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Elastase- and LPS-E...
Elastase- and LPS-Exposed Cpa3(Cre/+) and ST2(-/-) Mice Develop Unimpaired Obstructive Pulmonary Disease
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- Cardenas, Eduardo, I (författare)
- Karolinska Institutet,Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi,Karolinska Inst, Inst Environm Med, Div Lung & Airway Res, Stockholm, Sweden.
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- Alvarado-Vazquez, Perla Abigail (författare)
- Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi
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- Mendez-Enriquez, Erika (författare)
- Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi
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- Danielsson, Erik A. (författare)
- Uppsala universitet,Anestesiologi och intensivvård,Institutionen för medicinsk biokemi och mikrobiologi
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- Hallgren, Jenny (författare)
- Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi
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(creator_code:org_t)
- 2022-04-13
- 2022
- Engelska.
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Ingår i: Frontiers in Immunology. - : Frontiers Media S.A.. - 1664-3224. ; 13
- Relaterad länk:
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https://doi.org/10.3...
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https://uu.diva-port... (primary) (Raw object)
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https://urn.kb.se/re...
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https://doi.org/10.3...
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http://kipublication...
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Abstract
Ämnesord
Stäng
- IL-33 and its receptor ST2, as well as mast cells and their mediators, have been implicated in the development of chronic obstructive pulmonary disease (COPD). However, whether mast cells and the ST2 receptor play a critical role in COPD pathophysiology remains unclear. Here, we performed repeated intranasal administrations of porcine pancreatic elastase and LPS for four weeks to study COPD-like disease in wildtype, ST2-deficient, and Cpa3(Cre/+) mice, which lack mast cells and have a partial reduction in basophils. Alveolar enlargement and changes in spirometry-like parameters, e.g. increased dynamic compliance and decreased expiratory capacity, were evident one day after the final LPS challenge and worsened over time. The elastase/LPS model also induced mild COPD-like airway inflammation, which encompassed a transient increase in lung mast cell progenitors, but not in mature mast cells. While ST2-deficient and Cpa3(Cre/+) mice developed reduced pulmonary function uninterruptedly, they had a defective inflammatory response. Importantly, both ST2-deficient and Cpa3(Cre/+) mice had fewer alveolar macrophages, known effector cells in COPD. Elastase/LPS instillation in vivo also caused increased bronchiole contraction in precision cut lung slices challenged with methacholine ex vivo, which occurred in a mast cell-independent fashion. Taken together, our data suggest that the ST2 receptor and mast cells play a minor role in COPD pathophysiology by sustaining alveolar macrophages.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Lungmedicin och allergi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Respiratory Medicine and Allergy (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
Nyckelord
- COPD
- chronic obstructive pulmonary disease
- pulmonary function
- airway hyperresposiveness
- mast cell (MC)
- ST2
- IL-33
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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