Diesel exhaust (DE) aggravates pathology of delayed-type hypersensitivity (DTH) Induced by methyl-bovine serum albumin (mBSA) in mice

Abstract

It is well documented that air pollutants exacerbate respiratory diseases, such as asthma (Brunekreef and Holgate, 2002). Diesel exhaust particles (DEP), which are major contributors to the level of airborne particles less than 2.5 micrometers in aerodynamic diameter (PM2.5) in urban areas, consist of a carbon core upon which are absorbed various compounds, including polyaromatic hydrocarbons (PAH), nitroaromatic hydrocarbons, heterocyclics, quinones, aldehydes, aliphatic hydrocarbons and heavy metals (Vouk and Piver, 1983;Draper, 1986 ABSTRACT -Diesel exhaust particles (DEP), a well-known air pollutant, exacerbate type I hypersensitivity conditions, such as asthma and pollen allergy. In this study, we examined the effect of diesel exhaust (DE) exposure on delayed-type hypersensitivity (DTH), a type IV hypersensitivity, induced with methyl-bovine serum albumin (mBSA) in C57BL/6 mice. Mice were exposed to DE containing DEP at a dose of 1.78 mg/m 3 in an inhalation chamber for 14 days. On Day 7, DTH mice and DE-exposed DTH -tial sensitization. On Day 14, mice were injected s.c. into one footpad with 20 μl of 10 mg/ml mBSA disfootpad swelling (%) was observed in DTH mice compared with normal control mice, and this swell--ther enhanced by DE exposure. DE exposure increased production of IL-17, which enhances local tischange was observed in the percentage of CD4 + CD25 + + T regulatory (Treg) cells in splenic lymphocytes following DE exposure. IL-6 production was increased by DE, and this would facilitate the differentiation of naïve T cells to IL-17-producing Th17 cells, while concomitantly suppressing the competing differentiation pathway to IL-10-producing Treg cells. Our results indicate that DE inhalation may, in

Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice

“…The mice were exposed to DE in an inhalation chamber at the Nanoparticles Health Science Research Center, Tokyo University of Science, according to the method described in previous reports [46,47]. Briefly, a 2179 L, 39 Kw/3000 rpm diesel engine (Isuzu Motors Ltd., Tokyo, Japan) was used.…”

Anandamide Attenuates Th-17 Cell-Mediated Delayed-Type Hypersensitivity Response by Triggering IL-10 Production and Consequent microRNA Induction

“…This model of hypersensitivity has been used as a way to study the development of Th17 cells in vivo by injecting both intra-articularly into mice to induce arthritis [12] as well as subcutaneously to sensitize, and rechallenge the animals in the footpads [13] or the ear to induce DTH[14]. Th17 cells, besides their role in microbial immunity, are directly involved in the pathogenesis of autoimmune diseases such as arthritis [15], Experimental Autoimmune Encephalomyelitis [EAE] [16], [17], and myocarditis [18].…”

NiO and Co3O4nanoparticles induce lung DTH-like responses and alveolar lipoproteinosis

“…Some metal ions are known to induce contact dermatitis via delayedtype hypersensitivity (DTH) mediated by a cluster of differentiation (CD)4 T-cell-dependent inflammatory immune response that involve T-helper type 1 (Th1) and/or Th17 effector CD4 T-cells [3][4][5]. Those metal ions triggering immune responses may be regarded as haptens, low molecular weight species that are not themselves antigenic, but when bound to a host protein elicit sufficient structural change in the protein and its processed peptides that they can be recognised as nonself by T-cells [6].…”