Although silica-induced fibrosis and inflammation occurs independently of T, B, NK T, and
NK cells, lymphocytes regulate inflammation via modulation of the Nlrp3 inflammasome. The …

NLRP3 inflammasome activation occurs in response to hazardous particle exposures and is
critical for the development of particle-induced lung disease. Mechanisms of Lysosome …

Autophagy is an important metabolic mechanism that can promote cellular survival following
injury. The specific contribution of autophagy to silica-induced inflammation and disease is …

Epidemiological studies have shown a correlation between chronic biomass smoke exposure
and increased respiratory infection. Pulmonary macrophages are instrumental in both the …

Cellular and molecular mechanisms driving morbidity following SARS-CoV-2 infection have
not been well defined. The receptor for advanced glycation end products (RAGE) is a central …

Crystalline silica exposure can result in pulmonary fibrosis, where the pulmonary macrophage
is key as a result of its ability to react to silica particles. In the mouse silicosis model, there …

Dysregulated inflammation dominated by chemokine expression is a key feature of disease
following infection with the globally important human pathogens Zika virus (ZIKV) and …

Background Inhalation of crystalline silica is associated with pulmonary inflammation and
silicosis. Although silicosis remains a prevalent health problem throughout the world, effective …

Endotoxin is often used to activate NF-κB in vitro when assessing NLRP3 inflammasome
activation by various exogenous particles including nanoparticles. However, the endogenous …

Immunity to pulmonary infection typically requires elicitation of lung-resident T cells that
subsequently confer protection against secondary infection. The presence of tissue-resident T …