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@ARTICLE{Waern:289303,
      author       = {I. Waern and S. Akula and V. S. R. R. Allam and S. Taha and
                      T. B. Feyerabend$^*$ and M. Åbrink and S. Wernersson},
      title        = {{D}isruption of the mast cell carboxypeptidase {A}3 gene
                      does not attenuate airway inflammation and
                      hyperresponsiveness in two mouse models of asthma.},
      journal      = {PLOS ONE},
      volume       = {19},
      number       = {4},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DKFZ-2024-00698},
      pages        = {e0300668 -},
      year         = {2024},
      abstract     = {Mast cells are effector cells known to contribute to
                      allergic airway disease. When activated, mast cells release
                      a broad spectrum of inflammatory mediators, including the
                      mast cell-specific protease carboxypeptidase A3 (CPA3). The
                      expression of CPA3 in the airway epithelium and lumen of
                      asthma patients has been associated with a Th2-driven airway
                      inflammation. However, the role of CPA3 in asthma is unclear
                      and therefore, the aim of this study was to investigate the
                      impact of CPA3 for the development and severity of allergic
                      airway inflammation using knockout mice with a deletion in
                      the Cpa3 gene. We used the ovalbumin (OVA)- and house-dust
                      mite (HDM) induced murine asthma models, and monitored
                      development of allergic airway inflammation. In the OVA
                      model, mice were sensitized with OVA intraperitoneally at
                      seven time points and challenged intranasally (i.n.) with
                      OVA three times. HDM-treated mice were challenged i.n. twice
                      weekly for three weeks. Both asthma protocols resulted in
                      elevated airway hyperresponsiveness, increased number of
                      eosinophils in bronchoalveolar lavage fluid, increased
                      peribronchial mast cell degranulation, goblet cell
                      hyperplasia, thickening of airway smooth muscle layer,
                      increased expression of IL-33 and increased production of
                      allergen-specific IgE in allergen-exposed mice as compared
                      to mocktreated mice. However, increased number of
                      peribronchial mast cells was only seen in the HDM asthma
                      model. The asthma-like responses in Cpa3-/- mice were
                      similar as in wild type mice, regardless of the asthma
                      protocol used. Our results demonstrated that the absence of
                      a functional Cpa3 gene had no effect on several symptoms of
                      asthma in two different mouse models. This suggest that CPA3
                      is dispensable for development of allergic airway
                      inflammation in acute models of asthma in mice.},
      cin          = {D110},
      ddc          = {610},
      cid          = {I:(DE-He78)D110-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38578780},
      pmc          = {pmc:PMC10997103},
      doi          = {10.1371/journal.pone.0300668},
      url          = {https://inrepo02.dkfz.de/record/289303},
}