Trichloroethylene enhances TCR-CD3-induced proliferation of CD8&lt;sup&gt;+&lt;/sup&gt; rather than CD4&lt;sup&gt;+&lt;/sup&gt; T cells

Kobayashi, Ryo; Nakanishi, Takashi; Nagase, Hisamitsu

doi:10.2131/jts.37.381

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…Previous reports have indicated that various environmental pollutants activate splenocytes (Koike et al ., , ; Kobayashi et al ., ). Our result showed ASD1 and ASD2 increased proliferation of splenocytes, although its detailed cellular contribution has not been established.…”

Section: Discussionmentioning

confidence: 97%

Effects of Asian sand dust particles on the respiratory and immune system

Honda

Matsuda

Murayama

et al. 2013

J of Applied Toxicology

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Epidemiologic studies have reported that Asian sand dust (ASD) particles can affect respiratory health; however, the mechanisms remain unclear. We investigated the effects of ASD on airway epithelial cells and immune cells, and their contributing factors to the effects. Human airway epithelial cells were exposed to ASD collected on 1-3 May (ASD1) and on 12-14 May (ASD2) 2011 in Japan and heat-treated ASD1 for excluding heat-sensitive substances (H-ASD) at a concentration of 0, 3, 30 or 90 µg ml(-1) for 4 or 24 h. Furthermore, bone marrow-derived dendritic cells (BMDC) from atopic prone mice were differentiated by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) then these BMDC were exposed to the ASD for 24 h. Also splenocytes as mixture of immune cells were exposed to the ASD for 72 h. All ASD dose dependently reduced viability of airway epithelial cells. Non-heated ASD showed a dose-dependent increase in the protein release of interleukin (IL)-6 and IL-8. The raises induced by ASD1 were higher than those by ASD2. ASD1 and ASD2 also elevated ICAM-1 at the levels of mRNA, cell surface protein and soluble protein in culture medium. In contrast, H-ASD did not change most of these biomarkers. Non-heated ASD showed enhancement in the protein expression of DEC205 on BMDC and in the proliferation of splenocytes, whereas H-ASD did not. These results suggest that ASD affect airway epithelial cells and immune cells such as BMDC and splenocytes. Moreover, the difference in ASD events and components adhered to ASD can contribute to the health effects.

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Section: Discussionmentioning

confidence: 97%

Effects of Asian sand dust particles on the respiratory and immune system

Honda

Matsuda

Murayama

et al. 2013

J of Applied Toxicology

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“…A Japanese team reported that TCE enhances TCR-CD3-induced proliferation of CD8 + rather than CD4 + cells and disrupts various activities of peripheral T cells in male Balb/c mice. 27 Li et al 28 showed that TCEexposed mice show a shift in Th1/Th2 and Th17/Treg ratios. 28 In addition, liver injury caused by immune sensitization through TCE is also mediated by activation of the complement system.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular immunity and humoral immunity are also involved in TCEHS. A Japanese team reported that TCE enhances TCR‐CD3‐induced proliferation of CD8 + rather than CD4 + cells and disrupts various activities of peripheral T cells in male Balb/c mice 27 . Li et al 28 showed that TCE‐exposed mice show a shift in Th1/Th2 and Th17/Treg ratios 28 .…”

Section: Discussionmentioning

confidence: 99%

Trichloroethylene and trichloroethanol induce skin sensitization with focal hepatic necrosis in guinea pigs

Zhao

Song²,

Naito

et al. 2020

Journal of Occupational Health

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Objectives Occupational exposure to trichloroethylene (TCE) induces trichloroethylene hypersensitivity syndrome (TCEHS), which causes hypersensitivity dermatitis and hepatitis. However, whether TCE itself or its two metabolites, trichloroethanol (TCEOH) and trichloroacetic acid (TCA), are involved in TCEHS remains unclear. Therefore, in this study we explored the allergens causing TCEHS and characterized TCEHS‐related liver injury in guinea pigs. Method The guinea pig maximization test was performed using TCE, TCEOH, and TCA as candidate allergens. Skin inflammation was scored, and liver function and histopathological changes were evaluated by biochemical tests and hematoxylin and eosin staining, respectively. Results The sensitization rates for TCE, TCEOH, and TCA were 90.0%, 50.0%, and 0.0%, respectively. In the TCE and TCEOH experimental groups, the skin showed varying degrees of erythema with eosinophil granulocyte infiltration in the dermis. Additionally, serum alanine aminotransferase and γ‐glutamyl transpeptidase levels increased significantly, and histological analysis revealed focal hepatocellular necrosis with inflammatory cell infiltration in the liver. Conclusions TCE is the main cause of allergy and TCEOH is a secondary factor for allergy in guinea pigs. TCE and TCEOH can cause immune‐mediated skin sensitization complicated by focal hepatic necrosis.

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“…However, a limited understanding exists regarding the effects of ASD on other organs, including the lymphoid organs. Some reports have provided evidence indicating that various environmental pollutants can activate splenocytes (Kobayashi, Nakanishi, & Nagase, 2012;Koike, Inoue, Yanagisawa, & Takano, 2009). Honda et al showed that ASD increased splenocyte proliferation in vitro (Honda et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The toll like receptor 4‐myeloid differentiation factor 88 pathway is essential for particulate matter‐induced activation of CD4‐positive cells

Song

Ichinose

Morita

et al. 2018

J of Applied Toxicology

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Asian sand dust (ASD), a type of particulate matter (PM) found in Asia, can be transported to East Asia. We recently found that acute splenic inflammation is induced by ASD in mouse models. In this study, we examined the effect of sub‐chronic ASD exposure on mouse immune cells. Mice were intratracheally administered ASD once every 2 weeks for 8 weeks and killed 24 hours after the final administration. Wild‐type (WT) mice showed increased cell viability after ASD administration. In contrast, ASD administration induced splenocyte activation in toll‐like receptor (TLR)2−/−, but not TLR4−/− mice. Furthermore, concanavalin A‐induced interleukin‐2 production increased after ASD administration in WT and TLR2−/− mice, but not in TLR4−/− or myeloid differentiation factor (MyD)88−/− mice. Immunoblotting demonstrated that nuclear factor κB (NF‐κB) was activated in WT mice, but not in TLR4−/− or MyD88−/− mice. The NF‐κB‐dependent gene products CDK2 and intercellular cell adhesion molecule‐1 were upregulated upon ASD administration in WT mice, but not in TLR4−/− or MyD88−/− mice. Furthermore, the particles themselves, rather than particle constituents, activated NF‐κB in CD4‐positive cells through the TLR4 or MyD88 pathway. Taken together, these results indicate that particle‐induced splenic inflammation occurs via TLR4‐MyD88 signaling.

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Trichloroethylene enhances TCR-CD3-induced proliferation of CD8<sup>+</sup> rather than CD4<sup>+</sup> T cells

Cited by 6 publications

References 42 publications

Effects of Asian sand dust particles on the respiratory and immune system

Effects of Asian sand dust particles on the respiratory and immune system

Trichloroethylene and trichloroethanol induce skin sensitization with focal hepatic necrosis in guinea pigs

The toll like receptor 4‐myeloid differentiation factor 88 pathway is essential for particulate matter‐induced activation of CD4‐positive cells

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