House Dust Mite Aeroallergen Suppresses Leukocyte Phagocytosis and Netosis Initiated by Pneumococcal Lung Infection.

Asthmatics are highly susceptible to developing lower respiratory tract infections caused by (SPN, the pneumococcus). It has recently emerged that underlying allergic airway disease creates a lung microenvironment that is defective in controlling pneumococcal lung infections. In the present study, we examined how house dust mite (HDM) aeroallergen exposure altered immunity to acute pneumococcal lung infection.

G-CSFR antagonism reduces mucosal injury and airways fibrosis in a virus-dependent model of severe asthma.

Background And Purpose: Asthma is a chronic disease that displays heterogeneous clinical and molecular features. A phenotypic subset of late-onset severe asthmatics has debilitating fixed airflow obstruction, increased neutrophilic inflammation and a history of pneumonia. Influenza A virus (IAV) is an important viral cause of pneumonia and asthmatics are frequently hospitalised during IAV epidemics.

Novel Therapies for Pneumonia-Associated Severe Asthma Phenotypes.

Distinct asthma phenotypes are emerging from well-defined cohort studies and appear to be associated with a history of pneumonia. Asthmatics are more susceptible to infections caused by Streptococcus pneumoniae; however, the mechanisms that underlie defective immunity to this pathogen are still being elucidated. Here, we discuss how alternatively activated macrophages (AAMs) in asthmatics are defective in bacterial phagocytosis and how respiratory viruses disrupt essential host immunity to cause bacterial dispersion deeper into the lungs.

Excessive Reactive Oxygen Species Inhibit IL-17A γδ T Cells and Innate Cellular Responses to Bacterial Lung Infection.

Excessive reactive oxygen species (ROS) are detrimental to immune cellular functions that control pathogenic microbes; however, the mechanisms are poorly understood. Our aim was to determine the immunological consequences of increased ROS levels during acute bacterial infection. We used a model of S (Spn) lung infection and superoxide dismutase 3-deficient (SOD3) mice, as SOD3 is a major antioxidant enzyme that catalyses the dismutation of superoxide radicals.

The transcriptomic response of Streptococcus pneumoniae following exposure to cigarette smoke extract.

Exposure to cigarette smoke is a risk factor for respiratory diseases. Although most research has focused on its effects on the host, cigarette smoke can also directly affect respiratory pathogens, in some cases enhancing virulence. Streptococcus pneumoniae (the pneumococcus) is a leading cause of community-acquired pneumonia worldwide, however data on the effects of cigarette smoke on the pneumococcus are sparse.