Study on Persistent Uterine Infection, Ovarian Activity and Reproduction in Postpartum in Murrah Buffaloes

Wakayo, BU; Brar, P S; Prabhakar, S.; Arora, SPS

doi:10.5455/ijlr.20140910052449

Cited by 2 publications

(4 citation statements)

References 11 publications

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“…It causes inflammation of the uterus like metritis and endometritis. Usually, mammalian uterus is prone to bacterial infections during coitus and parturition (53) mainly during the first 5 weeks of postpartum (54). Moreover, infections of the reproductive system at calving cause prolonged acyclicity and reduced fertility upon artificial insemination, resulting in enhanced calving interval.…”

Section: Uterine Infections Lead To Ovarian Dysfunctionmentioning

confidence: 99%

“…Pathogenic organisms, mostly gram negative bacteria, in such infections adhere to the uterine mucosa, penetrate into the epithelium and release endotoxins like LPS into the circulation. These chemicals enter into ovarian follicular fluid to cause ovarian dysfunction and prolonged acyclicity (54). Persistent uterine infection reduces immune efficiency (55), which results into impaired functioning of the uterus and poor embryonic development (44).…”

Section: Uterine Infections Lead To Ovarian Dysfunctionmentioning

confidence: 99%

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Histone deacetylase A potential therapeutic target for ovarian dysfunction

et al. 2018

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Post-partum uterine disorders and reproductive tract infections cause ovarian dysfunction and infertility. Histone deacetylases (HDACs) prevent the relaxation of chromatin, and positively or negatively regulate transcription. Hence, HDACs play a pivotal role in altering the gene expression that impact different signalling pathways underling ovarian dysfunction. Thus, HDAC inhibitors (HDACi) may act as potential therapeutic targets in the treatment of an array of disorders impacting ovarian function.

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Section: Uterine Infections Lead To Ovarian Dysfunctionmentioning

confidence: 99%

Section: Uterine Infections Lead To Ovarian Dysfunctionmentioning

confidence: 99%

Histone deacetylase A potential therapeutic target for ovarian dysfunction

et al. 2018

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“…During uterine and mammary gland infections, endotoxin is known to accumulate in the follicular fluid . These endotoxins perturb the ovarian follicular growth and functions, which lead to ovarian dysfunction . Recently, we have also demonstrated that GCs exposed to the endotoxin (lipopolysaccharide [LPS], 1 µg/mL) are efficiently recognized by TLR4 present on GCs surface and induce the proinflammatory gene expression in 2 hours followed by downregulation to nearly normal level in next 6 hours .…”

Section: Introductionmentioning

confidence: 99%

“…1 These endotoxins perturb the ovarian follicular growth and functions, which lead to ovarian dysfunction. 2,3 Recently, we have also demonstrated that GCs exposed to the endotoxin (lipopolysaccharide [LPS], 1 µg/mL) are efficiently recognized by TLR4 present on GCs surface and induce the proinflammatory gene expression in 2 hours followed by downregulation to nearly normal level in next 6 hours. 4 Further, LPS induced proinflammatory gene expression can be attenuated with pretreatment of histone deacetylase inhibitor trichostatin A, which indicated that transient increase in proinflammatory cytokine expression was due to the chromatin remodeling.…”

mentioning

confidence: 99%

Inhibition of indoleamine 2,3‐dioxygenase attenuates endotoxin‐mediated tolerance in granulosa cells through kynurenine pathway

Dahiya

Onteru

Singh

2019

J of Cellular Biochemistry

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Ovarian granulosa cells (GCs) have been shown to have innate immune capabilities, which modulate their native endocrine functions through toll-like receptors (TLRs). We have recently shown that GCs exposed to lipopolysaccharide (LPS; 1.0 µg/mL) transiently regulate proinflammatory cytokine expression (interleukin 1β [IL-1β], IL-6, and tumor necrosis factor α) through chromatin remodeling. In the present study, we have demonstrated that GCs become tolerant to LPS on repeated exposure of LPS. To understand the mechanism of this endotoxin tolerance (ET) phenomenon in buffalo GCs, we have further studied the genome-wide transcriptomic analyses in buffalo GCs (unpublished data) and identified indoleamine 2,3-dioxygenase 1 (IDO1) gene, known to be involved in tryptophan catabolism, was found to be highly upregulated in endotoxin-tolerant GCs. Real-time gene expression analyses also showed similar results. Further analyses of tryptophan and tryptophan metabolite, kynurenine, showed that tryptophan was found to be depleted with the accumulation of kynurenine in the endotoxin-tolerant GCs. The effect of IDO1 induced ET was reversed when cells were pretreated with IDO1 inhibitor (1-methyl tryptophan, 1 mM). To the best of our knowledge, this is the first report describing the role of IDO1 gene in ET in GCs mimicked by repeated endotoxin exposure in vitro. In summary, the present study convincingly demonstrated that the tryptophan catabolism, through the kynurenine pathway, plays a crucial role as an immunomodulatory mechanism of ET in GCs. The finding could be exploited in developing potential therapeutics to treat impaired GCs function due to the ET underlying prolonged uterine or systemic infection leads to accumulation of endotoxin in follicular fluid. K E Y W O R D S1-methyl tryptophan, indoleamine 2,3-dioxygenase, endotoxin tolerance, granulosa cells, kynurenine, nuclear factor κB, tryptophan catabolism

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Study on Persistent Uterine Infection, Ovarian Activity and Reproduction in Postpartum in Murrah Buffaloes

Cited by 2 publications

References 11 publications

Histone deacetylase A potential therapeutic target for ovarian dysfunction

Histone deacetylase A potential therapeutic target for ovarian dysfunction

Inhibition of indoleamine 2,3‐dioxygenase attenuates endotoxin‐mediated tolerance in granulosa cells through kynurenine pathway

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