IL-33/ST2 signaling modulates Afghanistan particulate matter induced airway hyperresponsiveness in mice

Berman, Reena; Kopf, Katrina W; Min, Elysia; Huang, Jie; Downey, Gregory P.; Alam, Rafeul; Chu, Hong Wei; Day, Brian J.

doi:10.1016/j.taap.2020.115186

Cited by 13 publications

(14 citation statements)

References 65 publications

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“…Generally, inflammation is one of the key factors in inducing AHR. Here, we discuss the potential role of the IL-33/ST2 and regulator of G protein signaling 2 pathways in AHR …”

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

“…Limited research has been published concerning the combined effect of IL-33 and PM, including our recent manuscript highlighting APM-induced activation of IL-33 signaling in vivo . Using peripheral blood mononuclear cells isolated from chronic obstructive pulmonary disease (COPD) patients, de Falco et al demonstrated that treatment with ultrafine PM led to release of IL-33 .…”

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

“…The anti-AHR activities of RGS2 had never been studied in relation to PM or air pollution-related lung diseases until our recent work on the subject . Furthermore, whether or not RGS2 possesses any anti-inflammatory activities remains controversial.…”

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

“…Here, we discuss the potential role of the IL-33/ST2 and regulator of G protein signaling 2 pathways in AHR. 24 Interleukin-33 and the ST2 Receptor. A major player in inflammation and AHR in asthma is IL-33 and its receptor, ST2 (also known as interleukin 1 receptor-like 1 or IL1RL1).…”

Section: Airway Hyperresponsiveness Andmentioning

confidence: 99%

“…Conversely, manganese and SiO 2 were rarely found in the PM 2.5 fraction and tended to be concentrated in the PM 10 portion. Extensive characterization of the Afghanistan PM sample used in our own laboratory studies has been described previously. ,, It remains to be determined how composition of Afghanistan desert PM (APM) may differ among SWA sites and how the compositional variation of different PMs may impact the lung responses and related disease type and severity.…”

Section: Introductionmentioning

confidence: 99%

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Role of Particulate Matter from Afghanistan and Iraq in Deployment-Related Lung Disease

Berman

Rose

Downey

et al. 2021

Chem. Res. Toxicol.

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Approximately 3 million United States military personnel and contractors were deployed to Southwest Asia and Afghanistan over the past two decades. After returning to the United States, many developed persistent respiratory symptoms, including those due to asthma, rhinosinusitis, bronchiolitis, and others, which we collectively refer to as deployment-related lung diseases (DRLD). The mechanisms of different DRLD have not been well defined. Limited studies from us and others suggest that multiple factors and biological signaling pathways contribute to the onset of DRLD. These include, but are not limited to, exposures to high levels of particulate matter (PM) from sandstorms, burn pit combustion products, improvised explosive devices, and diesel exhaust particles. Once inhaled, these hazardous substances can activate lung immune and structural cells to initiate numerous cellsignaling pathways such as oxidative stress, Toll-like receptors, and cytokine-driven cell injury (e.g., interleukin-33). These biological events may lead to a pro-inflammatory response and airway hyperresponsiveness. Additionally, exposures to PM and other environmental hazards may predispose military personnel and contractors to more severe disease due to the interactions of those hazardous materials with subsequent exposures to allergens and cigarette smoke. Understanding how airborne exposures during deployment contribute to DRLD may identify effective targets to alleviate respiratory diseases and improve quality of life in veterans and active duty military personnel.

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“…Generally, inflammation is one of the key factors in inducing AHR. Here, we discuss the potential role of the IL-33/ST2 and regulator of G protein signaling 2 pathways in AHR …”

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

Section: Airway Hyperresponsiveness and Underlying Mechanismsmentioning

confidence: 99%

Section: Airway Hyperresponsiveness Andmentioning

confidence: 99%