Respiratory and systemic impacts following MWCNT inhalation in B6C3F1/N mice.

Background: A very pure multi-walled carbon nanotube (MWCNT) that was shown to have very low toxicity in vitro, was evaluated for lung and systemic effects and distribution following inhalation exposure.

Methods: B6C3F1/N mice were exposed to varying doses (0, 0.06, 0.

Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM Levels from Wildfire Smoke.

Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known.

Adverse effects of wood smoke PM(2.5) exposure on macrophage functions.

Epidemiological studies have shown a correlation between chronic biomass smoke exposure and increased respiratory infection. Pulmonary macrophages are instrumental in both the innate and the adaptive immune responses to respiratory infection. In the present study, in vitro systems were utilized where alveolar macrophages (AM) and bone marrow-derived macrophages (BMdM) were exposed to concentrated wood smoke-derived particulate matter (WS-PM) and mice were exposed in vivo to either concentrated WS-PM or inhaled WS.

IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung.

Allergic asthma is a chronic inflammatory disorder of the airway associated with bronchial obstruction, airway hyper-reactivity (AHR), and mucus production. The epithelium may direct and propagate asthmatic-like responses. Central to this theory is the observation that viruses, air pollution, and allergens promote epithelial damage and trigger the generation of IL-25, IL-33, and TSLP via innate pathways such as TLRs and purinergic receptors.

Innate immune processes are sufficient for driving silicosis in mice.

The lung is constantly exposed to potentially pathogenic particles and microorganisms. It has become evident recently that not only innate but also adaptive immune responses to particulates, such as SiO(2) entering the respiratory tract, are complex and dynamic events. Although the cellular mechanisms and anatomical consequences involved in the development of silicosis have been studied extensively, they still remain poorly understood.

Biomass smoke exposures: toxicology and animal study design.

The International Biomass Smoke Health Effects (IBSHE) conference was convened in Missoula, MT, to define our current knowledge of smoke exposure and the potential health effects. In an effort to ascertain the relative health effects of an exposure to biomass smoke, numerous studies have utilized either animal or in vitro systems. A wide variety of systems that have been employed ranged from more mainstream animal models (i.

Murine pulmonary inflammation model: a comparative study of anesthesia and instillation methods.

Various techniques have been utilized historically to generate acute pulmonary inflammation in the murine system. Crystalline silica exposure results in acute inflammation followed by pulmonary fibrosis. Methods of exposure are varied in their techniques, as well as types of anesthesia.

Urinary levoglucosan as a biomarker of wood smoke: results of human exposure studies.

Urinary levoglucosan was investigated as a potential biomarker of wood smoke exposure in two different controlled experimental settings. Nine subjects were exposed to smoke from a campfire in a controlled setting, and four were exposed to smoke from an older-model wood stove. All subjects were asked to provide urine samples before and after exposure, and to wear personal particulate matter with a diameter of < or =2.

Urinary levoglucosan as a biomarker of wood smoke exposure: observations in a mouse model and in children.

Background: Biomass smoke is an important source of particulate matter (PM), and much remains to be discovered with respect to the human health effects associated with this specific PM source. Exposure to biomass smoke can occur in one of two main categories: short-term exposures consist of periodic, seasonal exposures typified by communities near forest fires or intentional agricultural burning, and long-term exposures are chronic and typified by the use of biomass materials for cooking or heating. Levoglucosan (LG), a sugar anhydride released by combustion of cellulose-containing materials, is an attractive candidate as a biomarker of wood smoke exposure.

Critical role of MARCO in crystalline silica-induced pulmonary inflammation.

Chronic exposure to crystalline silica can lead to the development of silicosis, an irreversible, inflammatory and fibrotic pulmonary disease. Although, previous studies established the macrophage receptor with collagenous structure (MARCO) as an important receptor for binding and uptake of crystalline silica particles in vitro, the role of MARCO in regulating the inflammatory response following silica exposure in vivo remains unknown. Therefore, we determined the role of MARCO in crystalline silica-induced pulmonary pathology using C57Bl/6 wild-type (WT) and MARCO(-/-) mice.

Elevated asymmetric dimethylarginine alters lung function and induces collagen deposition in mice.

Increasing evidence suggests that lung mechanics and structure are maintained in part by an intimate balance between the L-arginine-metabolizing enzymes nitric oxide synthase (NOS) and arginase. Asymmetric dimethylarginine (ADMA) is a competitive endogenous inhibitor of NOS. The role of ADMA in the regulation of NOS and arginase in the airways has not yet been explored.

The IL-4Ralpha pathway in macrophages and its potential role in silica-induced pulmonary fibrosis.

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 is initial Th1-type inflammation, characterized by TNF-alpha and IFN-gamma. Previous studies determined that Th2 mediators (i.

Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure.

Silica inhalation results in chronic lung inflammation and fibrosis. While the role of the alveolar macrophage (AM) is considered key to the effects of silica on lung pathology, the etiology is not completely understood. Evidence suggests an increase in antigen presenting cell (APC) activity as a contributing factor to this process, as well as potential roles for both AM and interstitial macrophages (IM) in silicosis.

Evidence for a polytopic form of the E1 envelope glycoprotein of Hepatitis C virus.

The polyprotein precursor of the Hepatitis C virus (HCV) contains multiple membrane-spanning domains that define the membrane topology and subsequent maturation of the viral structural proteins. In order to examine the biogenesis of the E1-E2 heterodimeric complex, we inserted an affinity tag (S-peptide) at specific locations within the envelope glycoproteins. In particular, and based on the prediction that the E1 glycoprotein may be able to assume a polytopic topology containing two membrane-spanning domains, we inserted the affinity tag within a putative cytoplasmic loop of the E1 glycoprotein.