Background COVID-19 is an infectious disease characterized by multiple respiratory and extrapulmonary manifestations, including gastrointestinal symptoms. Although recent studies have linked gut microbiota to infectious diseases such as influenza, little is known about the role of the gut microbiota in COVID-19 pathophysiology. Methods To better understand the host-gut microbiota interactions in COVID-19, we characterized the gut microbial community and gut barrier function using metagenomic and metaproteomic approaches in 63 COVID-19 patients and 8 non-infected controls. Both immunohematological parameters and transcriptional profiles were measured to reflect the immune response in COVID-19 patients. Results Altered gut microbial composition was observed in COVID-19 patients, which was characterized by decreased commensal species and increased opportunistic pathogenic species. Severe illness was associated with higher abundance of four microbial species (i.e., Burkholderia contaminans, Bacteroides nordii, Bifidobacterium longum, and Blautia sp. CAG 257), six microbial pathways (e.g., glycolysis and fermentation), and 10 virulence genes. These severity-related microbial features were further associated with host immune response. For example, the abundance of Bu. contaminans was associated with higher levels of inflammation biomarkers and lower levels of immune cells. Furthermore, human-origin proteins identified from both blood and fecal samples suggested gut barrier dysfunction in COVID-19 patients. The circulating levels of lipopolysaccharide-binding protein increased in patients with severe illness and were associated with circulating inflammation biomarkers and immune cells. Besides, proteins of disease-related bacteria (e.g., B. longum) were detectable in blood samples from patients. Conclusions Our results suggest that the dysbiosis of the gut microbiome and the dysfunction of the gut barrier might play a role in the pathophysiology of COVID-19 by affecting host immune homeostasis.

BackgroundMen are at higher risk of developing chronic lymphocytic leukemia (CLL) than women. DNA methylation has been shown to play important roles in a number of cancers. There are differences in the DNA methylation pattern between men and women. In this study, we investigated whether this contributes to the sex-related difference of B cell CLL risk.MethodsUsing the HumanMethylation450 BeadChip, we profiled the genome-wide DNA methylation pattern of CD19+ B cells from 48 CLL patients (29 female patients and 19 male patients) and 28 healthy people (19 women and 9 men).ResultsWe identified 1043 sex-related differentially methylated positions (DMPs) related to CLL, 56 of which are located on autosomes and 987 on the X chromosome. Using published B cell RNA-sequencing data, we found 18 genes covered by the DMPs also have different expression levels in male and female CLL patients. Among them, TRIB1, an autosome gene, has been shown to promote tumor growth by suppressing apoptosis.ConclusionsOur study represents the first epigenome-wide association study (EWAS) that investigates the sex-related differences in cancer, and indicated that DNA methylation differences might contribute to the sex-related difference in CLL risk.Electronic supplementary materialThe online version of this article (10.1186/s13293-018-0213-7) contains supplementary material, which is available to authorized users.

Epidemiological studies are inconclusive regarding the association between dietary fiber intake and endometrial cancer risk. Thus, we aimed to conduct a meta-analysis to clarify the association between dietary fiber and endometrial cancer risk. We searched the PubMed and ISI Web databases for relevant studies through March 2018. The association between dietary fiber and endometrial cancer risk was evaluated by conducting a meta-analysis including 3 cohort and 12 case–control studies. A significant negative association was observed between total dietary fiber intake and endometrial cancer risk in 11 case–control studies (odds ratios (OR) 0.76, 95% confidence interval (CI): 0.64–0.89, I2 = 35.2%, p = 0.117), but a marginal positive association was observed in three cohort studies (relative risk (RR) 1.22, 95% CI: 1.00–1.49, I2 = 0.0%, p = 0.995). Particularly, a negative association was observed in North America (OR = 0.70, 95% CI: 0.59–0.83, I2 = 8.9%, p = 0.362). In addition, a positive association was observed in cereal fiber (RR = 1.26, 95% CI: 1.03–1.52, I2 = 0.0%, p = 0.530, 3 cohort studies) and a negative association was observed in vegetable fiber (OR = 0.74, 95% CI: 0.58–0.94, I2 = 0.0%, p = 0.445, 3 case–control studies). In conclusion, negative associations with endometrial cancer risk were observed for higher total dietary fiber intake and higher vegetable fiber intake in the case–control studies. However, results from the cohort studies suggested positive relationships of higher total fiber intake and higher cereal fiber intake with endometrial cancer risk.