cis9,trans11, but nottrans10,cis12 CLA isomer, impairs intestinal epithelial barrier function in IPEC-J2 cells and mice through activation of GPR120-[Ca2+]iand the MLCK signaling pathway

Han, Seung-Beom; Zhao, Weihua; Zhang, Fenglin; Song, Min; Liu, Fangfang; Zheng, Jisong; Ling, Mingfa; Yang, Xiaohua; Yang, Qiang; He, Haiwen; Chen, Lin; Lai, Xumin; Zhu, Xiaotong; Wang, Lina; Gao, Ping; Shu, Gang; Jiang, Qingyan; Wang, Songbo

doi:10.1039/d0fo00376j

Cited by 14 publications

(13 citation statements)

References 62 publications

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“…In the late stage, the effects of t10, c12-CLA changed to be inhibition while the effects of c9, t11-CLA remained unchanged . In addition, we previously found that trans 11, but not trans 10, cis 12 CLA isomer impairs intestinal epithelial barrier function in IPEC-J2 cells and mice . These reports indicated that although the c9, t11-CLA isomer and t10, c12-CLA isomer only have a change in the double-bond position, it may indeed lead to a great difference in physiological function, which has been further confirmed in the present study.…”

Section: Discussionmentioning

confidence: 95%

“…It has been shown that different isomers have different or opposite biological activities and physiological functions . For example, cis 9, trans 11, but not trans 10, cis 12 CLA isomer impairs intestinal epithelial barrier function in IPEC-J2 cells . In skeletal muscle, the CLA mixture has been implicated in promoting exercise endurance .…”

Section: Introductionmentioning

confidence: 99%

“…17 For example, cis 9, trans 11, but not trans 10, cis 12 CLA isomer impairs intestinal epithelial barrier function in IPEC-J2 cells. 18 In skeletal muscle, the CLA mixture has been implicated in promoting exercise endurance. 19 However, which isomer elicits this effect remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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trans 10, cis 12, but Not cis 9, trans 11 Conjugated Linoleic Acid Isomer Enhances Exercise Endurance by Increasing Oxidative Skeletal Muscle Fiber Type via Toll-like Receptor 4 Signaling in Mice

Duan

Yin

et al. 2021

J. Agric. Food Chem.

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Conjugated linoleic acid (CLA) has been implicated in regulating muscle fiber. However, which isomer elicits this effect and the underlying mechanisms remain unclear. Here, male C57BL6/J mice and C2C12 cells were treated with two CLA isomers, and the exercise endurance, skeletal muscle fiber type, and involvement of Toll-like receptor 4 (TLR4) signaling were assessed. The results demonstrated that dietary t10, c12, but not c9, t11-CLA isomer enhanced exercise endurance of mice (from 115.88 ± 11.21 to 130.00 ± 15.84 min, P < 0.05) and promoted the formation of oxidative muscle fiber type of gastrocnemius muscle (from 0.15 ± 0.04 to 0.24 ± 0.05, P < 0.05). Consistently, t10, c12-CLA isomer increased the mRNA expression of oxidative muscle fiber type in C2C12 myotubes (from 1.00 ± 0.08 to 2.65 ± 1.77, P < 0.05). In addition, t10, c12-CLA isomer increased TLR4 signaling expression in skeletal muscle and C2C12 myotubes. More importantly, knockdown of TLR4 eliminated the t10, c12-CLA isomer-induced enhancement of exercise endurance in mice and elevation of oxidative muscle fiber type in C2C12 myotubes and gastrocnemius muscle. Together, these findings showed that t10, c12, but not c9, t11-CLA isomer enhances exercise endurance by increasing oxidative skeletal muscle fiber type via TLR4 signaling.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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trans 10, cis 12, but Not cis 9, trans 11 Conjugated Linoleic Acid Isomer Enhances Exercise Endurance by Increasing Oxidative Skeletal Muscle Fiber Type via Toll-like Receptor 4 Signaling in Mice

Duan

Yin

et al. 2021

J. Agric. Food Chem.

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“…However, which CLA isomer is responsible for the observed benefits is sometimes controversial, with species-, tissueand cell-type-dependent specific effects reported [10][11][12][13]. In the study of Su et al [14], the isomers cis-9,trans-11-CLA impaired intestinal epithelial barrier function in both mice and IPEC-J2 cells, whereas trans-10,cis-12-CLA did not. However, in the study of Jaudszus et al [15], cis-9,trans-11-CLA significantly reduced the release of inflammatory cytokines in stimulated human bronchial epithelial cells and exerted better anti-inflammatory effects than trans-10,cis-12-CLA.…”

Section: Introductionmentioning

confidence: 99%

Isomer-Specific Effects of cis-9,trans-11- and trans-10,cis-12-CLA on Immune Regulation in Ruminal Epithelial Cells

Yang

Zhu

et al. 2021

Animals

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In this study, we used transcriptomics and qPCR to investigate the potential immunoprotective effects of different conjugated linoleic acid (CLA) isomers, the natural rumen microbial metabolites, on lipopolysaccharide (LPS)-induced inflammation of ruminal epithelial cells (RECs) in vitro. The results showed that 100 μM trans-10,cis-12-CLA exerted higher anti-inflammatory effects than cis-9,trans-11-CLA by significantly downregulating the expression of genes related to inflammation, cell proliferation and migration in RECs upon LPS stimulation. Transcriptomic analyses further indicated that pretreatment with trans-10,cis-12-CLA, but not cis-9,trans-11-CLA, significantly suppressed the biological signals of GO terms’ response to LPS, the regulation of signal transduction and cytokine production and KEGG pathways NF-κB, chemokine, NOD-like receptor, Hippo, PI3K-Akt, TGF-β and Rap1 signaling in RECs upon LPS stimulation. Furthermore, pretreatment with trans-10,cis-12-CLA significantly reduced the expression of lipogenic genes and the biosynthesis of the unsaturated fatty acid pathway in RECs compared with the LPS group, however, cis-9,trans-11-CLA exhibited the opposite results. These results suggest the distinct isomer differences of CLA in the regulation of inflammatory responses and adipocytokine signaling in RECs and will provide important references for determining their target use in the future.

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“…Cytokines further activated MLCK in a feed-forward mechanism, partly via altering ZO-1 and claudin 15 ( Lorentz et al, 2017 ). MLCK phosphorylates the myosin regulatory light chain, which leads to contraction of the actin-myosin ring, increasing intestinal permeability ( Su et al, 2020 ). Indeed, the significant increase of the intestinal permeability is closely interrelated to the occurrence and development of sepsis ( Assimakopoulos et al, 2018 ), such as sepsis secondary intratracheal instillation of Pseudomonas aeruginosa due to gut mucosal and microvascular injury and gut barrier dysfunction ( Yu and Martin, 2000 ).…”

Section: Introductionmentioning

confidence: 99%

Gut-Lung Crosstalk in Sepsis-Induced Acute Lung Injury

Zhou

Liao

2021

Front. Microbiol.

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common acute and severe cases of the respiratory system with complicated pathogenesis and high mortality. Sepsis is the leading indirect cause of ALI/ARDS in the intensive care unit (ICU). The pathogenesis of septic ALI/ARDS is complex and multifactorial. In the development of sepsis, the disruption of the intestinal barrier function, the alteration of gut microbiota, and the translocation of the intestinal microbiome can lead to systemic and local inflammatory responses, which further alter the immune homeostasis in the systemic environment. Disruption of homeostasis may promote and propagate septic ALI/ARDS. In turn, when ALI occurs, elevated levels of inflammatory cytokines and the shift of the lung microbiome may lead to the dysregulation of the intestinal microbiome and the disruption of the intestinal mucosal barrier. Thus, the interaction between the lung and the gut can initiate and potentiate sepsis-induced ALI/ARDS. The gut–lung crosstalk may be a promising potential target for intervention. This article reviews the underlying mechanism of gut-lung crosstalk in septic ALI/ARDS.

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cis9,trans11, but nottrans10,cis12 CLA isomer, impairs intestinal epithelial barrier function in IPEC-J2 cells and mice through activation of GPR120-[Ca²⁺]_iand the MLCK signaling pathway

Abstract: In vitro and in vivo studies show that c9, t11-CLA, but not t10, c12-CLA isomer, impairs intestinal epithelial barrier function in IPEC-J2 cells and mice via activation of GPR120-[Ca2+]i and the MLCK pathway.

Cited by 14 publications

References 62 publications

trans 10, cis 12, but Not cis 9, trans 11 Conjugated Linoleic Acid Isomer Enhances Exercise Endurance by Increasing Oxidative Skeletal Muscle Fiber Type via Toll-like Receptor 4 Signaling in Mice

trans 10, cis 12, but Not cis 9, trans 11 Conjugated Linoleic Acid Isomer Enhances Exercise Endurance by Increasing Oxidative Skeletal Muscle Fiber Type via Toll-like Receptor 4 Signaling in Mice

Isomer-Specific Effects of cis-9,trans-11- and trans-10,cis-12-CLA on Immune Regulation in Ruminal Epithelial Cells

Gut-Lung Crosstalk in Sepsis-Induced Acute Lung Injury

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