Dietary Eicosapentaenoic Acid Improves Ozone-Induced Pulmonary Inflammation in C57BL/6 Mice.

Background: Ambient concentrations of the air pollutant, ozone, are rising with increasing global temperatures. Ozone is known to increase incidence and exacerbation of chronic lung diseases, which will increase as ambient ozone levels rise. Studies have identified diet as a variable that is able to modulate the pulmonary health effects associated with ozone exposure.

Omega-3 Fatty Acids and Chronic Lung Diseases: A Narrative Review of Impacts from Womb to Tomb.

The lungs are a mucosal organ constantly exposed to potentially harmful compounds and pathogens. Beyond their role in gas exchange, they must perform a well-orchestrated protective response against foreign invaders. The lungs identify these foreign compounds, respond to them by eliciting an inflammatory response, and restore tissue homeostasis after inflammation to ensure the lungs continue to function.

Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK-mediated Efferocytosis.

Lung inflammation, caused by acute exposure to ozone (O), one of the six criteria air pollutants, is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung, and their number increases after O exposure. However, the role of AMØs in promoting or limiting O-induced lung inflammation has not been clearly defined.

Tissue-resident alveolar macrophages reduce O-induced inflammation via MerTK mediated efferocytosis.

Lung inflammation, caused by acute exposure to ozone (O) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O exposure. However, the role of AMØs in promoting or limiting O-induced lung inflammation has not been clearly defined.