Targeting the P2Y13 Receptor Suppresses IL-33 and HMGB1 Release and Ameliorates Experimental Asthma.

Rationale: The alarmins IL-33 and HMGB1 (high mobility group box 1) contribute to type 2 inflammation and asthma pathogenesis. Objectives: To determine whether P2Y13-R (P2Y13 receptor), a purinergic GPCR (G protein-coupled receptor) and risk allele for asthma, regulates the release of IL-33 and HMGB...

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Publicado en:American Journal of Respiratory & Critical Care Medicine Vol. 205; no. 3; pp. 300 - 340
Autores principales: Werder, Rhiannon B., Ullah, Md Ashik, Rahman, Muhammed Mahfuzur, Simpson, Jennifer, Lynch, Jason P., Collinson, Natasha, Rittchen, Sonja, Rashid, Ridwan B., Sikder, Md Al Amin, Handoko, Herlina Y., Curren, Bodie F., Sebina, Ismail, Hartel, Gunter, Bissell, Alec, Ngo, Sylvia, Yarlagadda, Tejasri, Hasnain, Sumaira Z., Wenying Lu, Sohal, Sukhwinder S., Martin, Megan
Formato: research Journal Article
Publicado: Oxford University Press / USA 2/1/2022
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 2/1/2022
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      pub: Oxford University Press / USA
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        10.1164/rccm.202009-3686OC
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        atl: Targeting the P2Y13 Receptor Suppresses IL-33 and HMGB1 Release and Ameliorates Experimental Asthma.
      aug:
        au:
          Werder, Rhiannon B.
          Ullah, Md Ashik
          Rahman, Muhammed Mahfuzur
          Simpson, Jennifer
          Lynch, Jason P.
          Collinson, Natasha
          Rittchen, Sonja
          Rashid, Ridwan B.
          Sikder, Md Al Amin
          Handoko, Herlina Y.
          Curren, Bodie F.
          Sebina, Ismail
          Hartel, Gunter
          Bissell, Alec
          Ngo, Sylvia
          Yarlagadda, Tejasri
          Hasnain, Sumaira Z.
          Wenying Lu
          Sohal, Sukhwinder S.
          Martin, Megan
        affil: Respiratory Immunology Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia
      sug:
        subj:
          Asthma Immunology
          Proteins Metabolism
          Receptors, Cell Surface Metabolism
          Mice
          Asthma Physiopathology
          Immunohistochemistry
          Disease Progression
          Human
          Epithelial Cells Metabolism
          Animal Studies
          Enzyme-Linked Immunosorbent Assay
          Asthma Metabolism
          Case Control Studies
          Comparative Studies
          Multicenter Studies
          Evaluation Research
          Validation Studies
      ab: Rationale: The alarmins IL-33 and HMGB1 (high mobility group box 1) contribute to type 2 inflammation and asthma pathogenesis. Objectives: To determine whether P2Y13-R (P2Y13 receptor), a purinergic GPCR (G protein-coupled receptor) and risk allele for asthma, regulates the release of IL-33 and HMGB1. Methods: Bronchial biopsy specimens were obtained from healthy subjects and subjects with asthma. Primary human airway epithelial cells (AECs), primary mouse AECs, or C57Bl/6 mice were inoculated with various aeroallergens or respiratory viruses, and the nuclear-to-cytoplasmic translocation and release of alarmins was measured by using immunohistochemistry and an ELISA. The role of P2Y13-R in AEC function and in the onset, progression, and exacerbation of experimental asthma was assessed by using pharmacological antagonists and mice with P2Y13-R gene deletion. Measurements and Main Results: Aeroallergen exposure induced the extracellular release of ADP and ATP, nucleotides that activate P2Y13-R. ATP, ADP, and aeroallergen (house dust mite, cockroach, or Alternaria antigen) or virus exposure induced the nuclear-to-cytoplasmic translocation and subsequent release of IL-33 and HMGB1, and this response was ablated by genetic deletion or pharmacological antagonism of P2Y13. In mice, prophylactic or therapeutic P2Y13-R blockade attenuated asthma onset and, critically, ablated the severity of a rhinovirus-associated exacerbation in a high-fidelity experimental model of chronic asthma. Moreover, P2Y13-R antagonism derepressed antiviral immunity, increasing IFN-λ production and decreasing viral copies in the lung. Conclusions: We identify P2Y13-R as a novel gatekeeper of the nuclear alarmins IL-33 and HMGB1 and demonstrate that the targeting of this GPCR via genetic deletion or treatment with a small-molecule antagonist protects against the onset and exacerbations of experimental asthma.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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