Background Earlier studies suggest that probiotics have protective effects in the prevention of respiratory tract infections (RTIs). Whether such benefits apply to RTIs of viral origin and mechanisms supporting the effect remain unclear. Aim To determine the role of gut microbiota modulation on clinical and laboratory outcomes of viral RTIs. Methods We conducted a systematic review of articles published in Embase and MEDLINE through 20 April 2020 to identify studies reporting the effect of gut microbiota modulation on viral RTIs in clinical studies and animal models. The incidence of viral RTIs, clinical manifestations, viral load and immunological outcomes was evaluated. Results We included 58 studies (9 randomized controlled trials; 49 animal studies). Six of eight clinical trials consisting of 726 patients showed that probiotics administration was associated with a reduced risk of viral RTIs. Most commonly used probiotics were Lactobacillus followed by Bifidobacterium and Lactococcus. In animal models, treatment with probiotics before viral challenge had beneficial effects against influenza virus infection by improving infection-induced survival (20/22 studies), mitigating symptoms (21/21 studies) and decreasing viral load (23/25 studies). Probiotics and commensal gut microbiota exerted their beneficial effects through strengthening host immunity. Conclusion Modulation of gut microbiota represents a promising approach against viral RTIs via host innate and adaptive immunity regulation. Further research should focus on next generation probiotics specific to viral types in prevention and treatment of emerging viral RTIs. Supplementary Information The online version contains supplementary material available at 10.1007/s00394-021-02519-x.

OBJECTIVE:Cigarette smoke extracts (CSE) could promote esophageal squamous cell carcinoma (ESCC) through upregulation of cyclooxygenase-2 (COX-2) expression. Promoter methylation mediates the transcriptional modulation of the COX-2 gene. The aim of the study was to explore whether COX-2 promoter methylation regulated COX-2 expression and functional activity in ESCC exposed to CSE. METHODS:The methylation status of COX-2 promoter in two human ESCC cell lines, EC109 and TE-1, was examined using bisulfite sequencing analysis. COX-2 mRNA and protein expression were detected by reverse-transcription polymerase chain reaction and Western blot. Prostaglandin E2 (PGE2) was examined by enzyme linked immunosorbent assay (ELISA). RESULTS:The promoter was hypermethylated in TE-1 which had a low level of COX-2 expression and was hypomethylated in EC109 with a relatively high level of COX-2 expression. Stimulation by cigarette smoke ethanol extract (EE) resulted in increased COX-2 expression in EC109, but not in TE-1. Treatment with 5-aza-2'-deoxycytidine (5-aza-DC) demethylated the promoter and upregulated COX-2 expression as well as PGE2 production in TE-1, especially followed by EE stimulation. No significant effect was observed in EC109. CONCLUSION:These findings suggest that promoter methylation may be one of the mechanisms regulating COX-2 expression in ESCC in response to stimulation of CSE.KEY WORD: cigarette smoke, cyclooxygenase-2, esophageal neoplasm, methylation. INTRODUCTIONEsophageal squamous cell carcinoma (ESCC) is the most common esophageal cancer and the fourth most common cause of cancer death in China. 1 Great efforts have been made since the etiology of ESCC has not been fully elucidated. Cigarette smoke contains over 3000 chemicals, many of which have been identified as carcinogens and are known to initiate and promote tumorigenesis.2 Epidemiological researches have shown that cigarette smoking is one of the risk factors Correspondence to: Shu Tian ZHANG, Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, 95 Yong'an Road, Xicheng District, Beijing 100050, China. Email: zhangxym2006@tom.com Xin Ying MENG and Sheng Tao ZHU contributed equally to this paper. 2012; 13; 208-213 doi: 10.1111/j.1751-2980.2012.00578.x 208 for the development of ESCC. 3,4 The chemicals may promote the formation of DNA adduct and modulate cell proliferation, apoptosis and angiogenesis in carcinogenesis. 5 However, the mechanism of cigarette smoke in ESCC carcinogenesis is still unclear. Journal of Digestive DiseasesCyclooxygenase-2 (COX-2) is a rate-limiting enzyme involved in the conversion of arachidonic acid to prostaglandin (PG). COX-2 expression can be induced by a variety of stimuli, such as mitogens, cytokines and growth factors. The overexpression of COX-2 has been observed in ESCC and its premalignant lesions, 6,7 which suggests that COX-2 may be associated with the carcinogenesis and/or the progression of ESCC. Our recent study reported that cigarette smoke could activa...

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Our diagnostic model is useful for diagnosing gastric precancerous lesions and GC.