Collagenous gastritis in a young Chinese woman: A case report

Hu, J. F.; Yi, Xiao-Yuan; Xiao, Xuejun; Zhou, Lanlan; Li, Bin; Bo, Xiao-Tong

doi:10.3748/wjg.v28.i41.5993

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…First, we established mouse models by BDL and then HE staining and Masson staining indicated that BDL could cause obvious portal vein fibrosis (Figure 1A,B). Activation of HSCs is key to fibrosis, [ 37 ] so we detected the protein levels of HSC activation markers Colla I, FN, and α‐SMA using WB, which revealed significantly increased protein levels of all the markers, indicating the formation of liver fibrosis after BDL ( p < 0.001, Figure 1C). Subsequently, Tβ4 expression was measured using RT‐qPCR and WB tests, which showed downregulated Tβ4 after BDL, inversely correlated with fibrosis progression ( p < 0.001, Figure 1D,E).…”

Section: Resultsmentioning

confidence: 99%

Mechanism of thymosin β4 in ameliorating liver fibrosis via the MAPK/NF‐κB pathway

Wang

Zhang

Wang³

et al. 2023

J Biochem & Molecular Tox

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Liver fibrosis is a grievous global challenge, where hepatic stellate cells (HSCs) activation is a paramount step. This study analyzed the mechanism of Tβ4 in ameliorating liver fibrosis via the MAPK/NF-κB pathway. The liver fibrosis mouse models were established via bile duct ligation (BDL) and verified by HE and Masson staining. TGF-β1-induced activated LX-2 cells were employed in vitro experiments. Tβ4 expression was determined using RT-qPCR, HSC activation markers were examined using Western blot analysis, and ROS levels were tested via DCFH-DA kits. Cell proliferation, cycle, and migration were examined by CCK-8, flow cytometry, and Transwell assays, respectively. Effects of Tβ4 on liver fibrosis, HSC activation, ROS production, and HSC growth were analyzed after transfection of constructed Tβ4-overexpressing lentiviral vectors. MAPK/NF-κB-related protein levels were tested using Western blotting and p65 expression in the nucleus was detected through immunofluorescence. Regulation of MAPK/NF-κB pathway in TGF-β1-induced LX-2 cells was explored by adding MAPK activator U-46619 or inhibitor SB203580. Furthermore, its regulating in liver fibrosis was verified by treating BDL mice overexpressing Tβ4 with MAPK inhibitor or activator. Tβ4 was downregulated in BDL mice. Tβ4 overexpression inhibited liver fibrosis. In TGF-β1induced fibrotic LX-2 cells, Tβ4 was reduced and cell migration and proliferation were enhanced with elevated ROS levels, while Tβ4 overexpression suppressed cell migration and proliferation. Tβ4 overexpression blocked the MAPK/NF-κB pathway activation by reducing ROS production, thus inhibiting liver fibrosis in TGF-β1 induced LX-2 cells and BDL mice. Tβ4 ameliorates liver fibrosis by impeding the MAPK/NF-κB pathway activation.

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Section: Resultsmentioning

confidence: 99%

Mechanism of thymosin β4 in ameliorating liver fibrosis via the MAPK/NF‐κB pathway

Wang

Zhang

Wang³

et al. 2023

J Biochem & Molecular Tox

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Probable collagenous gastritis via Epstein–Barr virus reactivation in the setting of coronavirus disease 2019: a case report

Duncan,

Veli,

Tsosie

et al. 2024

J Med Case Reports

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Background Recent biomedical research has shown the unusual, multisystem effects of coronavirus disease 2019 in humans. One specific sequela of a primary severe acute respiratory syndrome coronavirus 2 infection is the reactivation of latent viruses in various tissues, such as Epstein–Barr virus. Epstein–Barr virus has been identified in many inflammatory gastrointestinal lesions, such as microscopic gastritides and colitides. One subtype of these diseases is collagenous disease. “Long COVID” may be related to the reactivation of these latent viruses, and the following case describes a patient who developed vague symptoms consistent with “long COVID.” Case presentation A non-Hispanic white male in his 50s, with previous collagenous gastritis and colitis, developed a 10-kg weight loss and diffuse leg cramps over 3 months. The patient had coronavirus disease 2019 about 3 months prior to presentation. He had iron deficiency and tested positive for human immunodeficiency virus antibody. His heterophile antibody was also positive. Confirmatory testing for human immunodeficiency virus was negative, and his Epstein–Barr virus antibody panel was positive for early antigen immunoglobulin G. His Epstein–Barr virus viral load was undetectable. Minimal improvement was achieved with a 4-week course of oral budesonide, and upper endoscopy showed diffuse gastritis. He is now improving with proton pump inhibitor therapy and ferrous sulfate supplementation. Conclusion This case report explores outpatient management of microscopic gastritides and colitides. The evidence around coronavirus disease 2019 causing reactivation of Epstein–Barr virus, and Epstein–Barr virus’ presence in chronic gastrointestinal inflammatory lesions, is discussed. Practice recommendations include corticosteroid and acid-suppression therapy for patients suspected of having a recurrence of inflammatory lesions.

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Collagenous gastritis in a young Chinese woman: A case report

Cited by 2 publications

References 15 publications

Mechanism of thymosin β4 in ameliorating liver fibrosis via the MAPK/NF‐κB pathway

Mechanism of thymosin β4 in ameliorating liver fibrosis via the MAPK/NF‐κB pathway

Probable collagenous gastritis via Epstein–Barr virus reactivation in the setting of coronavirus disease 2019: a case report

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