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

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Luying Cui ◽  
Yali Wang ◽  
Heng Wang ◽  
Junsheng Dong ◽  
Zixiang Li ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Bacterial Infections ◽  
Gene Expressions ◽  
Tlr4 Mrna ◽  
Tnf Α ◽  
Peripartum Period ◽  
Inflammatory Action ◽  
Endometrial Epithelial Cells

Abstract Background Bacterial infections are common in postpartum dairy cows. Cortisol level has been observed to increase in dairy cows during peripartum period, and is associated with the endometrial innate immunity against pathogens like E.coli. However, the mechanism underlying how cortisol regulates E.coli-induced inflammatory response in bovine endometrial epithelial cells (BEEC) remains elusive. Results Cortisol decreased the expressions of IL1β, IL6, TNF-α, IL8, and TLR4 mRNA in BEEC treated with LPS or heat-killed E.coli, but up-regulated these gene expressions in BEEC stimulated by live E.coli. Conclusion Cortisol exerted the anti-inflammatory action on LPS- or heat-killed E.coli-stimulated BEEC, but the pro-inflammatory action on live E.coli-induced BEEC.

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

2019 ◽  
Author(s):  
Luying Cui ◽  
Yali Wang ◽  
Heng Wang ◽  
Junsheng Dong ◽  
Zixiang Li ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Bacterial Infections ◽  
Gene Expressions ◽  
Tlr4 Mrna ◽  
Tnf Α ◽  
Peripartum Period ◽  
Anti Inflammation ◽  
Endometrial Epithelial Cells

Abstract Background: Bacterial infections are common in postpartum dairy cows. Cortisol level has been observed to increase in dairy cows during peripartum period, and is associated with the endometrial innate immunity against pathogen like E.coli . However, the mechanism underlying how cortisol regulates E.coli -induced inflammatory response in bovine endometrial epithelial cells (BEEC) remains elusive. Results: Cortisol decreased the expressions of IL1β, IL6, TNF-α, IL8, and TLR4 mRNA in BEEC treated with LPS or heat-killed E.coli , but up-regulated the these gene expressions in BEEC stimulated by live E.coli . Conclusion: Cortisol exerted the anti-inflammation action on LPS- or heat-killed E.coli -stimulated BEEC, but the pro-inflammation action on live E.coli -induced BEEC.

scholarly journals MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.

Ssc-novel-miR-106-5p reduces lipopolysaccharide-induced inflammatory response in porcine endometrial epithelial cells by inhibiting the expression of the target gene mitogen-activated protein kinase kinase kinase 14 (MAP3K14)

2019 ◽  
Vol 31 (10) ◽  
pp. 1616
Author(s):  
Yu Lian ◽  
Yu Hu ◽  
Lu Gan ◽  
Yuan-Nan Huo ◽  
Hong-Yan Luo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Target Gene ◽  
Mitogen Activated Protein Kinase ◽  
Luciferase Reporter ◽  
Nuclear Factor ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Endometrial Epithelial Cells ◽  
Protein Kinase Kinase

As an important gram-negative bacterial outer membrane component, lipopolysaccharide (LPS) plays an important role in bacterial-induced endometritis in sows. However, how LPS induces endometritis is unclear. We stimulated sow endometrial epithelial cells (EECs) with LPS and detected cell viability and tumour necrosis factor-α (TNF-α) and interleukin-1 (IL-1) secretion. LPS affected EEC viability and TNF-α and IL-1 secretion in a dose-dependent manner. LPS induced differential expression in 10 of 393 miRNAs in the EECs (downregulated, nine; upregulated, one). MicroRNA (miRNA) high-throughput sequencing of the LPS-induced EECs plus bioinformatics analysis and the dual-luciferase reporter system revealed a novel miRNA target gene: mitogen-activated protein kinase kinase kinase 14 (MAP3K14). Ssc-novel-miR-106-5p mimic, inhibitor and the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) phosphorylation inhibitor Bay11–7085 were used to detect EEC nuclear factor-κB phosphorylation levels (p-NF-κB) and TNF-α and IL-1 secretion. MiR-106-5p mimic downregulated MAP3K14 mRNA and protein expression levels, inhibited p-NF-κB levels and decreased IL-1 and TNF-α secretion, whereas miR-106-5p inhibitor had the opposite effect. Bay11–7085 inhibited p-NF-κB expression and TNF-α and IL-1 secretion. These results suggest that LPS downregulates ssc-novel-miR-106-5p expression in sow EECs to increase MAP3K14 expression, which increases p-NF-κB to promote IL-1 and TNF-α secretion.

scholarly journals Inducible Expression of Human β-Defensin 2 byFusobacterium nucleatum in Oral Epithelial Cells: Multiple Signaling Pathways and Role of Commensal Bacteria in Innate Immunity and the Epithelial Barrier

2000 ◽  
Vol 68 (5) ◽  
pp. 2907-2915 ◽  
Author(s):  
Suttichai Krisanaprakornkit ◽  
Janet R. Kimball ◽  
Aaron Weinberg ◽  
Richard P. Darveau ◽  
Brian W. Bainbridge ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Cell Wall ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inducible Expression ◽  
Periodontal Pathogen ◽  
Gingival Tissue ◽  
Necrosis Factor Alpha ◽  
Tnf Α

ABSTRACT Human gingival epithelial cells (HGE) express two antimicrobial peptides of the β-defensin family, human β-defensin 1 (hBD-1) and hBD-2, as well as cytokines and chemokines that contribute to innate immunity. In the present study, the expression and transcriptional regulation of hBD-2 was examined. HBD-2 mRNA was induced by cell wall extract of Fusobacterium nucleatum, an oral commensal microorganism, but not by that of Porphyromonas gingivalis, a periodontal pathogen. HBD-2 mRNA was also induced by the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) and phorbol myristate acetate (PMA), an epithelial cell activator. HBD-2 mRNA was also expressed in 14 of 15 noninflamed gingival tissue samples. HBD-2 peptide was detected by immunofluorescence in HGE stimulated with F. nucleatum cell wall, consistent with induction of the mRNA by this stimulant. Kinetic analysis indicates involvement of multiple distinct signaling pathways in the regulation of hBD-2 mRNA; TNF-α and F. nucleatum cell wall induced hBD-2 mRNA rapidly (2 to 4 h), while PMA stimulation was slower (∼10 h). In contrast, each stimulant induced interleukin 8 (IL-8) within 1 h. The role of TNF-α as an intermediary in F. nucleatum signaling was ruled out by addition of anti-TNF-α that did not inhibit hBD-2 induction. However, inhibitor studies show that F. nucleatum stimulation of hBD-2 mRNA requires both new gene transcription and new protein synthesis. Bacterial lipopolysaccharides isolated from Escherichia coli andF. nucleatum were poor stimulants of hBD-2, although they up-regulated IL-8 mRNA. Collectively, our findings show inducible expression of hBD-2 mRNA via multiple pathways in HGE in a pattern that is distinct from that of IL-8 expression. We suggest that different aspects of innate immune responses are differentially regulated and that commensal organisms have a role in stimulating mucosal epithelial cells in maintaining the barrier that contributes to homeostasis and host defense.

Transcriptional profiling of primary endometrial epithelial cells following acute HIV-1 exposure reveals gene signatures related to innate immunity

2018 ◽  
Vol 79 (4) ◽  
pp. e12822 ◽  
Author(s):  
Muhammad Atif Zahoor ◽  
Matthew William Woods ◽  
Sara Dizzell ◽  
Aisha Nazli ◽  
Kristen M. Mueller ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Epithelial Cells ◽  
Transcriptional Profiling ◽  
Gene Signatures ◽  
Acute Hiv ◽  
Hiv 1 ◽  
Endometrial Epithelial Cells

scholarly journals Expression Pattern of Cathelicidins in Dairy Cows During Endometritis and Role of Bovine Endometrial Epithelial Cells in Production of Cathelicidins

2021 ◽  
Vol 8 ◽  
Author(s):  
Yajuan Li ◽  
Xiaoyu Ma ◽  
Jie Yang ◽  
Xiaohu Wu ◽  
Zuoting Yan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dairy Cows ◽  
Expression Pattern ◽  
Host Defense ◽  
Post Partum ◽  
Bacterial Disease ◽  
Host Defense Peptides ◽  
E Coli ◽  
Protein Levels ◽  
Endometrial Epithelial Cells

Endometritis is a common bacterial disease of dairy cows. Cathelicidins are host-defense peptides that play important roles in clearance of bacteria. However, the expression pattern of these peptides during endometritis is still unclear. We hypothesize that the levels of bovine cathelicidins increased during endometritis. This study was to investigate the changes of bovine cathelicidins during endometritis. Forty-four post-partum cows (28–35 days after calving) involved in this study were grouped according to the character of vaginal discharge (VD) into three groups. These were (1) cows with clear fluid (n = 8, healthy cows group, N); (2) cows with VD containing <50% off-white mucopurulent material (n = 20, moderate endometritis cows, M); (3) cows with VD containing > 50% yellow or white purulent material (n = 16, severe endometritis cows, S). The blood, VD, and endometrial biopsies samples were collected from each cow to assess the levels of cathelicidin 1–7. Furthermore, bovine endometrial epithelial cells (BEECs) were stimulated with different concentration of Escherichia coli (2 × 106 and 2 × 107 CFU/mL) to detect the cellular source of cathelicidins. Quantitative real-time PCR (RT-qPCR) was used to detect the relative mRNA expression of cathelicidins, and enzyme-linked immune sorbent assay (ELISA) method were used to measure the protein levels. The mRNA and protein levels of cathelicidin 1–7 significantly increased during bovine endometritis (both moderate and severe endometritis), while samples from severe cases showed lower levels of cathelicidins compared to moderate cases. BEECs can express cathelicidin 1–7, and E. coli triggered the release of these proteins. High concentration of E. coli decreased the mRNA and protein levels of cathelicidins. Taken together, our results supported that cathelicidins are released as host defense molecules against the bacteria during bovine endometritis, and BEECs play an active role in expression and production of cathelicidins.

scholarly journals Campylobacter fetus Induced Proinflammatory Response in Bovine Endometrial Epithelial Cells

2021 ◽  
Vol 70 (1) ◽  
pp. 99-106
Author(s):  
LIZETH GUADALUPE CAMPOS-MÚZQUIZ ◽  
ESTELA TERESITA MÉNDEZ-OLVERA ◽  
MONIKA PALACIOS MARTÍNEZ ◽  
DANIEL MARTÍNEZ-GÓMEZ
Keyword(s):  
Epithelial Cells ◽  
Proinflammatory Response ◽  
Expression Levels ◽  
Campylobacter Fetus ◽  
Tnf Α ◽  
Fetus Subsp ◽  
Ifn Γ ◽  
Intracellular Invasion ◽  
Endometrial Epithelial Cells ◽  
In Cells

Campylobacter fetus subsp. fetus is the causal agent of sporadic abortion in bovines and infertility that produces economic losses in livestock. In many infectious diseases, the immune response has an important role in limiting the invasion and proliferation of bacterial patho¬gens. Innate immune sensing of microorganisms is mediated by pattern-recognition receptors (PRRs) that identify pathogen-associated molecular patterns (PAMPs) and induces the secretion of several proinflammatory cytokines, like IL-1β, TNF-α, and IL-8. In this study, the expression of IL-1β, TNF-α, IL-8, and IFN-γ in bovine endometrial epithelial cells infected with C. fetus and Salmonella Typhimurium (a bacterial invasion control) was analyzed. The results showed that expression levels of IL-1β and IL-8 were high at the beginning of the infection and decreased throughout the intracellular period. Unlike in this same assay, the expression levels of IFN-γ increased through time and reached the highest peak at 4 hours post infection. In cells infected with S. Typhimurium, the results showed that IL8 expression levels were highly induced by infection but not IFN-γ. In cells infected with S. Typhimurium or C. fetus subsp. fetus, the results showed that TNF-α expression did not show any change during infection. A cytoskeleton inhibition assay was performed to determine if cytokine expression was modified by C. fetus subsp. fetus intracellular invasion. IL-1β and IL-8 expression were downregulated when an intracellular invasion was avoided. The results obtained in this study suggest that bovine endometrial epithelial cells could recognize C. fetus subsp. fetus resulting in early proinflammatory response.

scholarly journals Inhibitory Effect of Bovine Adipose-Derived Mesenchymal Stem Cells on Lipopolysaccharide Induced Inflammation of Endometrial Epithelial Cells in Dairy Cows

2021 ◽  
Vol 8 ◽  
Author(s):  
Wengeng Lu ◽  
Zheng-Mei Xu ◽  
Qing Liu ◽  
Nan-Nan Yu ◽  
Jia-Bin Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Osteogenic Differentiation ◽  
Surface Marker ◽  
Economic Damage ◽  
Expression Levels ◽  
Bax Protein ◽  
Endometrial Epithelial Cells

Endometritis is a disease that affects reproductive health in dairy cows and causes serious economic damage to the dairy industry world-wide. Although in recent years, the application of mesenchymal stem cell (MSC) therapy for the treatment of inflammatory diseases has attracted much attention, there are few reports of the use of MSCs in dairy cows. In the present study, our objective was to explore the inhibitory effects of bovine adipose-derived mesenchymal stem cells (bAD-MSCs) on lipopolysaccharide (LPS) induced inflammation in bovine endometrial epithelial cells (bEECs) along with the potential underlying molecular mechanisms. We characterized isolated bAD-MSCs using cell surface marker staining and adipogenic/osteogenic differentiation, and analyzed them using immunofluorescence, flow cytometry (surface marker staining), and adipogenic and osteogenic differentiation. Furthermore, to understand the anti-inflammatory effects of bAD-MSCs on LPS induced bEEC inflammation, we used a bAD-MSC/bEEC co-culture system. The results showed that bAD-MSC treatments could significantly decrease LPS induced bEEC apoptosis and pro-inflammatory cytokine expression levels, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Furthermore, our results showed that bAD-MSC treatments could also significantly downregulate LPS induced p38, IkB-a, and JAK1 phosphorylation and Bax protein expression levels, which are closely related to inflammatory progress and cellular apoptosis in bEECs. Our findings demonstrate that bAD-MSCs play an inhibitory role in LPS induced bEEC inflammation and provide new insights for the clinical therapy of endometritis in dairy cows.

scholarly journals Niacin Alleviates Dairy Cow Mastitis by Regulating the GPR109A/AMPK/NRF2 Signaling Pathway

2020 ◽  
Vol 21 (9) ◽  
pp. 3321 ◽  
Author(s):  
Wenjin Guo ◽  
Juxiong Liu ◽  
Wen Li ◽  
He Ma ◽  
Qian Gong ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Dairy Cows ◽  
Dairy Cow ◽  
Mammary Epithelial Cells ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Economic Losses ◽  
Mrna Levels ◽  
Tnf Α

Mastitis is one of three bovine diseases recognized as a cause of substantial economic losses every year throughout the world. Niacin is an important feed additive that is used extensively for dairy cow nutrition. However, the mechanism by which niacin acts on mastitis is not clear. The aim of this study is to investigate the mechanism of niacin in alleviating the inflammatory response of mammary epithelial cells and in anti-mastitis. Mammary glands, milk, and blood samples were collected from mastitis cows not treated with niacin (n = 3) and treated with niacin (30 g/d, n = 3) and healthy cows (n = 3). The expression of GPR109A, IL-6, IL-1β, and TNF-α in the mammary glands of the dairy cows with mastitis was significantly higher than it was in the glands of the healthy dairy cows. We also conducted animal experiments in vivo by feeding rumen-bypassed niacin. Compared with those in the untreated mastitis group, the somatic cell counts (SCCs) and the expression of IL-6, IL-1β, and TNF-α in the blood and milk were lower. In vitro, we isolated the primary bovine mammary epithelial cells (BMECs) from the mammary glands of the healthy cows. The mRNA levels of IL-6, IL-1β, TNF-α, and autophagy-related genes were detected after adding niacin, shRNA, compound C, trans retinoic acid, 3-methyladenine to BMECs. Then GPR109A, AMPK, NRF-2, and autophagy-related proteins were detected by Western blot. We found that niacin can activate GPR109A and phosphorylate AMPK, and promote NRF-2 nuclear import and autophagy to alleviate LPS-induced inflammatory response in BMECs. In summary, we found that niacin can reduce the inflammatory response of BMECs through GPR109A/AMPK/NRF-2/autophagy. We also preliminarily explored the alleviative effect of niacin on mastitis in dairy cows.

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