Effects of Capsaicin Desensitization on Nasal Allergy-like Symptoms and Histamine Release in the Nose Induced by Toluene Diisocyanate in Guinea Pigs

Abe, Yoshiyuki; Takeda, Noriaki; Irifune, Morihiro; Ogino, Satoshi; Kalubi, Bukasa; Imamura, Ikuo; Fukui, Hirokazu; Wada, Hiroshi; Matsunaga, Toru

doi:10.3109/00016489209137463

Cited by 43 publications

(30 citation statements)

References 20 publications

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“…Nasal allergic-like symptom was measured by means of the number of sneezes and the extent of watery rhinorrhea using the method of Abe et al (9). After TDI provocation, animals were placed in a plastic cage (one animal per cage) and the number of sneezes and severity of watery rhinorrhea were examined for 10 min.…”

Section: Evaluation Of Nasal Allergic-like Symptommentioning

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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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: Evaluation Of Nasal Allergic-like Symptommentioning

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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“…Our previous works (7,8) have demonstrated that repeated intranasal application of toluene 2,4-diisocyanate (TDI) induced release of histamine from mast cells via neurogenic inflammation and leads to the development of nasal hypersensitivity behavior in guinea pigs. We also showed that both H1R mRNA and H1R protein level were up-regulated in TDI sensitized allergic rats and H1R mRNA was significantly suppressed by the treatment of d-chlorpheniramine, an H1R antagonist (9).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Histamine H1 Receptor Up-Regulates Histamine H1 Receptor Itself Through Activation of Receptor Gene Transcription

et al. 2007

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Abstract. Histamine is a major mediator in allergy acting mainly through the histamine H 1 receptor (H1R). Although H1R up-regulation has been suggested as an important step for induction of allergic symptoms, little is known about the regulation of H1R level. Here we report that the activation of H1R up-regulates H1R through augmentation of H1R mRNA expression in HeLa cells. Histamine stimulation significantly increased both H1R promoter activity and mRNA level without alteration in mRNA stability. H1R protein was also up-regulated by histamine. An H1R antagonist but not histamine H 2 receptor antagonist blocked histamine-induced up-regulation of both promoter activity and mRNA expression. A protein kinase C (PKC) activator, phorbol-12-myristate-13-acetate, increased H1R mRNA expression, whereas an activator of PKA or PKG (8-Br-cAMP or 8-Br-cGMP, respectively) did not. Furthermore, histamine-induced upregulation of both promoter activity and mRNA level were completely suppressed by the PKC inhibitor Ro-31-8220. H1R antagonists have long been thought to block H1R and inhibit immediate allergy symptoms. In addition to this short-term effect, our data propose their longterm inhibitory effect against allergic diseases by suppressing PKC-mediated H1R gene transcription. This finding provides new insights into the therapeutic target of H1R antagonist in allergic diseases.

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“…It is well known that irritation of sensory nerves with certain chemical irritants such as toluene diisocyanate (Takeda et al, 1993;Abe et al, 1992), capsaicin (Gepetti et al, 1988), formaline (Lundblad et al, 1984), and nicotine (Lundblad et al, 1984) induces sneezing, nasal secretion, and nasal congestion. These irritants induce the release of neuropeptides such as substance P (SP), calcitonin gene-related peptide (CGRP), and other neuropeptides from peripheral terminals of the trigeminal nerve Kokumai et al, 1992;.…”

Section: Discussionmentioning

confidence: 99%

Short-Term Exposure to Diesel Exhaust Induces Nasal Mucosal Hyperresponsiveness to Histamine in Guinea Pigs

Kobayashi

Ikeue²,

Ito

et al. 1997

Toxicol Sci

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The increasing prevalence of allergic rhinitis in many countries is becoming a social problem. It is important to determine whether air pollutants are related to the increase in the prevalence rate of allergic rhinitis or not. In this respect, it is necessary to elucidate whether exposure to air pollutants affects the nasal mucosa and causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. A previous study revealed that diesel exhaust particulates are potent in augmenting increases in nasal congestion and nasal secretion induced by histamine (T. Kobayashi and T. Ito, 1995, Fundam. Appl. Toxicol. 27,195-202). In the present study, using a rhinitis model of guinea pigs, we investigated whether short-term (3-hr) exposure to diesel exhaust induces nasal mucosal hyperresponsiveness to histamine. Guinea pigs of each group were exposed to filtered air or to a low or high concentration of diesel exhaust (1 and 3.2 mg/m 3 particulates in diluted diesel exhaust, respectively) for 3 hr. After diesel exhaust exposure, sneezing frequency, nasal secretion from the nostril, and intranasal airway resistance induced by histamine were measured as indices of sneezing response, rhinorrhea, and nasal congestion, respectively. Short-term exposure to a low or high concentration of diesel exhaust itself did not induce sneezing, nasal secretion, or nasal congestion. However, short-term exposure to a high concentration of diesel exhaust augmented sneezing and nasal secretion, but not nasal congestion, induced by histamine. In conclusion, short-term exposure to diesel exhaust potently induces nasal mucosal hyperresponsiveness. C 1997Socfc(jrofTajdco4ogy.The recent increase in the prevalence of allergic rhinitis (Kaneko et al, 1980;Crawford and Cohen, 1985;Aberg, 1989;Barbee et al, 1991;Lundback et al, 1992) in many countries is becoming an increasingly important social prob-' To whom correspondence and reprint requests should be addressed. Fax: 81-298-50-2439. lem. A positive relationship between the prevalence rate of allergic rhinitis and concentrations of atmospheric pollutants (Kaneko et al, 1980;Ishizaki et al, 1987) has been suggested from epidemiological studies. Therefore, it is important to clarify whether diesel exhaust (DE) could be related to the increase in the prevalence rate of allergic rhinitis. From this point of view, it is necessary to elucidate whether exposure to DE enhances IgE production and whether exposure to diesel exhaust particulates (DEP) causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. It has been reported that administration of DEP or exposure to DE enhances IgE antibody production in mice (Muranaka et al, 1986;Takafuji et al, 1987;Fujimaki et al, 1994) and in humans (Diaz-Sanchez etal, 1994; Takenaka etal, 1995). In nasal hyperresponsive animals, increases in nasal airway resistance, nasal secretion, and sneezing elicited by major mediators released during an allergic attack were induced by the lowering ...

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Effects of Capsaicin Desensitization on Nasal Allergy-like Symptoms and Histamine Release in the Nose Induced by Toluene Diisocyanate in Guinea Pigs

Cited by 43 publications

References 20 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

Stimulation of Histamine H1 Receptor Up-Regulates Histamine H1 Receptor Itself Through Activation of Receptor Gene Transcription

Short-Term Exposure to Diesel Exhaust Induces Nasal Mucosal Hyperresponsiveness to Histamine in Guinea Pigs

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