Do the current house dust mite-driven models really mimic allergic asthma?

Birrell, Mark A.; Oosterhout, Antoon J. M. van; Belvisi, Maria G.

doi:10.1183/09031936.00069110

Cited by 19 publications

(15 citation statements)

References 9 publications

(10 reference statements)

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“…However, there is little evidence that HDMs induce robust IgE production in mice in short-term models (Birrell et al, 2010). Furthermore, mice deficient in IL-21R developed normal GC B cell responses and displayed higher concentrations of circulating total IgE as previously reported (Ozaki et al, 2002), arguing that IgE production from B cells plays a limited role in this model.…”

Section: Discussionmentioning

confidence: 91%

Interleukin-21-Producing CD4+ T Cells Promote Type 2 Immunity to House Dust Mites

et al. 2015

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Asthma is a T helper 2 (Th2)-cell-mediated disease; however, recent findings implicate Th17 and innate lymphoid cells also in regulating airway inflammation. Herein, we have demonstrated profound interleukin-21 (IL-21) production after house dust mite (HDM)-driven asthma by using T cell receptor (TCR) transgenic mice reactive to Dermatophagoides pteronyssinus 1 and an IL-21GFP reporter mouse. IL-21-producing cells in the mediastinal lymph node (mLN) bore characteristics of T follicular helper (Tfh) cells, whereas IL-21(+) cells in the lung did not express CXCR5 (a chemokine receptor expressed by Tfh cells) and were distinct from effector Th2 or Th17 cells. Il21r(-/-) mice developed reduced type 2 responses and the IL-21 receptor (IL-21R) enhanced Th2 cell function in a cell-intrinsic manner. Finally, administration of recombinant IL-21 and IL-25 synergistically promoted airway eosinophilia primarily via effects on CD4(+) lymphocytes. This highlights an important Th2-cell-amplifying function of IL-21-producing CD4(+) T cells in allergic airway inflammation.

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Section: Discussionmentioning

confidence: 91%

Interleukin-21-Producing CD4+ T Cells Promote Type 2 Immunity to House Dust Mites

et al. 2015

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“…However, in the context of the murine model of house dust mite-induced allergic airway disease, rhinovirus infection does not induce eosinophilia [99]. The contrasting results from the two mouse models perhaps tell us more about the utility of the models [100] than the putative role of the eosinophil. In animal models of RSV and Sendai (parainfluenza) infection, eosinophils have been found to be important in viral clearance [101,102], raising the possibility that eosinophilic inflammation is beneficial under certain circumstances.…”

Section: Clues From Virus-induced Inflammationmentioning

confidence: 93%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

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“…However, it should be pointed out that levels of IgE in the serum were low in our HDM-sensitized mice model compared to other mouse models of allergic airway inflammation [26]. This poor antibody response is characteristic of the HDM mouse model [27] and represents a potential limitation. However, we were able to induce a robust inflammatory response, which included a significant influx of eosiniphils, in the mice allowing us to test the effect of inflammation on circulating 25(OH)D levels.…”

Section: Discussionmentioning

confidence: 79%

House Dust Mite Induced Lung Inflammation Does Not Alter Circulating Vitamin D Levels

et al. 2014

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Low circulating levels of 25-hydroxyvitamin D [25(OH)D] are associated with chronic lung diseases such as asthma. However, it is unclear whether vitamin D is involved in disease pathogenesis or is modified by the inflammation associated with the disease process. We hypothesized that allergic inflammation decreases the level of circulating 25(OH)D and tested this using a mice model of house dust mite (HDM) induced allergic airway inflammation. Cellular influx was measured in bronchoalvelar lavage (BAL) fluid, and allergic sensitization and 25(OH)D levels were measured in serum. Exposure to HDM caused a robust inflammatory response in the lung that was enhanced by prior influenza infection. These responses were not associated with any change in circulating levels of 25(OH)D. These data suggest that alterations in circulating 25(OH)D levels induced by Th-2 driven inflammation are unlikely to explain the cross-sectional epidemiological association between vitamin D deficiency and asthma.

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Do the current house dust mite-driven models really mimic allergic asthma?

Cited by 19 publications

References 9 publications

Interleukin-21-Producing CD4+ T Cells Promote Type 2 Immunity to House Dust Mites

Interleukin-21-Producing CD4+ T Cells Promote Type 2 Immunity to House Dust Mites

Viral infections and asthma: an inflammatory interface?

House Dust Mite Induced Lung Inflammation Does Not Alter Circulating Vitamin D Levels

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