Recruitment and training of alveolar macrophages after pneumococcal pneumonia.

Recovery from pneumococcal pneumonia remodels the pool of alveolar macrophages so that they exhibit new surface marker profiles, transcriptomes, metabolomes, and responses to infection. Mechanisms mediating alveolar macrophage phenotypes after pneumococcal pneumonia have not been delineated. IFN-γ and its receptor on alveolar macrophages were essential for certain, but not all, aspects of the remodeled alveolar macrophage phenotype.

Unique Roles for Phosphodiesterase 2 in Cyclic di-AMP Catabolism and Macrophage Responses.

Cyclic di-AMP (c-di-AMP) is an important signaling molecule for pneumococci, and as a uniquely prokaryotic product it can be recognized by mammalian cells as a danger signal that triggers innate immunity. Roles of c-di-AMP in directing host responses during pneumococcal infection are only beginning to be defined. We hypothesized that pneumococci with defective c-di-AMP catabolism due to phosphodiesterase deletions could illuminate roles of c-di-AMP in mediating host responses to pneumococcal infection.

Lung CD4 resident memory T cells remodel epithelial responses to accelerate neutrophil recruitment during pneumonia.

Previous pneumococcal experience establishes lung-resident IL-17A-producing CD4 memory T cells that accelerate neutrophil recruitment against heterotypic pneumococci. Herein, we unravel a novel crosstalk between CD4 T cells and lung epithelial cells underlying this protective immunity. Depletion of CD4 cells in pneumococcus-experienced mice diminished CXCL5 (but not CXCL1 or CXCL2) and downstream neutrophil accumulation in the lungs.

miR-155 in the progression of lung fibrosis in systemic sclerosis.

Background: MicroRNA (miRNA) control key elements of mRNA stability and likely contribute to the dysregulated lung gene expression observed in systemic sclerosis associated interstitial lung disease (SSc-ILD). We analyzed the miRNA gene expression of tissue and cells from patients with SSc-ILD. A chronic lung fibrotic murine model was used.

Investigating the role of ankyrin-rich membrane spanning protein in human immunodeficiency virus type-1 Tat-induced microglia activation.

Long-term persistence of human immunodeficiency virus type-1 (HIV) in the central nervous system (CNS) results in mild to severe neurocognitive impairment in a significant proportion of the HIV-infected population. These neurological deficits are known as HIV-associated neurocognitive disorders (HAND). Microglia are CNS-resident immune cells that are directly infected by HIV and consequently secrete proinflammatory molecules that contribute to HIV-induced neuroinflammation.