scholarly journals A new house dust mite–driven and mast cell–activated model of asthma in the guinea pig

2020 ◽  
Vol 50 (10) ◽  
pp. 1184-1195
Author(s):  
Patricia Ramos‐Ramírez ◽  
Malin Noreby ◽  
Jielu Liu ◽  
Jie Ji ◽  
Suado M. Abdillahi ◽  
...  
Keyword(s):  
Mast Cell ◽  
Guinea Pig ◽  
House Dust ◽  
House Dust Mite ◽  
Dust Mite

scholarly journals Mast cell‐derived serotonin enhances methacholine‐induced airway hyperresponsiveness in house dust mite‐induced experimental asthma

Allergy ◽  
2021 ◽  
Author(s):  
Erika Mendez‐Enriquez ◽  
Perla Abigail Alvarado‐Vazquez ◽  
Willem Abma ◽  
Oscar E. Simonson ◽  
Sergey Rodin ◽  
...  
Keyword(s):  
Mast Cell ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Hyperresponsiveness ◽  
Dust Mite

Mast cell-derived serotonin enhances methacholine-induced airway hyperresponsiveness in house dust mite-induced experimental asthma

2021 ◽  
Author(s):  
Erika Haide Mendez ◽  
Perla Abigail Alvarado Vazquez ◽  
Willem Abma ◽  
Oscar Simonson ◽  
Sergey Rodin ◽  
...  
Keyword(s):  
Mast Cell ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Hyperresponsiveness ◽  
Dust Mite

scholarly journals Mast Cell-Deficient KitW-shMice Develop House Dust Mite-Induced Lung Inflammation despite Impaired Eosinophil Recruitment

2014 ◽  
Vol 6 (2) ◽  
pp. 219-226 ◽  
Author(s):  
J. Daan de Boer ◽  
Jack Yang ◽  
Florry E. van den Boogaard ◽  
Arie J. Hoogendijk ◽  
Regina de Beer ◽  
...  
Keyword(s):  
Mast Cell ◽  
House Dust ◽  
House Dust Mite ◽  
Lung Inflammation ◽  
Eosinophil Recruitment ◽  
Dust Mite

scholarly journals The Allergen Der p3 from House Dust Mite Stimulates Store-Operated Ca2+ Channels and Mast Cell Migration through PAR4 Receptors

2018 ◽  
Vol 70 (2) ◽  
pp. 228-241.e5 ◽  
Author(s):  
Yu-Ping Lin ◽  
Charmaine Nelson ◽  
Holger Kramer ◽  
Anant B. Parekh
Keyword(s):  
Mast Cell ◽  
Cell Migration ◽  
House Dust ◽  
House Dust Mite ◽  
Dust Mite ◽  
Ca2 Channels

scholarly journals Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma

2018 ◽  
Vol 314 (3) ◽  
pp. L484-L492 ◽  
Author(s):  
A. M. Zoltowska Nilsson ◽  
Y. Lei ◽  
M. Adner ◽  
G. P. Nilsson
Keyword(s):  
Mast Cell ◽  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Hyperresponsiveness ◽  
Causative Role ◽  
Cell Functions ◽  
Cell Responses ◽  
Cellular Inflammation ◽  
Dust Mite

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.

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