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Title: Emerging etiological role of microbiome in human disease Early in 1840, Edward Hitchcock demonstrated the evolutionary relationships among plants and animals using a "paleontological chart," and now various forms of life on the earth can be outlined in the same phylogenetic tree based on rRNA gene. Bacteria, a branch in the phylogenetic tree, share the same root as humans. Besides commensally residing around human beings (or vice versa), bacteria form a complex flora in the human body. The implantation occurs at the moment when a child get born, or even earlier. Bacterial flora in the human body, referred to as the microbiome, fluctuates dramatically during the first three years of life before stabilizing[1]. Commensalism with bacteria is beneficial for human health in copious aspects, such as nutrition supplements, immunity stimulation, and cell protection. However, remarkable differences in microbiota are observed between healthy individuals and patients with kind of disorders. For instance, the gut microbiota signatures are varied between obese and healthy individuals[2]. Although the full extent is unknown, microbial dysbiosis was observed in diseases, and its vital role in pathogenesis becomes a hot spot in medical microbiology. D'Souza et al. reviewed the studies concerning microbial dysbiosis and esophageal mucosal disease and summarized that the pathogenesis of the esophageal mucosal disease is tightly connected with esophageal dysbiosis[3]. Multiple factors influence the microbiome, and dysbiosis responds to these factors, which causes and aggravates the pathogenesis. Two types of the esophageal microbiome are characterized between gastroesophageal reflux disease (GERD) patients and healthy controls, of which type II with a higher relative abundance of gram-negative anaerobes are in GERD. The lipopolysaccharides (LPS) "shell" around gram-negative organisms is responsible for the induction of the Toll-like-receptor (TLR) and inflammatory cascade. Higher abundant gram-negative bacteria excessively express LPS and subsequently activate the TLR-4-NF-B pathway, associated with expression of downstream mediators such as IL-8 and cyclooxygenase (COX)-2. Chemical-mediated mucosal injury and inflammation due to reflux of gastric acid and/or duodenal bile salts have been thought responsible for GERD. The etiological role of bacteria in this pathogenesis is underestimated. D'Souza et al. pointed out comprehensively that multifactor-driven dysbiosis contributes to a pro-inflammatory, cytokine-mediated state that starts in the submucosa and subsequently develops to esophageal mucosal diseases. The underestimation of the etiological role of the microbiome also exists in other diseases. For instance, metabolic disorders, like obesity, are related to gut dysbiosis. Although it is known that gut microbiota can regulate the host metabolism via fermenting end-products, such as SCFAs, modulating gut peptide signaling, and causing low-grade inflammation[4], the bacterial etiology of metabolic disorders is still not fully revealed. Synchronous evolution maintained the balance between the host and bacteria. Dysbiosis, an imbalance state of commensal bacteria, might contribute to the pathogenesis while achieving another balance. Further studies are warranted to illustrate the etiological role of dysbiosis on the host diseases, which is profound to health management and the essence of life evolution. Reference 1. Gilbert J, Blaser MJ, Caporaso JG, Jansson J, Susan V. Current understanding of the human microbiome. Nat Med 2018;24:392–400 [DOI: 10.1038/nm.4517.Current] 2. Zhao L. The gut microbiota and obesity: From correlation to causality. Nat Rev Microbiol 2013;11:639–47 [PMID: 23912213 DOI: 10.1038/nrmicro3089] 3. D’Souza SM, Houston K, Keenan L, Yoo BS, Parekh PJ, Johnson DA. Role of micriobial dysbiosis in the pathogenesis of esophageal mucosal disease--A paradigm shift from acid to bacteria. World J Gastroenterol 2021;27:2054–72 4. Muscogiuri G, Cantone E, Cassarano S, Tuccinardi D, Barrea L, Savastano S, Colao A. Gut microbiota: a new path to treat obesity. Int J Obes Suppl [Internet] 2019;9:10–9 [DOI: 10.1038/s41367-019-0011-7]Available from: http://dx.doi.org/10.1038/s41367-019-0011-7

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