IL-22 regulates inflammatory responses to agricultural dust-induced airway inflammation.

IL-22 is a unique cytokine that is upregulated in many chronic inflammatory diseases, including asthma, and modulates tissue responses during inflammation. However, the role of IL-22 in the resolution of inflammation and how this contributes to lung repair processes are largely unknown. Here, we tested the hypothesis that IL-22 signaling is critical in inflammation resolution after repetitive exposure to agricultural dust.

Lung Inflammatory Response to Environmental Dust Exposure in Mice Suggests a Link to Regional Respiratory Disease Risk.

Purpose: The Salton Sea, California's largest lake, is designated as an agricultural drainage reservoir. In recent years, the lake has experienced shrinkage due to reduced water sources, increasing levels of aerosolized dusts in surrounding regions. Communities surrounding the Salton Sea have increased asthma prevalence versus the rest of California; however, a connection between dust inhalation and lung health impacts has not been defined.

Estradiol-17β stimulates H S biosynthesis by ER-dependent CBS and CSE transcription in uterine artery smooth muscle cells in vitro.

Endogenous hydrogen sulfide (H S), synthesized by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), is a potent vasodilator that can be stimulated by estradiol-17β (E β) in uterine artery (UA) smooth muscle (UASMC) in vivo; however, the underlying mechanisms are unknown. This study tested a hypothesis that E β stimulates H S biosynthesis by upregulating CBS expression via specific estrogen receptor (ER). Treatment with E β stimulated time- and concentration- dependent CBS and CSE messenger RNA (mRNA) and protein expressions, and H S production in cultured primary UASMC isolated from late pregnant ewes, which were blocked by ICI 182,780.