Loss of pulmonary tissue protection and neutrophil microbicidal defects promote severe infection during influenza A virus infection.

Invasive pulmonary aspergillosis (IPA) is a severe fungal disease caused by () that may spread hematogenously to extrapulmonary organs. IPA is typically associated with a broad spectrum of immunocompromised conditions and constitutes a high mortality rate. While the association of influenza as a risk for secondary bacterial infections is well appreciated, emerging evidence indicates that influenza-hospitalized patients demonstrate increased susceptibility to severe aspergillosis infection.

The vaccine dosing effect overcomes the reduced immunogenic potential and in vivo efficacy of 33F pneumococcal serotype.

Serotype 33F is an emerging Streptococcus pneumoniae (Spn) serotype associated with asymptomatic nasopharyngeal (NP) colonization and invasive pneumococcal disease (IPD). Serotype 33F is a component in the advanced version of the pneumococcal conjugate vaccine 15 (PCV 15) formulation. However, in the murine vaccination model, serotype 33F exhibits reduced immunogenicity, correlating with reduced protection against 33F.

The chemokine receptor CXCR3 promotes CD8 T cell-dependent lung pathology during influenza pathogenesis.

The dual role of CD8 T cells in influenza control and lung pathology is increasingly appreciated. To explore whether protective and pathological functions can be linked to specific subsets, we dissected CD8 T responses in influenza-infected murine lungs. Our single-cell RNA-sequencing (scRNA-seq) analysis revealed notable diversity in CD8 T subpopulations during peak viral load and infection-resolved state.

IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection.

The upper respiratory tract (nasopharynx or NP) is the first site of influenza replication, allowing the virus to disseminate to the lower respiratory tract or promoting community transmission. The host response in the NP regulates an intricate balance between viral control and tissue pathology. The hyper-inflammatory responses promote epithelial injury, allowing for increased viral dissemination and susceptibility to secondary bacterial infections.

Cellular Heterogeneity and Molecular Reprogramming of the Host Response during Influenza Acute Lung Injury.

An exuberant host response contributes to influenza A virus (IAV) (or influenza)-mediated lung injury. However, despite significant information on the host response to IAV, the cellular framework and molecular interactions that dictate the development of acute injury in IAV-infected lungs remain incompletely understood. We performed an unbiased single-cell RNA sequencing (scRNAseq) analysis to examine the cellular heterogeneity and regulation of host responses in the IAV model of acute lung injury.

Assessment of Total, PTEN, and AR-V7 Circulating Tumor Cell Count by Flow Cytometry in Patients with Metastatic Castration-Resistant Prostate Cancer Receiving Enzalutamide.

Introduction: Metastatic castration-resistant prostate cancer (mCRPC) is a deadly disease. Enzalutamide is an oral second-generation anti-androgen that is active in mCRPC. Circulating tumor cells (CTC) count correlates with overall survival (OS) in mCRPC, whereas detection of the androgen-receptor splice variant 7 (AR-V7) in CTC predicts poor response to oral second-generation anti-androgens.