Increased airway hyperresponsiveness to adenosine in patients with aspirin intolerant asthma

Isogai, Sumito; Niwa, Yoshikazu; Yatsuya, Hiroshi; Hayashi, Masamichi; Yamamoto, Naoki; Okamura, Takuya; Minezawa, Tomoyuki; Gotô, Yasuhiro; Yamaguchi, Teppei; Takeyama, Tomoko; Sakakibara, Yosuke; Morikawa, S.; Horiguchi, Tomoya; Gotoh, Y.; Mieno, Yuki; Uozu, Sakurako; Nakanishi, Tōru; Okazawa, Mitsushi; Sakakibara, Hiroki; Imaizumi, Kazuyoshi

doi:10.1016/j.alit.2016.10.001

Cited by 7 publications

(5 citation statements)

References 9 publications

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“…Mast cell activation biomarkers are increased during aspirin challenge, significantly correlating with decreased lung function and increased urinary cysLT concentration. 73,91,92 Airway reactivity to adenosine monophosphate, a specific mast cell stimulus, is increased, 93 whereas cromolyn, a mast cell stabilizer, shows specific bronchodilation. 94 The role of mast cells is further confirmed by a randomized controlled trial, which has demonstrated that omalizumab reduces mast cell activation, aspirin sensitivity and cysLT overproduction.…”

Section: Nsaid-exacerbated Respiratory Diseasementioning

confidence: 99%

Adult‐onset eosinophilic airway diseases

Asano

Ueki

Tamari

et al. 2020

Allergy

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Allergic diseases in the upper and the lower airways such as allergic rhinitis and atopic asthma are usually accompanied by local eosinophilia and sometimes by peripheral blood eosinophilia. Chronic rhinosinusitis with nasal polyps (CRSwNP) and nonatopic asthma are also characterized by local and systemic eosinophilia; however, there are substantial differences in the age of onset and the presence of atopy. Atopic asthma and allergic rhinitis develop during childhood in most cases and mediated by type 1 hypersensitivity reactions to allergen(s), as are other childhood-onset allergic diseases such as food allergies and eczema. Patients often develop these diseases consecutively as an allergic march (Figure 1), suggesting the presence of common genetic backgrounds and pathophysiology. In contrast to childhood-onset disease, adult-onset asthma frequently presents as a nonatopic and eosinophilic condition, 1-6

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Section: Nsaid-exacerbated Respiratory Diseasementioning

confidence: 99%

Adult‐onset eosinophilic airway diseases

Asano

Ueki

Tamari

et al. 2020

Allergy

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“…Ectonucleotidases readily cleave the naturally occurring 5′-phosphoesters of adenosine 5′-phosphates to produce adenosine in situ . Adenosine 5′-monophosphate (AMP) is used diagnostically in inhalation challenge testing (Basoglu et al, 2005; Isogai et al, 2017). AMP readily forms adenosine in situ and thus most of its actions occur through ARs, but not all of its in vivo effects arise from AR activation (Carlin et al, 2018; Xiao et al, 2019).…”

Section: Ar Agonists For Clinical Developmentmentioning

confidence: 99%

Historical and Current Adenosine Receptor Agonists in Preclinical and Clinical Development

Jacobson

Tosh

Jain

et al. 2019

Front. Cell. Neurosci.

163

189

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Adenosine receptors (ARs) function in the body’s response to conditions of pathology and stress associated with a functional imbalance, such as in the supply and demand of energy/oxygen/nutrients. Extracellular adenosine concentrations vary widely to raise or lower the basal activation of four subtypes of ARs. Endogenous adenosine can correct an energy imbalance during hypoxia and other stress, for example, by slowing the heart rate by A 1 AR activation or increasing the blood supply to heart muscle by the A 2A AR. Moreover, exogenous AR agonists, antagonists, or allosteric modulators can be applied for therapeutic benefit, and medicinal chemists working toward that goal have reported thousands of such agents. Thus, numerous clinical trials have ensued, using promising agents to modulate adenosinergic signaling, most of which have not succeeded. Currently, short-acting, parenteral agonists, adenosine and Regadenoson, are the only AR agonists approved for human use. However, new concepts and compounds are currently being developed and applied toward preclinical and clinical evaluation, and initial results are encouraging. This review focuses on key compounds as AR agonists and positive allosteric modulators (PAMs) for disease treatment or diagnosis. AR agonists for treating inflammation, pain, cancer, non-alcoholic steatohepatitis, angina, sickle cell disease, ischemic conditions and diabetes have been under development. Multiple clinical trials with two A 3 AR agonists are ongoing.

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“…18,21,33,[38][39][40] In addition, patients with N-ERD are more sensitive to adenosine inhalation (which is a mast cell activator stimulant in the airways) than are patients with aspirintolerant asthma. 41 Mast cell activation in N-ERD is influenced by endogenous CysLT, local IgE, and the innate cytokine milieu. 38,42 Mast cells express high-affinity receptors for the Fc region (FcεRI) of IgE and cysteinyl leukotriene receptors (CysLT1R and CysLT2R).…”

Section: Role Of Mast Cellsmentioning

confidence: 99%