QFQiang Feng

Qiang Feng

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

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Previous Organizations / Institutes

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Qiang Feng has a total of 13 co-authors. Here are the top co-authors by number of shared publications:

  • Chuan Liu

    BGI-Shenzhen, Shenzhen, 518083, China

    1 shared publication
  • Jun Zhang

    Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, Shandong, People’s Republic of China

    1 shared publication
  • Liang Xiao

    BGI-Shenzhen

    1 shared publication
  • Lili Su

    BGI-Shenzhen, Shenzhen, 518083, China

    1 shared publication
  • Lingling Li

    Nutrition Department, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510655, China

    1 shared publication
  • Qing He

    Department of Gastroenterology, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510655, China

    1 shared publication

Latest Publications

  • Open Access

    Linking Periodontitis with Inflammatory Bowel Disease through the Oral–Gut Axis: The Potential Role of Porphyromonas gingivalis

    by Xinyi Huang, Yilin Li, Jun Zhang, Qiang Feng

    Periodontitis and inflammatory bowel disease (IBD) are both chronic inflammatory diseases that are characterized by abnormal host immune responses and microbiota dysbiosis. Emerging evidence implies potential associations between periodontitis and IBD. Porphyromonas gingivalis (P. gingivalis), a primary cause of periodontitis, is thought to play a role in the development of IBD through the oral–gut disease axis. However, the precise mechanisms of its involvement remain enigmatic. In this narrative review, we begin with a discussion of the bidirectional relationship between periodontitis and IBD and the involvement of P. gingivalis in each of the two diseases. Further, we summarize the possible routes by which P. gingivalis links periodontitis and IBD through the oral–gut axis, as well as the underlying mechanisms of its involvement in the pathogenesis of IBD. Collectively, P. gingivalis participates in the progression of IBD through gut dysbiosis, impairment of the intestinal barrier, release of inflammatory mediators, and disturbance of the immune response. The above findings may provide new insights for exploring novel biomarkers and potential therapeutic approaches for IBD.


  • Dysbiosis of the fecal microbiota in the TNBS-induced Crohn’s disease mouse model

    by Qing He, Xiaoping Li, Chuan Liu, Lili Su, Zhongkui Xia, Xin Li, Ying Li, Lingling Li, Ting Yan, Qiang Feng, et al.

    Crohn’s disease (CD) is characterized by chronic transmural inflammation. The symptom of the mice model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) is closed to human under CD condition, so this kind of animal is widely used in the related researches. Although the dysbiosis of the fecal microbiota has been proved to play an important role in the patients with CD, the composition of the gastrointestinal microbiota in the mouse model under disease condition is still unclear. In the current study, male 7-week BALB/c mice were anesthetized and intrarectal administrated by ethanol (ET group), TNBS in ethanol (TN group), and phosphate buffered saline (PBS) (CK group) as control. The symptoms of individuals under the CD condition were observed, and the changes of the bacterial taxonomic structure and functional composition were revealed by next-generation sequencing (NGS) 16S sequencing. The BALB/c mice in TN group demonstrated CD-like symptoms and the damages in the intestinal tract. The NGS 16S results exhibited that the diversity and microbial composition under CD condition are significantly different with those in ET group. The KEGG Orthology (KO) profile were generated from PICRUSt, and function modules such as methanogenesis (M00347) and microcin C transport system (M00349) were found enriched in the individuals in the TN group. This study proved that mouse model induced by TNBS could develop the similar symptom to CD patient, and we firstly showed the significant intestinal microbe changes on both taxonomic structure and functional composition in this mouse model.