TDI can induce respiratory allergy with Th2-dominated response in mice

Ban, M.; Morel, G.; Langonné, Isabelle; Huguet, Nelly; Pépin, Elsa; Binet, Stéphane

doi:10.1016/j.tox.2005.09.013

Cited by 69 publications

(56 citation statements)

References 36 publications

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“…Although AR, defined as an IgE-mediated disease, could be different from TDI-induced, non-IgE-mediated rhinitis, nasal allergic-like symptoms induced by TDI are similar to those observed in AR patients (38,39). Additionally, TDI-sensitized rats also display many of the characteristic features of AR in humans, including infiltration of eosinophils and mast cells (40), increase in the level of cytokines (8,(41)(42)(43), elevation of H1R mRNA and protein level (12), increase in the HDC mRNA level, HDC activity, and histamine content (13), even though histamine release was triggered by neuropeptide, but not IgE, in TDI-sensitized animals. Furthermore, the expression of IL-4 and IL-5 mRNAs was also up-regulated in the nasal mucosa of TDI-sensitized rats after provocation with TDI (16,17).…”

Section: Discussionmentioning

confidence: 99%

“…Toluene-2,4-diisocyanate (TDI), a highly reactive industrial chemical, is one of the leading causes of occupation-related asthma in industrialized countries (8). We demonstrated previously that repeated intranasal application of TDI induced release of histamine from mast cells via neurogenic inflammation and led to the development of nasal hypersensitivity in guinea pigs and rats (9 -11).…”

Section: A Llergic Rhinitis (Ar)mentioning

confidence: 99%

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Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Shahriar

Mizuguchi

Maeyama

et al. 2009

The Journal of Immunology

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Allergic rhinitis (AR) is an inflammatory disorder typified by symptoms such as sneezing, congestion, and rhinorrhea. Histamine plays important roles in eliciting AR symptoms. Up-regulation of the histamine H1 receptor (H1R) and histidine decarboxylase (HDC) mRNAs was observed in AR patients. Th2 cytokines are also involved in the pathogenesis of AR. We examined the effect of suplatast tosilate on nasal symptoms, and H1R, HDC, and IL-4 gene expression using toluene-2,4-diisocyanate (TDI)-sensitized rats and HeLa cells expressing endogenous H1R. Provocation with TDI increased nasal symptoms, HDC activity, the histamine content of nasal lavage fluid, and the expression of H1R, HDC, and IL-4 mRNAs in TDI-sensitized rats. Pretreatment with suplatast for 2 wk significantly suppressed TDI-induced nasal symptoms and elevation of H1R, HDC, and IL-4 mRNAs. Suplatast also suppressed HDC activity in the nasal mucosa and the histamine content of the nasal lavage fluid. Bilateral injection of IL-4 into the nasal cavity of normal rats up-regulated H1R mRNA, while intranasal application of histamine up-regulated IL-4 mRNA. Suplatast suppressed IL-4-induced up-regulation of H1R mRNA in HeLa cells. However, it did not inhibit histamine-induced H1R mRNA elevation. These results suggest that suplatast alleviates nasal symptoms by inhibiting histamine signaling in TDI-sensitized rats through the suppression of histamine- and IL-4-induced H1R gene expression by the inhibitions of HDC and IL-4 gene transcriptions, respectively.

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Section: Discussionmentioning

confidence: 99%

Section: A Llergic Rhinitis (Ar)mentioning

confidence: 99%

Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Shahriar

Mizuguchi

Maeyama

et al. 2009

The Journal of Immunology

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“…Topical application followed by intra-tracheal instillations of TDI resulted in local and systemic Th2-dominated immune responses associated with a rise in IL-4, IL-5 and IL-13. On the other hand, the experimental design, in which TDI was administrated by inhalation only, failed to provoke a vigorous Th2 immune response, with a slight increase in IL-5 production and serum total IgE [ 23]. However, other authors have observed the significant increase of Th2 cytokines after inhalation exposure of TDI.…”

Section: Ethicsmentioning

confidence: 95%

“…Numerous data are accessible from works considering the type of immune response and determinants in TDI-induced asthma. Ban et al [23] described four models of TDI-induced asthma, where the immune-mediated mechanisms depended on the route of administration. Topical application followed by intra-tracheal instillations of TDI resulted in local and systemic Th2-dominated immune responses associated with a rise in IL-4, IL-5 and IL-13.…”

Section: Ethicsmentioning

confidence: 99%

Immunological determinants in a murine model of toluene diisocyanate-induced asthma

Świerczyńska-Machura

Walusiak‐Skorupa

Nowakowska‐Świrta

et al. 2012

International Journal of Occupational Medicine and Environmental Health

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Objectives: Diisocyanates (DIC) are highly reactive, low-molecular-weight chemicals which are the leading cause of occupational asthma (OA). The aim of the study was to analyze certain aspects of the pathogenesis of allergic inflammation in the airways induced by toluene diisocyanate (TDI) in an experimental model in mice. Materials and Methods: The experiment was carried out on 50 female BALB/cJ/Han/IMP mice, which were exposed by inhalation (intranasal and in the inhalation chamber) to toluene diisocyanate (2,4-TDI). After the experiment, the bronchoalveolar lavage fluid (BALF) was collected from the animals, and the composition of the induced inflammatory cells, and the concentrations of certain cytokines (IL-4, IL-5, TNF-α) were evaluated. Results: The total number of cells in BALF of the examined group of mice was significantly higher compared to the control mice. There was also a significant increase in neutrophils and eosinophils in the study group compared to the controls. The number of lymphocytes and macrophages did not differ significantly between the two groups. A statistically significant increase in the level of TNF-α was shown to occur in the group exposed to toluene diisocyanate in comparison to the control group. The concentration of IL-4 increased in the study group, compared to the control one, but the differences did not reach the level of significance, p > 0.05. Such difference was not observed for IL-5. Conclusions: We developed a murine model of TDI-induced asthma which caused the influx of inflammatory cells like eosinophils and neutrophils in the bronchoalveolar lavage fluid (BALF) in the TDI-treated mice. The increase of the concentration of some proinflammatory cytokines (TNF-α, IL-4) in BALF from the exposed mice was also observed.

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“…Therefore, we chose to test PPD and PTD in an exposure regimen in BALB/c mice where the antigen-specific hypersensitivity response to the contact allergens 2,4-dinitrofluorobenzene (DNFB) and toluene 2,4-diisocyanate (TDI) was T H 2-like upon five repeated topical applications within 12 or 28 days (Dearman et al, 1996;Nagai et al, 1997;Warbrick et al, 1998). The respiratory sensitizer TDI was only used as a positive control since both T H 1 and T H 2 responses can be generated to this chemical in animal models (Matheson et al, 2005;Ban et al, 2006) and in man (Liippo and Lammintausta, 2008). The study was not designed to compare potencies of PPD or PTD to TDI or to each other.…”

Section: R E S E a R C H A R T I C L Ementioning

confidence: 99%

The hair dyes PPD and PTD fail to induce a T_H2 immune response following repeated topical application in BALB/c mice

Rothe

Sarlo

Scheffler

et al. 2011

Journal of Immunotoxicology

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TDI can induce respiratory allergy with Th2-dominated response in mice

Cited by 69 publications

References 36 publications

Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Immunological determinants in a murine model of toluene diisocyanate-induced asthma

The hair dyes PPD and PTD fail to induce a T_H2 immune response following repeated topical application in BALB/c mice

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TDI can induce respiratory allergy with Th2-dominated response in mice

Cited by 69 publications

References 36 publications

Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Suplatast Tosilate Inhibits Histamine Signaling by Direct and Indirect Down-Regulation of Histamine H1 Receptor Gene Expression through Suppression of Histidine Decarboxylase and IL-4 Gene Transcriptions

Immunological determinants in a murine model of toluene diisocyanate-induced asthma

The hair dyes PPD and PTD fail to induce a TH2 immune response following repeated topical application in BALB/c mice

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Product

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The hair dyes PPD and PTD fail to induce a T_H2 immune response following repeated topical application in BALB/c mice