Comparative Role of Peptide Leukotrienes and Histamine in the Development of Nasal Mucosal Swelling in Nasal Allergy

Numata, Tsutomu; Hanazawa, Toyoyuki; Konno, Akiyoshi; Terada, Nobuhisa; Yamakoshi, Takayuki; Nagata, Hiroshi

doi:10.1177/000348949910800509

Cited by 52 publications

(42 citation statements)

References 19 publications

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“…Because sneezing and watery rhinorrhea in allergic rhinitis could be inhibited by treating patients with antihistaminics, these symptoms are triggered mainly via the stimulation of nasal terminals of the trigeminus nerve by histamine (4). Although the detailed sequence of events leading to the occurrence of allergic nasal blockage are not yet fully elucidated, it has been reported that a cysteinyl leukotriene (CysLT)-receptor antagonist reduced nasal blockage (5,6).…”

Section: Introductionmentioning

confidence: 99%

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

et al. 2003

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Abstract. Whether a state of nasal hyperresponsiveness influences antigen-induced biphasic nasal blockage and sneezing were examined using a guinea pig model of allergic rhinitis. Sensitized animals were challenged with an antigen, Japanese cedar pollen, once every week. Before the 13th challenge, the animals were randomly divided into 2 groups, and then the 13th challenge was performed (Groups A-0 and B-0). The 14th challenge was done on day 2 (Group A-2) and on day 7 (Group B-7) after the 13th challenge, on which nasal hyperresponsiveness was present and absent, respectively. Biphasic nasal blockage and sneezing after the challenge in Group A-2 were more severe than those in Group A-0, while those of Group B-7 were almost the same as those of Group B-0. An anti-histaminic, mepyramine, inhibited sneezing but not the biphasic nasal blockage in Group B-7. A cysteinyl leukotriene (CysLT) antagonist, pranlukast, suppressed the late nasal blockage but not the early blockage and sneezing in Group B-7. In contrast, in Group A-2, mepyramine significantly attenuated not only sneezing but also the early nasal blockage. Pranlukast significantly inhibited both nasal blockage and sneezing in Group A-2. In conclusion, nasal hyperresponsiveness aggravated the antigen-induced nasal responses, to which histamine and CysLTs considerably contributed.

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Section: Introductionmentioning

confidence: 99%

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

et al. 2003

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“…Bisgaard et al (13) demonstrated that, even in normal control subjects, a high dose of LTD4 may induce nasal mucosal blood flow and NAR in the absence of nasal discharge. Furthermore, Numata et al (19) reported that nasal mucosal swelling induced by nasal challenge was prevented by LTRA administration.…”

Section: Discussionmentioning

confidence: 99%

“…Miadonna et al (20) and Howarth (21) demonstrated that the symptoms of AR such as nasal secretion, nasal obstruction in particular, was more strongly correlated with the release of arachidonic acid metabolites than histamine in the nasal secretion or specimen during natural exposure. However, when stimulated with histamine or cysLT there was a different result; sneezing, itching, rhinorrhea and nasal obstruction could be induced by histamine rapidly (within a few seconds), while cysLT caused a more pronounced and longer lasting nasal obstruction (13,19). These phenomena implied that not only one, probably many mediators were involved in the development of symptoms, even involved with nervous reflex.…”

Section: Discussionmentioning

confidence: 99%

Leukotriene D4 nasal provocation test: Rationale, methodology and diagnostic value

Zhu

Xie

Guan

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Cysteinyl leukotrienes (LT) play a vital role in the pathogenesis of allergic rhinitis (AR), but few studies have investigated the nasal mucosal physiological response to LTs in AR patients. The aim of the present study was to establish the methodology and investigate the diagnostic value and safety of a leukotriene D4 (LTD4) nasal provocation test. LTD4 nasal provocation tests were performed in 26 AR patients and 16 normal control subjects. Nasal airway responsiveness was assessed by calculating the concentration of LTD4 required to cause a 60% increase in nasal airway resistance (PC 60 NAR-LTD4), which was measured using rhinomanometry and a composite symptom score. Receiver operating characteristic (ROC) curve was applied to evaluate the diagnostic value of LTD4 nasal provocation test, and adverse events were recorded. The study protocol was registered with the U.S. National Institutes of Health (https://clinicaltrials. gov/ct2/show/NCT01963741). PC 60 NAR-LTD4 in AR was significantly lower compared with that of normal controls . No serious adverse events were observed. Thus, the present results indicate that AR patients exhibited nasal hyperactivity to LTD4, and the established procedure of LTD4 nasal provocation testing is effective and safe for use in the diagnosis of AR. IntroductionThe levels of cysteinyl leukotrienes(LTs) in nasal secretions are elevated following allergen challenge or during natural exposure to allergens in allergic rhinitis (AR) patients (1,2). LTs play a vital role in the pathogenesis of AR and asthma (3,4), and as asthma patients frequently exhibit AR, patients that suffered from asthma and AR were particular good candidates for anti-LT therapy (5).Anti-LT therapy has been indicated to be effective in relieving the symptoms of AR or asthma in large-scale randomized, double-blind, placebo-controlled clinical trials (6,7). Nasal congestion and rhinorrhea in AR were reduced via the administration of montelukast, a LT receptor antagonist (LTRA), to a degree similar to that of antihistamines (8,9); however, the results of other trials were inconsistent with this (6,7,10). It remains unclear which population group may benefit most since the efficacy of the LTRA varied among asthmatic patients. Since it is difficult to predict responsiveness to anti-LT therapy in an individual patient, it is critical to develop a simplified method to identify the treatment response.LTC and LTD can induce an increase in nasal mucosal blood flow and nasal airway resistance (NAR); however, inhalation of LTD4 is associated with higher potency (11) and slow deactivation in vivo (12) as compared with LTC4 and LTE4. It has been reported that LTC4 is ~10 times (13), while LTD4 was ~5,000 times, as potent as histamine in achieving a 150% increase in NAR (14), as measured by rhinomanometry. Furthermore, LTD4 has been suggested to be an effective bronchial provocation agent in our previous studies (15,16). Consequently, LTD4 is speculated to be a potentially useful provocation agent (15). To the best of our...

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“…However, the oral doses of olopatadine that inhibited the increase in histamine and lipid mediators in NALF after antigen challenge in sensitized guinea pigs were nearly equivalent to the doses that inhibited the experimental allergic rhinitis in guinea pigs. Recently, the involvement of peptide LTs and TXA 2 have been suggested because pranlukast, a peptide LTs-receptor antagonist and ramatroban, a TXA 2 -receptor antagonist, showed clinical efficacy in the treatment of nasal obstruction (34,35). Consequently, it is thought that the inhibitory effects of olopatadine on the release of peptide LTs and TX may contribute to the suppressive effect of olopatadine on nasal obstruction.…”

Section: -2 Mode Of Action 2-2-1 Histamine H1-receptor Antagonistimentioning

confidence: 99%

Pharmacological, Pharmacokinetic and Clinical Properties of Olopatadine Hydrochloride, a New Antiallergic Drug

Ohmori

Hayashi

Kaise

et al. 2002

Japanese Journal of Pharmacology

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ABSTRACT-Olopatadine hydrochloride (olopatadine, 11-[(Z)-3-(dimethylamino)propylidene]-6,11-dihydrodibenz [b,e]oxepin-2-acetic acid monohydrochloride) is a novel antiallergic/ histamine H 1 -receptor antagonistic drug that was synthesized and evaluated in our laboratories. Oral administration of olopatadine at doses of 0.03 mg/ kg or higher inhibited the symptoms of experimental allergic skin responses, rhinoconjunctivitis and bronchial asthma in sensitized guinea pigs and rats. Olopatadine is a selective histamine H 1 -receptor antagonist possessing inhibitory effects on the release of inflammatory lipid mediators such as leukotriene and thromboxane from human polymorphonuclear leukocytes and eosinophils. Olopatadine also inhibited the tachykininergic contraction in the guinea pig bronchi by prejunctional inhibition of peripheral sensory nerves. Olopatadine exerted no significant effects on action potential duration in isolated guinea pig ventricular myocytes, myocardium and human ether-a-go-go-related gene channel. Olopatadine was highly and rapidly absorbed in healthy human volunteers. The urinary excretion of olopatadine accounted for not less than 58% and the contribution of metabolism was considerably low in the clearance of olopatadine in humans. Olopatadine is one of the few renal clearance drugs in antiallergic drugs. Olopatadine was shown to be useful for the treatment of allergic rhinitis and chronic urticaria in double-blind clinical trials. Olopatadine was approved in Japan for the treatment of allergic rhinitis, chronic urticaria, eczema dermatitis, prurigo, pruritis cutaneous, psoriasis vulgaris and erythema exsudativum multiforme in December, 2000. Ophthalmic solution of olopatadine was also approved in the United States for the treatment of seasonal allergic conjunctivitis in December, 1996 (Appendix: also in the European Union, it was approved in February 2002).

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Comparative Role of Peptide Leukotrienes and Histamine in the Development of Nasal Mucosal Swelling in Nasal Allergy

Cited by 52 publications

References 19 publications

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

Leukotriene D4 nasal provocation test: Rationale, methodology and diagnostic value

Pharmacological, Pharmacokinetic and Clinical Properties of Olopatadine Hydrochloride, a New Antiallergic Drug

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