Effect of Glucocorticoid on Upregulation of Histamine H<sub>1</sub>Receptor mRNA in Nasal Mucosa of Rats Sensitized by Exposure to Toluene Diisocyanate

Kitamura, Yoshiaki; Miyoshi, Ayako; Murata, Yuki; Kalubi, Bukasa; Fukui, Hirokazu; Takeda, Noriaki

doi:10.1080/00016480410022525

Cited by 54 publications

(50 citation statements)

References 20 publications

(17 reference statements)

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“…This expression was maximal after 4 h of TDI provocation (12). Pretreatment with suplatast significantly reduced H1R expression in the nasal mucosa of the TDI-sensitized rats (Fig.…”

Section: Effect Of Suplatast On Tdi-induced Increases In H1r Mrna Expmentioning

confidence: 96%

“…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%

“…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). Up-regulation of H1R at both the mRNA and protein level was also observed in the nasal mucosa of TDI-sensitized nasal allergic model rats (12,13). As histidine decarboxylase (HDC) is the only enzyme that synthesizes histamine from histidine in mammals, control of HDC activity is another important target for regulation of histamine signaling.…”

Section: A Llergic Rhinitis (Ar)mentioning

confidence: 99%

“…Rats were sensitized with TDI by the method described by Kitamura et al (12) with slight modifications. Briefly, 10 l of a 10% solution of TDI in ethyl acetate (Wako Pure Chemical) was applied bilaterally to the nasal vestibule once a day for 5 consecutive days.…”

Section: Tdi Sensitization and Provocation And Administration Of Suplmentioning

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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“…This expression was maximal after 4 h of TDI provocation (12). Pretreatment with suplatast significantly reduced H1R expression in the nasal mucosa of the TDI-sensitized rats (Fig.…”

Section: Effect Of Suplatast On Tdi-induced Increases In H1r Mrna Expmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: A Llergic Rhinitis (Ar)mentioning

confidence: 99%

Section: Tdi Sensitization and Provocation And Administration Of Suplmentioning

confidence: 99%

See 2 more Smart Citations

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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“…The strength of H1R signaling depends on the H1R expression level (8). Our recent studies have demonstrated that the level of H1R gene expression is strongly correlated with the severity of allergic symptoms in model rats and patients with pollinosis (9,10), and compounds that suppress H1R gene up-regulation alleviate allergic symptoms (11)(12)(13)(14)(15)(16). These findings suggest that the H1R gene is an allergy-sensitive gene, i.e.…”

mentioning

confidence: 90%

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Mizuguchi

Terao

Kitai

et al. 2011

Journal of Biological Chemistry

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The histamine H 1 receptor (H1R) gene is up-regulated in patients with allergic rhinitis. However, the mechanism and reason underlying this up-regulation are still unknown. Recently, we reported that the H1R expression level is strongly correlated with the severity of allergic symptoms. Therefore, understanding the mechanism of this up-regulation will help to develop new anti-allergic drugs targeted for H1R gene expression. Here we studied the molecular mechanism of H1R up-regulation in HeLa cells that express H1R endogenously in response to histamine and phorbol 12- Histamine is a major chemical mediator of allergic reactions, and its action is mainly mediated by the histamine H 1 receptor (H1R), 2 which is one of the four histamine receptor isoforms. H1R, which is a G protein-coupled receptor, is coupled to the G q protein. The stimulation of H1R activates inositol phospholipid hydrolysis and intracellular Ca 2ϩ mobilization. Typically, the activation of G protein-coupled receptors by their agonists induces down-regulation of the receptors. However, to date, a few reports have demonstrated up-regulation of G proteincoupled receptors by their agonists (1-4). Previously, we found that histamine stimulation up-regulated H1R at both the mRNA and protein level via activation of H1R in HeLa cells that express H1R endogenously (5). Up-regulation of H1R has been observed in patients with allergic rhinitis (6, 7). The strength of H1R signaling depends on the H1R expression level (8). Our recent studies have demonstrated that the level of H1R gene expression is strongly correlated with the severity of allergic symptoms in model rats and patients with pollinosis (9, 10), and compounds that suppress H1R gene up-regulation alleviate allergic symptoms (11-16). These findings suggest that the H1R gene is an allergy-sensitive gene, i.e. its expression level affects the severity of symptoms. Hence, understanding the molecular mechanism of H1R up-regulation may be useful for developing new anti-allergic drugs that target H1R gene expression. However, the mechanism of H1R up-regulation in response to histamine is unknown.Previously, we demonstrated that PKC-dependent signaling is involved in up-regulation of H1R gene expression in HeLa cells (5). PKC consists of at least 11 isoforms, and based on their structures and cofactor requirements, the PKC isoforms are divided into three subgroups; that is, conventional PKC (␣, ␤, and ␥), novel PKC (␦, ⑀, , and ), and atypical PKC ( and /) (17). It has been reported that PKC ␣, ␤, ␦, ⑀, and isoforms are expressed in HeLa cells (18 -20).Coupling of H1R signaling with PKC␣ has been reported in H1R-overexpressing CHO cells (21) and native human epidermal keratinocytes (22). In these cells, however, no up-regulation of H1R gene expression was observed. In addition, NF-B (23), the cAMP response element-binding protein (CREB) (24)), the nuclear factor of activated T-cell (25), and the serumresponsive element (26)

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Effects of narrow‐band UVB on nasal symptom and upregulation of histamine H₁ receptor mRNA in allergic rhinitis model rats

Kamimura

Kitamura

Fujii

et al. 2021

Laryngoscope Investig Oto

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Background Phototherapy with narrow‐band ultraviolet B (narrow‐band UVB) is clinically effective treatment for atopic dermatitis. In the present study, we examined the effects of intranasal irradiation with narrow‐band UVB on nasal symptom, upregulation of histamine H1 receptor (H1R) gene expression and induction of DNA damage in the nasal mucosa of allergic rhinitis (AR) model rat. Methods AR model rats were intranasally irradiated with 310 nm of narrow‐band UVB. Nasal mucosal levels of H1R mRNA were measured using real‐time quantitative reverse transcriptase (RT)‐PCR. DNA damage was evaluated using cyclobutane pyrimidine dimer (CPD) immunostaining. Results In toluene 2,4‐diisocyanate (TDI)‐sensitized rats, TDI provoked sneezes and H1R gene expression in the nasal mucosa. Intranasal pre‐irradiation with 310 nm narrow‐band UVB at doses of 600 and 1400, but not 200 mJ/cm2 significantly inhibited the number of sneezes and upregulation of H1R gene expression provoked by TDI. CPD‐positive cells appeared in the nasal mucosa after intranasal narrow‐band UVB irradiation at a dose of 1400, but not 200 and 600 mJ/cm2. The suppression of TDI‐provoked sneezes and upregulation of H1R gene expression lasted 24 hours, but not 48 hours, after narrow‐band UVB irradiation with a dose of 600 mJ/cm2. Conclusions Intranasal pre‐irradiation with narrow‐band UVB dose‐dependently inhibited sneezes and upregulation of H1R gene expression of the nasal mucosa in AR model rats, suggesting that the inhibition of nasal upregulation of H1R gene expression suppressed nasal symptom. The suppression after narrow‐band UVB irradiation at a dose of 600 mJ/cm2 was reversible without induction of DNA damage. These findings indicated that low‐dose narrow‐band UVB phototherapy could be effectively and safely used for AR treatment in a clinical setting. Level of Evidence NA.

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Effect of Glucocorticoid on Upregulation of Histamine H₁Receptor mRNA in Nasal Mucosa of Rats Sensitized by Exposure to Toluene Diisocyanate

Cited by 54 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

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Effects of narrow‐band UVB on nasal symptom and upregulation of histamine H₁ receptor mRNA in allergic rhinitis model rats

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Effect of Glucocorticoid on Upregulation of Histamine H1Receptor mRNA in Nasal Mucosa of Rats Sensitized by Exposure to Toluene Diisocyanate

Cited by 54 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

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Effects of narrow‐band UVB on nasal symptom and upregulation of histamine H1 receptor mRNA in allergic rhinitis model rats

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Effect of Glucocorticoid on Upregulation of Histamine H₁Receptor mRNA in Nasal Mucosa of Rats Sensitized by Exposure to Toluene Diisocyanate

Effects of narrow‐band UVB on nasal symptom and upregulation of histamine H₁ receptor mRNA in allergic rhinitis model rats