Periodontitis may induce gut microbiota dysbiosis via salivary microbiota

The aim of this study was to identify whether periodontitis induces gut microbiota dysbiosis via invasion by salivary microbes.First,faecal and salivary samples were collected from periodontally healthy participants(PH group,n=16)and patients with severe periodontitis(SP group,n=21)and analysed by 16S ribosomal RNA sequencing.Significant differences were observed in both the faecal and salivary microbiota between the PH and SP groups.Notably,more saliva-sourced microbes were observed in the faecal samples of the SP group.Then,the remaining salivary microbes were transplanted into C57BL6/J mice(the C-PH group and the C-SP group),and it was found that the composition of the gut microbiota of the C-SP group was significantly different from that of the C-PH group,with Porphyromonadaceae and Fusobacterium being significantly enriched in the C-SP group.In the colon,the C-SP group showed significantly reduced crypt depth and zonula occludens-1 expression.The m RNA expression levels of pro-inflammatory cytokines,chemokines and tight junction proteins were significantly higher in the C-SP group.To further investigate whether salivary bacteria could persist in the intestine,the salivary microbiota was stained with carboxyfluorescein diacetate succinimidyl ester and transplanted into mice.We found that salivary microbes from both the PH group and the SP group could persist in the gut for at least 24 h.Thus,our data demonstrate that periodontitis may induce gut microbiota dysbiosis through the influx of salivary microbes.

Gut microbiota dysbiosis involves in host non-alcoholic fatty liver disease upon pyrethroid pesticide exposure

A growing body of evidence has demonstrated the significance of the gut microbiota in host health,while the association between gut microbiota dysbiosis and multiple diseases is yet elusive in the scenario of exposure to widely used pesticides.Here,we show that gut microbiota dysbiosis involves in host's abnormal lipid metabolism and consequently the non-alcoholic fatty liver disease in Xenopus laevis upon exposure to cis-bifenthrin,one of the most prevalent pyrethroid insecticides in the world.With the guidance of gut microbiota analysis,we found that cis-bifenthrin exposure significantly perturbed the gut microbial community,and the specific taxa that served as biomarkers were identified.Metabolomics profiling and association analysis further showed that a significant change of intestinal metabolites involved in lipid metabolic pathways were induced along with the microbiota dysbiosis upon exposure to cis-bifenthrin.Detailed investigation showed an altered functional regulation of lipids in the liver after cis-bifenthrin exposure and the accumulation of lipid droplets in hepatocytes.Specifically,a change in deoxycholic acid alters bile acid hepatoenteral circulation,which affects lipid metabolism in the liver and ultimately causes the development of fatty liver disease.Collectively,these findings provide novel insight into the gut microbiota dysbiosis upon pesticide exposure and their potential implication in the development of chronic host diseases related to liver metabolic syndrome.

When smoke meets gut:deciphering the interactions between tobacco smoking and gut microbiota in disease development

Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Although previous research has explored the detrimental health effects of tobacco smoking,recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes.Numerous tobacco smoke components,such as nicotine,are found in the gastrointestinal tract and interact with gut microbiota,leading to lasting impacts on host health and diseases.This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality.We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health.Furthermore,this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.

Pathophysiological mechanisms underlying gastrointestinal symptoms in patients with COVID-19

Gastrointestinal(GI)symptoms,such as diarrhea,abdominal pain,vomiting,and anorexia,are frequently observed in patients with coronavirus disease 2019(COVID-19).However,the pathophysiological mechanisms connecting these GI symptoms to severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infections remain elusive.Previous studies indicate that the entry of SARS-CoV-2 into intestinal cells leads to downregulation of angiotensin converting enzyme 2(ACE2)receptors resulting in impaired barrier function.While intestinal ACE2 functions as a chaperone for the amino acid transporter B0AT1,the B0AT1/ACE2 complex within the intestinal epithelium acts as a regulator of gut microbiota composition and function.Alternations to the B0AT1/ACE2 complex lead to microbial dysbiosis through increased local and systemic immune responses.Previous studies have also suggested that altered serotonin metabolism may be the underlying cause of GI disorders involving diarrhea.The findings of elevated plasma serotonin levels and high fecal calprotectin in COVID-19 patients with diarrhea indicate that the viral infection evokes a systemic inflammatory response that specifically involves the GI.Interestingly,the elevated proinflammatory cytokines correlate with elevated serotonin and fecal calprotectin levels further supporting the evidence of GI inflammation,a hallmark of functional GI disorders.Moreover,the finding that rectal swabs of COVID-19 patients remain positive for SARS-CoV-2 even after the nasopharynx clears the virus,suggests that viral replication and shedding from the GI tract may be more robust than that of the respiratory tract,further indicating fecal-oral transmission as another important route of viral spread.This review summarized the evidence for pathophysiological mechanisms(impaired barrier function,gut inflammation,altered serotonin metabolism and gut microbiota dysbiosis)underlying the GI symptoms in patients with COVID-19.