Magic™ Anti-IAV Monoclonal antibody, Clone N9232832

Influenza A viruses (IAVs) cause annual epidemic and severe pandemic outbreaks worldwide and result in high mortality. Despite the importance of surveillance for preventing IAV infection, the existing techniques are inefficient for ultrasensitive diagnosis in real time. In this study, we performed protein nanopore-based measurements to detect the highly conserved IAV RNA promoter at the single-molecule level. The binding of specific DNA probes to the IAV RNA promoter generated two types of characteristic nanopore signatures with single or double spikes of current blockade and substantially increased dwell times, which facilitated the discrimination of the IAV promoter from nonspecific macromolecules. Our DNA probe-mediated nanopore sensor will serve as an ultrasensitive, real-time, point-of-care diagnostic tool for highly pathogenic IAVs.

Secondary methicillin-resistantStaphylococcus aureus(MRSA) infection is a cause of severe pneumonia with high mortality during influenza A virus (IAV) pandemics. Alveolar macrophages (AMs) mount cellular defenses against IAV and MRSA infection, which occurs via the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. However, the activity and function of the NLRP3 inflammasome in MRSA pneumonia secondary to IAV infection remain unclear. To clarify this, we studied MRSA infection secondary to IAV both in vitro and in mouse model. The expression of the NLRP3 inflammasome was evaluated by quantitative reverse transcription polymerase chain reaction, immunofluorescence, Western blot, and enzyme-linked immunosorbent assay. The lung pathology and the rate of weight change were observed. We found that IAV infection for 1 week activated NLRP3 inflammasome. The enhanced expression of NLRP3, caspase-1, and cleaved caspase-1 was associated with MRSA infection secondary to IAV, but the expression of interleukin (IL)-1 beta decreased in superinfection with MRSA both in vitro and in vivo. The aggravated inflammatory pathology in MRSA pneumonia secondary to IAV infection was associated with decreased expression of IL-1 beta. And increased weight loss in MRSA pneumonia secondary to IAV infection was related to decreased concentration of IL-1 beta in serum. It infers that superinfection with MRSA reduces expression of IL-1 beta someway, and decreased expression of IL-1 beta impairs the host immunity and leads to aggravated pneumonia. These results contributed to our understanding of the detailed activity of the NLRP3 inflammasome, IL-1 beta, and their relationship with aggravation of MRSA pneumonia secondary to IAV infection. Immunotherapy targeting the IL-1 beta signaling pathway could be possible therapeutic strategy for secondary MRSA pneumonia.