Correction: Budesonide promotes airway epithelial barrier integrity following double-stranded RNA challenge.

[This corrects the article DOI: 10.1371/journal.pone.

The gene regulatory basis of bystander activation in CD8 T cells.

CD8 T cells are classically recognized as adaptive lymphocytes based on their ability to recognize specific foreign antigens and mount memory responses. However, recent studies indicate that some antigen-inexperienced CD8 T cells can respond to innate cytokines alone in the absence of cognate T cell receptor stimulation, a phenomenon referred to as bystander activation. Here, we demonstrate that neonatal CD8 T cells undergo a robust and diverse program of bystander activation, which corresponds to enhanced innate-like protection against unrelated pathogens.

Protein kinase D3 promotes neutrophil migration during viral infection.

Protein kinase D (PKD) is a serine/threonine kinase family with three isoforms (PKD1-3) that are expressed in most cells and implicated in a wide array of signaling pathways, including cell growth, differentiation, transcription, secretion, polarization and actin turnover. Despite growing interest in PKD, relatively little is known about the role of PKD in immune responses. We recently published that inhibiting PKD limits proinflammatory cytokine secretion and leukocyte accumulation in mouse models of viral infection, and that PKD3 is highly expressed in the murine lung and immune cell populations.

Budesonide promotes airway epithelial barrier integrity following double-stranded RNA challenge.

Airway epithelial barrier dysfunction is increasingly recognized as a key feature of asthma and other lung diseases. Respiratory viruses are responsible for a large fraction of asthma exacerbations, and are particularly potent at disrupting epithelial barrier function through pattern recognition receptor engagement leading to tight junction dysfunction. Although different mechanisms of barrier dysfunction have been described, relatively little is known about whether barrier integrity can be promoted to limit disease.

Inhibiting Protein Kinase D Promotes Airway Epithelial Barrier Integrity in Mouse Models of Influenza A Virus Infection.

Rationale: Protein kinase D (PKD) is a serine/threonine kinase family that is involved in a wide array of signaling pathways. Although PKD has been implicated in immune responses, relatively little is known about the function of PKD in the lung or during viral infections.

Objectives: We investigated the hypothesis that PKD is involved in multiple aspects of host response to viral infection.

Lung megakaryocytes are immune modulatory cells.

Although platelets are the cellular mediators of thrombosis, they are also immune cells. Platelets interact both directly and indirectly with immune cells, impacting their activation and differentiation, as well as all phases of the immune response. Megakaryocytes (Mks) are the cell source of circulating platelets, and until recently Mks were typically only considered bone marrow-resident (BM-resident) cells.

Diesel exhaust particle exposure reduces expression of the epithelial tight junction protein Tricellulin.

Background: While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelial barrier. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems.

Methods: 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 μg/cm SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls.

Distinct roles for MDA5 and TLR3 in the acute response to inhaled double-stranded RNA.

The airway epithelial barrier is critical for preventing pathogen invasion and translocation of inhaled particles into the lung. Epithelial cells also serve an important sentinel role after infection and release various pro-inflammatory mediators that recruit and activate immune cells. Airway epithelial barrier disruption has been implicated in a growing number of respiratory diseases including viral infections.

The leaky lung test: a pilot study using inhaled mannitol to measure airway barrier function in asthma.

: Airway epithelial barrier dysfunction is emerging as an important feature of asthma pathogenesis, but this is difficult to measure in individual subjects. We aimed to develop a noninvasive way to measure airway permeability in asthma. : Healthy controls and subjects with mild asthma inhaled dry powder mannitol in a dose-escalating manner on two separate occasions, stopping at 155 mg or 315 mg.