Gestational exposure to titanium dioxide, diesel exhaust, and concentrated urban air particles affects levels of specialized pro-resolving mediators in response to allergen in asthma-susceptible neonate lungs

• DOI: 10.1080/15287394.2021.2000906
• Publication Date: 2021-11-22T07:28:39Z
• Authors: Mohan Kumar; Naohiro Yano; Alexey V. Fedulov
• Keywords: Titanium; Inhalation Exposure; Mice, Inbred BALB C; Ovalbumin; Allergens; 01 natural sciences; Asthma; 3. Good health; Mice; Animals, Newborn; Maternal Exposure; 13. Climate action; Eosinophilia; 11. Sustainability; Animals; Female; Particulate Matter; Disease Susceptibility; Inflammation Mediators; Lung; Vehicle Emissions; 0105 earth and related environmental sciences

Maternal gestational exposures to traffic and urban air pollutant particulates have been linked increased risk and/or worsening asthma in children; however, mechanisms underlying this vertical transmission are not entirely understood. It was postulated that particle exposure might affect the ability elicit specialized proresolving mediator (SPM) responses upon allergen encounter neonates. Lipidomic profiling of 50 SPMs performed lungs neonates born mice exposed concentrated particles (CAP), diesel exhaust (DEP), or less immunotoxic titanium dioxide (TiO2). While asthma-like phenotypes were induced with identical eosinophilia intensity across all particle-exposed mothers, levels LXA4, HEPE HETE isoforms, HDoHe only decreased by CAP DEP but TiO2. However, RvE2 RvD1 inhibited particles. In contrast, isomers Maresin1 Protectin D1 variably elevated DEP, whereas DX, PGE2, TxB2 groups. Only D1/DX, MaR1(n-3,DPA), 5(S),15(S)-DiHETE, RvE3 correlated majority other analytes, inhibited, showed no marked correlation inflammation intensity. Evidence indicates leads both particle-specific nonspecific effects on SPM network.