Human menstrual blood-derived mesenchymal stem cells (MenSCs) and their secreted small extracellular vesicles (EVs) had been proven to relieve inflammation, tissue damage, and fibrosis in various organs. The microenvironment induced by inflammatory cytokines can promote mesenchymal stem cells (MSCs) to secrete more substances (including EVs) that could regulate inflammation. Inflammatory bowel disease (IBD) is a chronic idiopathic intestinal inflammation, the etiology and mechanism of which are unclear. At present, the existing therapeutic methods are ineffective for many patients and have obvious side effects. Hence, we explored the role of tumor necrosis factor α- (TNF-α-) pretreated MenSC-derived small EV (MenSCs-sEV^TNF-α) in a mouse model of dextran sulfate sodium- (DSS-) induced colitis, expecting to find better therapeutic alterations. In this research, the small EVs of MenSCs were obtained by ultracentrifugation. MicroRNAs of small EVs derived from MenSCs before and after TNF-α treatment were sequenced, and the differential microRNAs were analyzed by bioinformatics. The small EVs secreted by TNF-α-stimulating MenSCs were more effective in colonic mice than those secreted directly by MenSCs, as evidenced by the results of histopathology analysis of colonic tissue, immunohistochemistry for tight junction proteins, and enzyme-linked immunosorbent assay (ELISA) for cytokine expression profiles in vivo. The process of MenSCs-sEV^TNF-α relieving colonic inflammation was accompanied by the polarization of M2 macrophages in the colon and miR-24-3p upregulation in small EVs. In vitro, both MenSC-derived sEV (MenSCs-sEV) and MenSCs-sEV^TNF-α reduced the expression of proinflammatory cytokines, and MenSCs-sEV^TNF-α can increase the portion of M2 macrophages. In conclusion, after TNF-α stimulation, the expression of miR-24-3p in small EVs derived from MenSCs was upregulated. MiR-24-3p was proved to target and downregulate interferon regulatory factor 1 (IRF1) expression in the murine colon and then promoted the polarization of M2 macrophages. The polarization of M2 macrophages in colonic tissues then reduced the damage caused by hyperinflammation.

The H10 subtype avian influenza virus (AIV), an important zoonotic pathogen, is widely prevalent in host species (wild fowl) and continues to infect humans, imposing a huge threat to public health. Thus, the H10 subtype AIV is considered a potential pandemic strain and has drawn the attention of scholars worldwide. Therefore, a fast, sensitive, and economical detection method for H10 subtype AIV needs to be developed for the surveillance and prevention of this infection. Quantum dot fluorescent microsphere‐based immunochromatographic strip (QDFM‐ICS) has a great application prospect in the rapid detection of the virus. In this study, two monoclonal antibodies (1E8 and 2G9) were generated by immunizing mice with the purified hemagglutinin (HA) protein, and QDFM‐ICS was designed to detect the H10 subtype influenza antigen. We illustrated that the limit of detection (LOD) of QDFM‐ICS for the HA titer and purified HA protein of the H10 subtype AIV was 0.125 per 80 μL of the sample and 4 ng/mL, respectively. The specificity of QDFM‐ICS was 100%, which indicated that mAb 2G9 specifically bound to the H10 subtype influenza antigen without cross‐reacting with other subtype AIVs. The method has good reproducibility. Additionally, the results of preliminary tests on clinical samples showed high consistency between QDFM‐ICS and real‐time reverse transcription‐polymerase chain reaction. The QDFM‐ICS has simple analysis steps and can produce objective results within 15 min. Hence, it can be suggested that QDFM‐ICS can be used to monitor and prevent the infection caused by H10 subtype AIVs.

Diabetes imposes a huge burden worldwide. Islet transplantation is an alternative therapy for diabetes. However, tacrolimus, a kind of immunosuppressant after organ transplantation, is closely related to post-transplant diabetes mellitus. Mesenchymal stem cells (MSCs) have attracted interest for their potential to alleviate diabetes. In vivo experiments revealed that human menstrual blood-derived stem cells (MenSCs) treatment improved tacrolimus-induced blood glucose, body weight, and glucose tolerance disorders in mice. RNA sequencing was used to analyze the potential therapeutic targets of MenSCs. In this study, we illustrated that cystathionine β-synthase (CBS) contributed to tacrolimus -induced islet dysfunction. Using β-cell lines (MIN6, β-TC-6), we demonstrated that MenSCs ameliorated tacrolimus-induced islet dysfunction in vitro. Moreover, MenSC reduced the tacrolimus-induced elevation of CBS levels and significantly enhanced the viability, anti-apoptotic ability, glucose-stimulated insulin secretion (GSIS), and glycolytic flux of β-cells. We further revealed that MenSCs exerted their therapeutic effects by inhibiting CBS expression to activate the IL6/JAK2/STAT3 pathway. In conclusion, we showed that MenSCs may be a potential strategy to improve tacrolimus-induced islet dysfunction.