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Your search keyword '"Shu-Jun Ma"' showing total 5 results
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5 results on '"Shu-Jun Ma"'

1. E3 ligase c-Cbl regulates intestinal inflammation through suppressing fungi-induced noncanonical NF-κB activation

Author

Jie-Lin Duan, Hui-Hui Ma, Quan-Zhen Lv, Xin-Ming Jia, Fan Li, De-Dong Li, Hui-Qian He, Xin Lin, Yao Yu, Yan-Shan Jiang, Tao Liu, and Shu-Jun Ma

Subjects
Ubiquitin-Protein Ligases, Immunology, 03 medical and health sciences, Mice, 0302 clinical medicine, Ubiquitin, Transcription (biology), hemic and lymphatic diseases, medicine, Animals, Proto-Oncogene Proteins c-cbl, Colitis, Research Articles, 030304 developmental biology, Inflammation, 0303 health sciences, Multidisciplinary, biology, Chemistry, RELB, fungi, Fungi, NF-kappa B, SciAdv r-articles, Dendritic cell, medicine.disease, Ubiquitin ligase, Cell biology, Interleukin 10, 030220 oncology & carcinogenesis, biology.protein, Tyrosine kinase, Research Article, Signal Transduction
Abstract

c-Cbl suppresses RelB activation to facilitate protective benefits of commensal fungi and maintain intestinal homeostasis., Intestinal fungi are critical for modulating host immune homeostasis and underlying mechanisms remain unclear. We show that dendritic cell (DC)–specific deficiency of casitas B-lineage lymphoma (c-Cbl) renders mice susceptible to dextran sodium sulfate (DSS)–induced colitis. Mechanistically, we identify that c-Cbl functions downstream of Dectin-2 and Dectin-3 to mediate the ubiquitination and degradation of noncanonical nuclear factor κB subunit RelB. Thus, c-Cbl deficiency in DCs promotes α-mannan–induced activation of RelB, which suppresses p65-mediated transcription of an anti-inflammatory cytokine gene, il10, thereby aggravating DSS-induced colitis. Moreover, suppressing fungal growth with fluconazole or inhibition of RelB activation in vivo attenuates colitis in mice with DC-specific deletion of c-Cbl. We also demonstrate an interaction between c-Cbl and c-Abl tyrosine kinase and find that treatment with DPH, a c-Abl agonist, synergistically increases fungi-induced c-Cbl activation to restrict colitis. Together, these findings unravel a previously unidentified fungi-induced c-Cbl/RelB axis that sustains intestinal homeostasis and protects against intestinal inflammation.

Published
2021

2. Interaction between intestinal mycobiota and microbiota shapes lung inflammation.

Author

Wang, Youxia, He, Fang, Liu, Bingnan, Wu, Xiaoyan, Han, Ziyi, Wang, Xuefei, Liao, Yuexia, Duan, Jielin, and Ren, Wenkai

Subjects
PNEUMONIA, ESCHERICHIA coli, GUT microbiome, LUNG infections, GLUCANS
Abstract

Gut microbiota is an intricate microbial community containing bacteria, fungi, viruses, archaea, and protozoa, and each of them contributes to diverse aspects of host health. Nevertheless, the influence of interaction among gut microbiota on host health remains uncovered. Here, we showed that the interaction between intestinal fungi and bacteria shaped lung inflammation during infection. Specifically, antifungal drug‐induced dysbiosis of gut mycobiota enhanced lung inflammation during infection. Dysbiosis of gut mycobiota led to gut Escherichia coli (E. coli) overgrowth and translocation to the lung during infection, which induced lung accumulation of the CD45+F4/80+Ly6G−Ly6C−CD11b+CD11c+ macrophages. Clearance of macrophages or deletion of TLR4 (Toll‐like receptor 4, recognition of LPS) rather than Dectin‐1 (recognition of beta‐1,3/1,6 glucans on fungi) blocked the antifungal drug‐induced aggravation of lung inflammation during infection. These findings suggest that the interaction between intestinal mycobiota and commensal bacteria affects host health through the gut–lung axis, offering a potential therapeutic target for ameliorating lung inflammation during infection. Highlights: Antifungal drug‐induced dysbiosis of gut mycobiota aggravates lung inflammation during infection.Dysbiosis of intestinal mycobiota results in gut Escherichia coli overgrowth and translocation to the lung during infection.E. coli induces lung accumulation of the CD45+F4/80+Ly6G−Ly6C−CD11b+CD11c+ macrophages.Clearance of macrophages or deletion of TLR4 blocks the antifungal drug‐induced aggravation of lung inflammation during infection. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Study Findings on Hypercholesterolemia Detailed by Researchers at Ningbo First Hospital (Two Novel Disease-Causing Mutations in the LDLR of Familial Hypercholesterolemia)

Subjects
Gene mutations -- Genetic aspects -- Reports, Medical research -- Reports, Medicine, Experimental -- Reports, Genetic research -- Genetic aspects -- Reports, Hypercholesterolemia -- Genetic aspects, Low density lipoproteins -- Reports -- Genetic aspects, Physical fitness -- Reports, Health
Abstract

2022 JAN 1 (NewsRx) -- By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Investigators publish new report on hypercholesterolemia. According to news originating from Ningbo, [...]

Published
2022

5. Study Data from Tongji University Update Understanding of Transcription Factors (E3 Ligase C-cbl Regulates Intestinal Inflammation Through Suppressing Fungi-induced Noncanonical Nf-kappa B Activation)

Subjects
Inflammation -- Research, Ligases -- Research, Fungi -- Research, DNA binding proteins -- Research, Biological sciences, Health
Abstract

2021 JUN 1 (NewsRx) -- By a News Reporter-Staff News Editor at Life Science Weekly -- Investigators publish new report on Proteins - Transcription Factors. According to news reporting from [...]

Published
2021

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