In Utero Ultrafine Particulate Matter Exposure Causes Offspring Pulmonary Immunosuppression
In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression Kristal A. Rychlika,1,2, Jeremiah R. Secrestb,2, Carmen Lauc, Jairus Pulczinskia,1, Misti L. Zamorad,1, Jeann Lealc, Rebecca Langleya, Louise G. Myatta, Muppala Rajue, Richard C.-A. Changf, Yixin Lib, Michael C. Goldingf, Aline Rodrigues-Hoffmannc, Mario J. Molinag,3, Renyi Zhangb,d, and Natalie M. Johnsona,2,3 aDepartment of Environmental and Occupational Health, Texas A&M University, College Station, TX 77843; bDepartment of Chemistry, Texas A&M University, College Station, TX 77843; cDepartment of Veterinary Pathobiology, Texas A&M University, College Station, TX 77843; dDepartment of Atmospheric Sciences, Texas A&M University, College Station, TX 77843; eDepartment of Epidemiology and Biostatistics, Texas A&M University, College Station, TX 77843; fDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX 77843; and gDepartment of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093 Contributed by Mario J. Molina, December 6, 2018 (sent for review September 19, 2018; reviewed by Alexandra Noel and Tong Zhu) Early life exposure to fine particulate matter (PM) in air is predominance of T helper (Th) 2 cell-associated cytokine pro- associated with infant respiratory disease and childhood asthma, duction classically define the phenotypic response. This frame- but limited epidemiological data exist concerning the impacts of work has been extended to include an imbalanced Th17 and ultrafine particles (UFPs) on the etiology of childhood respiratory regulatory T cell (Treg) response (13). Knowledge on the disease. Specifically, the role of UFPs in amplifying Th2- and/or Th17- mechanisms of allergic inflammation has largely been derived driven inflammation (asthma promotion) or suppressing effector from murine models of asthma, which can replicate key features T cells (increased susceptibility to respiratory infection) remains unclear.
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