Microbiological evidences for gastric cardiac microflora dysbiosis inducing the progression of inflammation. Issue 6 (29th January 2020)

• Record Type: Journal Article
• Authors: Yan, Ruijing; Guo, Yi; Gong, Qingyun; Chen, Man; Guo, Yuanning; Yang, Peng; Huang, Hao; Huang, Haihua; Huang, Wen; Ma, Zikai; Zheng, Zhijian; Tian, Dongping; Su, Min
• Is Part Of: Journal of gastroenterology and hepatology. Volume 35:Issue 6(2020)
• Page Start: 1032
• Page End: 1041
• Publication Date: 2020-01-29
• Subjects: DNA repair -- gastroscopy -- Helicobacter pylori -- inflammation -- microbiome; Gastroenterology -- Periodicals; Digestive organs -- Diseases -- Periodicals; Liver -- Diseases -- Periodicals; Gastroenterology -- Periodicals; Liver Diseases -- Periodicals; 616.33
• DOI: 10.1111/jgh.14946
• Languages: English
• ISSNs: 0815-9319

Abstract

Abstract: Background and Aim: Nowadays, anti‐inflammation treatment is a promising approach for preventing tumorigenesis, and human microflora is closely related to inflammation. This study aimed to investigate the gastric cardiac microbiome and identify inflammation‐related microorganisms for gastric cardiac inflammation. Methods: We performed 16S rRNA sequencing on a total of 11 healthy individuals and 89 individuals with different degree of gastric cardiac inflammation. Immunohistochemistry was used for verifying candidate bacteria. Phylogenetic reconstruction of unobserved states (picrust ) was used for predicting the pathways involved by cardiac microflora. Results: The resident phyla in normal were Proteobacteria, Firmicutes, Bacteroides, and Actinobacteria, and the dominant genus in normal were Halomonas, shewanella, and Comamonas . In the progression of gastric cardiac inflammation, the diversity of cardiac microflora did not change ( P > 0.05). However, the composition structure of cardiac microflora varied between healthy and inflamed tissues ( P < 0.05). Meanwhile, there were 64 species parallel increased with inflammation degree, especially Helicobacter pylori, Lactobacillus spp. Additionally, inflammation‐related species were detected ( P < 0.05), including H. pylori, Acinetobacter ursingii, and Streptococcus agalactiae . Higher H. pylori colonization was positively related to the progression of cardiac inflammation ( γ coefficient = 0.678, P < 0.001), and it also influenced the cardiac microbial community structure. Cardiac microflora also participated in DNA repair pathways and is affected by the relative abundance of H. pylori ( P < 0.0001). Conclusions: Cardiac microflora dysbiosis, especially the increasing of the relevant abundance of H. pylori, promotes the progression of cardiac inflammation.