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Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma.
Am J Physiol Lung Cell Mol Physiol 2018; 314(3):L484-L492AJ

Abstract

Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated with the pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell functions, there is a need to further characterize IL-33/ST2-dependent mast cell responses and their significance in the context of asthma. This study aimed to investigate how IL-33/ST2-dependent mast cell responses contribute to the development of airway hyperresponsiveness (AHR) and airway inflammation in a mouse model of house dust mite (HDM)-induced asthma. Mast cell-deficient C57BL/6-KitW-sh (Wsh) mice engrafted with either wild-type (Wsh + MC-WT) or ST2-deficient bone marrow-derived mast cells (Wsh + MC-ST2KO) were exposed to HDM delivered intranasally. An exacerbated development of AHR in response to HDM was seen in Wsh + MC-ST2KO compared with Wsh + MC-WT mice. The contribution of this IL-33/ST2-dependent mast cell response to AHR seems to reside within the smaller airways in the peripheral parts of the lung, as suggested by the isolated yet marked effect on tissue resistance. Considering the absence of a parallel increase in cellular inflammation in bronchoalveolar lavage fluid (BALF) and lung, the aggravated AHR in Wsh + MC-ST2KO mice seems to be independent of cellular inflammation. We observed an association between the elevated AHR and reduced PGE2 levels in BALF. Due to the protective properties of PGE2 in airway responses, it is conceivable that IL-33/ST2-dependent mast cell induction of PGE2 could be responsible for the dampening effect on AHR. In conclusion, we reveal that IL-33/ST2-dependent mast cell responses can have a protective, rather than causative role, in the development of AHR.

Authors+Show Affiliations

Immunology and Allergy Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital , Stockholm , Sweden.Immunology and Allergy Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital , Stockholm , Sweden.Centre for Allergy Research, Karolinska Institutet , Stockholm , Sweden. Unit of Experimental Asthma and Allergy Research, Institute of Environmental Medicine, Karolinska Institutet , Stockholm . Sweden.Immunology and Allergy Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital , Stockholm , Sweden. Centre for Allergy Research, Karolinska Institutet , Stockholm , Sweden. Department of Medical Sciences, Uppsala University , Uppsala , Sweden.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29146574

Citation

Zoltowska Nilsson, A M., et al. "Mast Cell-dependent IL-33/ST2 Signaling Is Protective Against the Development of Airway Hyperresponsiveness in a House Dust Mite Mouse Model of Asthma." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 314, no. 3, 2018, pp. L484-L492.
Zoltowska Nilsson AM, Lei Y, Adner M, et al. Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma. Am J Physiol Lung Cell Mol Physiol. 2018;314(3):L484-L492.
Zoltowska Nilsson, A. M., Lei, Y., Adner, M., & Nilsson, G. P. (2018). Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma. American Journal of Physiology. Lung Cellular and Molecular Physiology, 314(3), pp. L484-L492. doi:10.1152/ajplung.00270.2017.
Zoltowska Nilsson AM, et al. Mast Cell-dependent IL-33/ST2 Signaling Is Protective Against the Development of Airway Hyperresponsiveness in a House Dust Mite Mouse Model of Asthma. Am J Physiol Lung Cell Mol Physiol. 2018 03 1;314(3):L484-L492. PubMed PMID: 29146574.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma. AU - Zoltowska Nilsson,A M, AU - Lei,Y, AU - Adner,M, AU - Nilsson,G P, Y1 - 2017/11/16/ PY - 2017/11/18/pubmed PY - 2019/1/10/medline PY - 2017/11/18/entrez KW - AHR KW - HDM mouse model KW - IL-33 KW - ST2 KW - airway hyperresponsiveness KW - mast cells SP - L484 EP - L492 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am. J. Physiol. Lung Cell Mol. Physiol. VL - 314 IS - 3 N2 - Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated with the pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell functions, there is a need to further characterize IL-33/ST2-dependent mast cell responses and their significance in the context of asthma. This study aimed to investigate how IL-33/ST2-dependent mast cell responses contribute to the development of airway hyperresponsiveness (AHR) and airway inflammation in a mouse model of house dust mite (HDM)-induced asthma. Mast cell-deficient C57BL/6-KitW-sh (Wsh) mice engrafted with either wild-type (Wsh + MC-WT) or ST2-deficient bone marrow-derived mast cells (Wsh + MC-ST2KO) were exposed to HDM delivered intranasally. An exacerbated development of AHR in response to HDM was seen in Wsh + MC-ST2KO compared with Wsh + MC-WT mice. The contribution of this IL-33/ST2-dependent mast cell response to AHR seems to reside within the smaller airways in the peripheral parts of the lung, as suggested by the isolated yet marked effect on tissue resistance. Considering the absence of a parallel increase in cellular inflammation in bronchoalveolar lavage fluid (BALF) and lung, the aggravated AHR in Wsh + MC-ST2KO mice seems to be independent of cellular inflammation. We observed an association between the elevated AHR and reduced PGE2 levels in BALF. Due to the protective properties of PGE2 in airway responses, it is conceivable that IL-33/ST2-dependent mast cell induction of PGE2 could be responsible for the dampening effect on AHR. In conclusion, we reveal that IL-33/ST2-dependent mast cell responses can have a protective, rather than causative role, in the development of AHR. SN - 1522-1504 UR - https://www.unboundmedicine.com/medline/citation/29146574/Mast_cell_dependent_IL_33/ST2_signaling_is_protective_against_the_development_of_airway_hyperresponsiveness_in_a_house_dust_mite_mouse_model_of_asthma_ L2 - http://www.physiology.org/doi/full/10.1152/ajplung.00270.2017?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -