Rapid and sensitive lateral flow biosensor for the detection of GII human norovirus based on immunofluorescent nanomagnetic microspheres.

Human norovirus (HuNoV) is the most predominant viral agents of acute gastroenteritis. Point-of-care testing (POCT) based on lateral flow immunochromatography (LIFC) has become an important tool for rapid diagnosis of HuNoVs. However, low sensitivity and lack of quantitation are the bottlenecks of traditional LIFC. Thus, we established a rapid and accurate technique that combined immunomagnetic enrichment (IM) with LFIC to identify GII HuNoVs in fecal specimens. Before preparing immunofluorescent nanomagnetic microspheres and achieving the effect of HuNoV enrichment in IM and fluorescent signal in LFIC, amino-functionalized magnetic beads (MBs) and carboxylated quantum dots (QDs) were coupled at a mass ratio of 4:10. Anti-HuNoV monoclonal antibody was then conjugated with QDs-MB. The limit of detection was 1.56 × 104 copies/mL, and the quantitative detection range was 1.56 × 104 copies/mL-1 × 106 copies/mL under optimal circumstances. The common HuNoV genotypes GII.2, GII.3, GII.4, and GII.17 can be detected, there was no cross-reaction with various enteric viruses, including rotavirus, astrovirus, enterovirus, and sapovirus. A comparison between IM-LFIC and RT-qPCR for the detection of 87 fecal specimens showed a high level of agreement (kappa = 0.799). This suggested that the method is rapid and sensitive, making it a promising option for point-of-care testing in the future.

Exosomes derived from mycobacterium tuberculosis-infected MSCs induce a pro-inflammatory response of macrophages.

Tuberculosis (TB) is a common infectious disease caused by Mycobacterium tuberculosis (M.tb), and macrophages serve as the primary natural host of M.tb. Mesenchymal stem cells (MSCs)-derived exosomes play an essential role in inflammatory responses. This study aimed to determine the role of exosomes derived from M.tb-infected MSCs (Exo-MSCs-M.tb) on macrophages in vitro and in vivo and the underlying mechanisms. Here, we demonstrated that M.tb infection promoted the production of Exo-MSCs-M.tb, but did not influence MSCs proliferation. Exo-MSCs-M.tb were taken up by macrophages and then induced the pro-inflammatory response of macrophages through elevating the production of TNF-α, RANTES, and iNOS. Also, pro-inflammatory response induced by Exo-MSCs-M.tb displayed a time-dependent pattern in macrophages, in which the highest level of inflammatory response was observed at 72 hours post-infection of MSCs. In addition, the effect of Exo-MSCs-M.tb was mediated through TLR2/4 and MyD88 signaling pathways. Furthermore, Exo-MSCs-M.tb could induce the pro-inflammatory response in mice in vivo, and exosomes isolated from Exo-MSCs-M.tb-treated mice could also promote the pro-inflammatory response. Taken together, these results indicate that Exo-MSCs-M.tb induced the pro-inflammatory response of macrophages through TLRs signaling. This study provides new insight into the potential of MSCs-derived exosomes for the treatment of TB.