Association Between Fine Particulate Matter (PM_(2.5)) and the Reproductive System: A Narrative Review

In the last two decades,the issue on exposure to air pollution,especially fine particulate matter(PM_(2.5)),and its health effects has been a global concern.PM2.5 can enter the bronchi,lung cells,and subsequently the body,thus causing adverse health effects.One of these health effects include damage to the reproductive system.However,this has not gained much attention.In addition,PM_(2.5) contain toxic compounds,such as heavy metals or PAHs,which can cross various barriers,including epithelial barrier and blood-testis barrier,causing hormonal disorders in both,men and women,thus resulting in infertility.In this review,an attempt was made to provide useful information about effects of PM_(2.5) on the reproductive system.

Double-side role of short chain fatty acids on host health via the gut-organ axes

Short chain fatty acids(SCFA)exist in dietary foods and are produced by the fermentation of gut microbiota,and are considered an important element for regulating host health.Through blood circulation,SCFA produced in the gut and obtained from foods have an impact on the intestinal health as well as vital organs of the host.It has been recognized that the gut is the“vital organ”in the host.As the gut microbial metabolites,SCFA could create an“axis”connecting the gut and to other organs.Therefore,the“gut-organ axes”have become a focus of research in recent years to analyze organism health.In this review,we summarized the sources,absorption properties,and the function of SCFA in both gut and other peripheral tissues(brain,kidney,liver,lung,bone and cardiovascular)in the way of“gut-organ axes”.Short chain fatty acids exert both beneficial and pathological role in gut and other organs in various ways,in which the beneficial effects are more pronounced.In addition,the beneficial effects are reflected in both preventive and therapeutic effects.More importantly,the mechanisms behinds the gut and other tissues provided insight into the function of SCFA,assisting in the development of novel preventive and therapeutic strategies for maintaining the host health.

Over-activation of TLR5 signaling by high-dose flagellin induces liver injury in mice

Flagellin is a potent activator of a broad range of cell types that are involved in innate and adaptive immunity. Therefore, it is a good adjuvant candidate for vaccines, and it might function as a biological protectant against both major acute radiation syndrome during cancer radiotherapy and a mitigator of radiation emergencies. However, accumulating evidence has implicated flagellin in the occurrence of some inflammatory diseases, such as acute lung inflammation, cardiovascular collapse and inflammatory bowel disease. The aim of this study was to elucidate whether only flagellin-TLR5 signaling activation plays a role in the pathophysiology of liver or whether some other flagellin activity also contributes to liver injury either via bacterial infections or during clinical applications. Recombinant flagellin proteins with or without TLR5-stimulating activity were used to evaluate the role of flagellin-TLR5 signaling in liver injury in wild-type and TLR5 KO mice. Gross lesions and large areas of hepatocellular necrosis were observed in liver tissue 12 h after the intraperitoneal administration of 100 or 200 pg flagellin （FliC） in a dose-and time-dependent manner in wild-type mice, but not in TLR5 KO mice. Deletion of the N-terminal or TLR5 binding domain of flagellin inhibited flagellin-induced inflammatory responses and the subsequent acute liver function abnormality and damage. These data confirmed that flagellin is an essential determinant of liver injury and demonstrated that the over-activation of TLR5 signaling by high-dose flagellin caused acute inflammatory responses, neutrophil accumulation and oxidative stress in the liver, which contributes to the progression and severity of flagellin-induced liver injury.