Deficient neutrophil responses early in influenza infection promote viral replication and pulmonary inflammation.

Neutrophils play key protective roles in influenza infections, yet excessive neutrophilic inflammation is a hallmark of acute lung injury during severe infections. Phenotypic heterogeneity is increasingly recognized in neutrophil populations; however, how functional variation in neutrophils between individuals determine the diverse outcomes of influenza remains unclear. To examine immunologic responses that may drive varying outcomes in influenza, we infected C57BL/6 (B6) and A/J mice with mouse-adapted influenza A virus A/PR/8/34 H1N1.

Senolytic treatment attenuates immune cell infiltration without improving IAV outcomes in aged mice.

Aging is a major risk factor for poor outcomes following respiratory infections. In animal models, the most severe outcomes of respiratory infections in older hosts have been associated with an increased burden of senescent cells that accumulate over time with age and create a hyperinflammatory response. Although studies using coronavirus animal models have demonstrated that removal of senescent cells with senolytics, a class of drugs that selectively kills senescent cells, resulted in reduced lung damage and increased survival, little is known about the role that senescent cells play in the outcome of influenza A viral (IAV) infections in aged mice.

Spatiotemporal control of cell ablation using Ronidazole with Nitroreductase in Drosophila.

The ability to induce cell death in a controlled stereotypic manner has led to the discovery of evolutionary conserved molecules and signaling pathways necessary for tissue growth, repair, and regeneration. Here we report the development of a new method to genetically induce cell death in a controlled stereotypic manner in Drosophila. This method has advantages over other current methods and relies on expression of the E.

Factors influencing pursuit of management roles by clinically trained pharmacists: A modified Delphi survey.

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Deficiency in the mitophagy mediator Parkin accelerates murine skin allograft rejection.

Alterations in mitochondrial function and associated quality control programs, including mitochondrial-specific autophagy, termed mitophagy, are gaining increasing recognition in the context of disease. However, the role of mitophagy in organ transplant rejection remains poorly understood. Using mice deficient in Parkin, a ubiquitin ligase that tags damaged or dysfunctional mitochondria for autophagic clearance, we assessed the impact of Parkin-dependent mitophagy on skin-graft rejection.