Assessment of Sub-micrometer-Sized Particles with Practical Activities in an Underground Coal Mine.

Unlabelled: This assessment was designed to explore and characterize the airborne particles, especially for the sub-micrometer sizes, in an underground coal mine. Airborne particles present in the breathing zone were evaluated by using both (1) direct reading real-time instruments (RTIs) to measure real-time particle number concentrations in the workplaces and (2) gravimetric samplers to collect airborne particles to obtain mass concentrations and conduct further characterizations. Airborne coal mine particles were collected via three samplers: inhalable particle sampler (37 mm cassette with polyvinyl chloride (PVC) filter), respirable dust cyclone (10 mm nylon cyclone with 37 mm Zefon cassette and PVC filter), and a Tsai diffusion sampler (TDS).

Regulation of versican expression in macrophages is mediated by canonical type I interferon signaling via ISGF3.

Growing evidence supports a role for versican as an important component of the inflammatory response, with both pro- and anti-inflammatory roles depending on the specific context of the system or disease under investigation. Our goal is to understand the regulation of macrophage-derived versican and the role it plays in innate immunity. In previous work, we showed that LPS triggers a signaling cascade involving Toll-like receptor (TLR)4, the Trif adaptor, type I interferons, and the type I interferon receptor, leading to increased versican expression by macrophages.

MAP2K1 dampens cigarette smoke-induced inflammation via suppression of type I interferon pathway activation.

Chronic obstructive pulmonary disease (COPD), comprised of chronic bronchitis and emphysema, is a leading cause of morbidity and mortality worldwide. Mitogen-activated protein 2 kinase (MAP2K) pathway activation is present in COPD lung tissue and a genetic polymorphism in associates with FEV1 decline in COPD, suggesting it may contribute to disease pathogenesis. To test the functional contribution of in cigarette smoke (CS)-induced lung inflammation, we used a short-term CS exposure model in mice deficient in myeloid () and wild-type mice ().