested LTA induced mammary gland inflammation was mild and self-limiting. LTA treatment revealed a good anti-inflammation effect through downregulating the transduction of NLRP3/MAPK and NF-κB signaling pathways in mouse mastitis induced by S. aureus. Our research highlights the importance of an LTA during the innate immune response of the mammary gland and offer novel insights for new approaches concerning effective immunomodulation against a local bacterial infection.

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Different effects of cortisol on pro-inflammatory gene expressions in LPS-, heat-killed E.coli-, or live E.coli-stimulated bovine endometrial epithelial cells

Cited by 12 publications

References 35 publications

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

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

Residual effects of intra‐articular betamethasone and triamcinolone acetonide in an equine acute synovitis model

S. Aureus Lipoteichoic Acid Failed to Activate NLRP3, but Downregulated the Transduction of NLRP3/MAPK and NF-κB Signaling Pathway in Mouse Mastitis Induced by S. Aureus

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