Thymocytes are activated by toluene inhalation through the transcription factors NF‐<i>κ</i>B, STAT5 and NF‐AT

Liu, Jiqin; Yoshida, Yasuhiro; Kunugita, Naoki; Noguchi, Junko; Sugiura, Teiichi; Ding, Ning; Arashidani, Keiichi; Fujimaki, Hidekazu; Yamashita, Uki

doi:10.1002/jat.1536

Cited by 4 publications

(1 citation statement)

References 23 publications

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“…However, in the present study, there were no significant changes of the DNA binding activity of the NF-κB and AP-1 subunits in the lung from C3H/HeN mice exposed to toluene and OVA. Exposure to 50 ppm toluene in mice resulted in the induction of IL-2 production and the activation of the transcription factors NF-κB, STAT5 and NF-AT in thymocytes (Liu et al, 2010), suggesting that lowlevel toluene exposure can modulate the inflammatory response via a signal transduction pathway. To elucidate the mechanism of the effect of toluene and OVA interaction in the lung and the role of transcription factors, the mRNA expression of NF-κB and AP-1 subunits, subunit dimerization and phosphorylation process must be studied.…”

Section: Discussionmentioning

confidence: 99%

Activation of transcription factors in a mouse lung following exposure to environmental chemical and biological agents

Win-Shwe

Fujimaki

2015

J. Toxicol. Sci.

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-Environmental biological and chemical agents can modulate innate and acquired immunity in the lung via the stimulation of Toll-like receptors (TLRs). To investigate the effect of environmental chemical agents on the activation of NF-κB and activator protein (AP)-1 subunits and the role of TLR4 signaling in the lung, C3H/HeN and C3H/HeJ (TLR4-defective) mice were exposed to 0 or 50 ppm of toluene for 6 hr/day, 5 days/week for 6 weeks. Some groups of mice were also stimulated with OVA or LPS as a biological agent. The DNA-binding activities of the NF-κB subunits (p50, p52, p65 and RelB) and AP-1 family members (FosB, c-Fos, +c-Jun, JunD) were compared using TransAM TM ELISA kits. Exposure to toluene alone produced no significant changes in both mice. Although stimulation with OVA or LPS alone significantly increased the DNA binding activities of p50 and p52 in C3H/HeN mice, there were no interactions between biological factors and toluene. In the C3H/HeJ mice, stimulation with OVA or LPS increased p65 and p52 binding activity and the combination of exposure to toluene and OVA significantly increased the DNA binding activities of the p65 and p52 in the lung. During AP-1 activation, co-exposure to toluene and OVA increased JunD binding activity in C3H/HeJ mice, while co-exposure to toluene and LPS influenced c-Fos binding activity in C3H/HeN mice. These results indicate that TLR4 may play an important role in activation of NF-κB or AP-1 family following exposure to environmental biological and chemical agents.

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Section: Discussionmentioning

confidence: 99%

Activation of transcription factors in a mouse lung following exposure to environmental chemical and biological agents

Win-Shwe

Fujimaki

2015

J. Toxicol. Sci.

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Silica‐carrying particulate matter enhances Bjerkandera adusta‐induced murine lung eosinophilia

Ichinose

Liu

et al. 2014

Environmental Toxicology

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Bjerkandera adusta (B. adusta) causes fungus-associated chronic cough. However, the inflammatory response is not yet fully understood. Recently, B. adusta was identified in Asian sand dust (ASD) aerosol. This study investigated the enhancing effects of ASD on B. adusta-induced lung inflammation. B. adusta was inactivated by formalin. ASD was heated to remove toxic organic substances. ICR mice were intratracheally instilled with saline, B. adusta 0.2 µg, or B. adusta 0.8 µg with or without heated ASD 0.1 mg (H-ASD), four times at 2-week intervals. Two in vitro experiments were conducted to investigate any enhancing effects using bone marrow-derived macrophages (BMDM) from Toll-like receptor (TLR) knockout mice and ICR mice. Co-exposure to H-ASD and B. adusta, especially at high doses, caused eosinophil infiltration, proliferation of goblet cells in the airway, and fibrous thickening of the subepithelial layer, and remarkable increases in expression of Th2 cytokines and eosinophil-related cytokine and chemokine expression in bronchoalveolar lavage fluid. In the in vitro study using BMDM from wild-type, TLR2-/-, and TLR4-/- mice, the TLR-signaling pathway for cytokine production caused by B. adusta was predominantly TLR2 rather than TLR4. H-ASD increased the expression of NF-κB and cytokine production by B. adusta in BMDM from ICR mice. The results suggest that co-exposure to H-ASD and B. adusta caused aggravated lung eosinophilia via remarkable increases of pro-inflammatory mediators. The aggravation of inflammation may be related, at least in part, to the activation of the TLR2-NF-κB signaling pathway in antigen presenting cells by H-ASD.

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SVα-MSH, a novel α-melanocyte stimulating hormone analog, ameliorates autoimmune encephalomyelitis through inhibiting autoreactive CD4+ T cells activation

Fang

Han

Hong

et al. 2014

Journal of Neuroimmunology

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Thymocytes are activated by toluene inhalation through the transcription factors NF‐κB, STAT5 and NF‐AT

Cited by 4 publications

References 23 publications

Activation of transcription factors in a mouse lung following exposure to environmental chemical and biological agents

Activation of transcription factors in a mouse lung following exposure to environmental chemical and biological agents

Silica‐carrying particulate matter enhances Bjerkandera adusta‐induced murine lung eosinophilia

SVα-MSH, a novel α-melanocyte stimulating hormone analog, ameliorates autoimmune encephalomyelitis through inhibiting autoreactive CD4+ T cells activation

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