Evaluation of serum concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-2, IL-10, and nitric oxide (NO) during the estrous cycle, early pregnancy and abortion in goats

Chen, Youwang; Lv, Wenting; Jia, Jingliang; Wang, Jiantao; Yang, Jianhui

doi:10.1016/j.anireprosci.2016.09.007

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…In animal models, NOS and HO facilitate the T h 1/T h 2 shift. Lymphocyte NO synthesis increases during bovine pregnancy, and in pregnant goat serum NO 3 − correlates with T h 2 cytokines [214,215]. Maturation of rat naïve T cells into cytotoxic effectors (T CTX ) requires downregulation of antigen-presenting cells' iNOS and HO-1 [216].…”

Section: Immune Adaptationmentioning

confidence: 99%

Gasotransmitters in pregnancy: from conception to uterine involution†

Guerra

Hurt

2019

Biology of Reproduction

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Gasotransmitters are endogenous small gaseous messengers exemplified by nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S or sulfide). Gasotransmitters are implicated in myriad physiologic functions including many aspects of reproduction. Our objective was to comprehensively review basic mechanisms and functions of gasotransmitters during pregnancy from conception to uterine involution and highlight future research opportunities. We searched PubMed and Web of Science databases using combinations of keywords nitric oxide, carbon monoxide, sulfide, placenta, uterus, labor, and pregnancy. We included English language publications on human and animal studies from any date through August 2018 and retained basic and translational articles with relevant original findings. All gasotransmitters activate cGMP signaling. NO and sulfide also covalently modify target protein cysteines. Protein kinases and ion channels transduce gasotransmitter signals, and co-expressed gasotransmitters can be synergistic or antagonistic depending on cell type. Gasotransmitters influence tubal transit, placentation, cervical remodeling, and myometrial contractility. NO, CO, and sulfide dilate resistance vessels, suppress inflammation, and relax myometrium to promote uterine quiescence and normal placentation. Cervical remodeling and rupture of fetal membranes coincide with enhanced oxidation and altered gasotransmitter metabolism. Mechanisms mediating cellular and organismal changes in pregnancy due to gasotransmitters are largely unknown. Altered gasotransmitter signaling has been reported for preeclampsia, intrauterine growth restriction, premature rupture of membranes, and preterm labor. However, in most cases specific molecular changes are not yet characterized. Nonclassical signaling pathways and the crosstalk among gasotransmitters are emerging investigation topics.

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Section: Immune Adaptationmentioning

confidence: 99%

Gasotransmitters in pregnancy: from conception to uterine involution†

Guerra

Hurt

2019

Biology of Reproduction

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“…Therefore, the inhibition of these inammatory mediators has been considered as an effective strategy against inammatory diseases. 5 Nuclear factor kappa-B (NF-kB) plays a remarkable role in regulating the inammatory responses by increasing the expressions of inammatory mediators and pro-inammatory cytokines. It remains in an inactive form with the linkage to the inhibitor of kB (IkB) protein normally, while it is released through the phosphorylation and degradation of IkB when induced by inammatory stimuli such as LPS and cytokines and the fatal elements of oxidative stress, namely, reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the inhibition of these inflammatory mediators has been considered as an effective strategy against inflammatory diseases. 5 …”

Section: Introductionmentioning

confidence: 99%

Structural characterization and anti-inflammatory potency of Mesobuthus martensii Karsch oligopeptides in lipopolysaccharide (LPS)-induced RAW264.7 macrophages

Zheng

Chen

et al. 2019

RSC Adv.

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“…Maternal immune tolerance to semiallogeneic trophoblast cells of fetal origin is required for successful implantation and maintenance of pregnancy [ 5 ], and multiple mechanisms are believed to promote maternal-fetal immune tolerance. A number of studies have reported that defects in the balance of Th1/Th2 together with overfunctioning of Th1 are involved in abnormal immune responses and pathologic pregnancies, including miscarriage, preeclampsia, and fetal growth restriction [ 6 ]. The production of Th2-type cytokines, such as interleukin-4 (IL-4), IL-5, and IL-10, locally at the maternal-fetal interface assists in maintaining pregnancy; while Th1-type cytokines, such as interferon- γ (IFN- γ ), IL-2, and tumor necrosis factor- α (TNF- α ) mediate fetal rejection [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Impaired Gal-9 Dysregulates the PBMC-Induced Th1/Th2 Imbalance in Abortion-Prone Matings

Jiang

Zhou

et al. 2018

Journal of Immunology Research

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Recurrent miscarriage is defined as the loss of 3 or more consecutive pregnancies; however, the underlying immunologic mechanisms that trigger pregnancy loss remain largely unelucidated. Galectin-9 (Gal-9) may modulate a variety of biologic functions and play an important role in Th1/Th2 immune deviation. To analyze the mechanism of Gal-9 in abortion, we used the classical abortion-prone mouse model (DBA/2-mated CBA/J mice) to detect the expression of Gal-9 at the maternal-fetal interface. We also mimicked the immune environment of pregnancy by culturing trophoblast cells with peripheral blood mononuclear cells (PBMCs) to explore how Gal-9 might be involved in the pathogenesis of abortion. We found that the expression levels of Gal-9 in abortion-prone matings were lower than that for controls. Using a coculture system, we detected a Th1 preponderance in the coculture from abortion-prone matings. Furthermore, Gal-9 blockade augmented the imbalance of Th1/Th2 immunity in abortion-prone matings by promoting the secretion of Th1-derived cytokines in coculture, while there was a Th2 preponderance when we administered recombinant Gal-9. In conclusion, our results suggest that the Gal-9 signal is important for the regulation of PBMC function toward a Th2 bias at the maternal-fetal interface, which is beneficial for the maintenance of a normal pregnancy.

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Evaluation of serum concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-2, IL-10, and nitric oxide (NO) during the estrous cycle, early pregnancy and abortion in goats

Cited by 6 publications

References 27 publications

Gasotransmitters in pregnancy: from conception to uterine involution†

Gasotransmitters in pregnancy: from conception to uterine involution†

Structural characterization and anti-inflammatory potency of Mesobuthus martensii Karsch oligopeptides in lipopolysaccharide (LPS)-induced RAW264.7 macrophages

Impaired Gal-9 Dysregulates the PBMC-Induced Th1/Th2 Imbalance in Abortion-Prone Matings

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