title: PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia.
abstract: PM2.5 can exacerbate asthma. Organic substances adsorbed on PM2.5-rich dust (PM2.5rd) were inactivated by heating at 360 °C. To characterize the role of organic substances, the effects of PM2.5rd and heated PM2.5-rich dust (H-PM2.5 rd) on allergic lung inflammation were investigated. BALB/c mice were intratracheally administered PM2.5rd or H-PM2.5rd with or without ovalbumin (OVA) four times at 2-week intervals. PM2.5rd, but not H-PM2.5rd, caused neutrophilic alveolitis and bronchitis. In the presence of OVA, PM2.5rd caused severe eosinophil infiltration and goblet cells proliferation in airways, along with a marked induction of the Th2 cytokines interleukin (IL)-4 and IL-13, and the eosinophil-related cytokine IL-5 in bronchoalveolar lavage fluid (BALF). OVA + H-PM2.5rd caused a weaker response. PM2.5rd showed adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production, but H-PM2.5rd showed minimal effects. These findings suggested that PM2.5rd-bound substances might aggravate lung eosinophilia. To clarify the roles of TLR2, TLR4, and MyD88 on cytokine production in PM2.5rd, murine bone marrow-derived macrophages (BMDMs) from wild-type (WT), TLR2(-/-), TLR4(-/-), and MyD88(-/-) BALB/c mice were stimulated with dust. Cytokine production was low or undetectable in TLR4(-/-) cells, but occurred from TLR2(-/-) cells, and production by MyD88(-/-) cells was higher than by TLR4(-/-) cells. These results suggest that TLR4 and TLR2 ligands (LPS and β-glucan, respectively) mainly contributed to cytokines production induced by PM2.5rd. In addition to chemical substances, PM2.5-bound microbial substances might act in inflammatory and allergic lung diseases.
authors.affiliation: Environment and Non-communicable Disease Research Center, School of Public Health, China Medical University , Shenyang , China .
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Yahao
authors.initials: Y
authors.lastname: Ren
authors.forename: Yuan
authors.initials: Y
authors.lastname: Song
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Keiichi
authors.initials: K
authors.lastname: Arashidani
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D004391:Dust; D018836:Inflammation Mediators / Q000378:metabolism; D007564:Japan; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D052638:Particulate Matter / Q000633:toxicity*; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000378:metabolism* / Q000473:pathology
chemical_list: D000393:Air Pollutants; D004391:Dust; D018836:Inflammation Mediators; D052638:Particulate Matter
keywords: Asthma; MyD88 deficient; PM2.5-rich dust; TLR deficient; bone marrow macrophages; knockout mice; lung eosinophilia