In mouse asthma models that use ovalbumin (Kim et al., 2012), house dust mite (HDM Wilhelmlm et al., 2011; Halim et al., 2012a; Klein Wolterink et al., 2012), papain (Halim et al., 2012a), and fungal allergens, ILC2s uniformly increase in number and are the major source of IL-5 or/and IL-13, especially in the early phases of the disease.
In guinea pig and mouse asthma models, DAS181 does not cause airway hyperreactivity (unpublished data).
Some researchers have demonstrated that synthetic TLR7 ligands can inhibit Th2 responses, airway remodeling and attenuate airway inflammation in mouse asthma models [19] [21].
Here, we will review how research utilizing mouse asthma models has generated clinically relevant findings regarding the pathogenesis of severe asthma and has revealed targets to exploit in the development of new treatments.
One approach to solving the challenge of developing new treatments for severe asthma is to use experimental mouse asthma models to improve our understanding of the processes implicated in disease pathogenesis, which include airway inflammation, airway remodeling and airway hyperresponsiveness (AHR).
An example of this is provided by pro-resolution lipid mediators, such as lipoxins, protectins and resolvins, which were reported as being able to attenuate disease severity in mouse asthma models (Haworth et al., 2011; Haworth et al., 2008; Levy et al., 2005; Levy et al., 2002; Levy et al., 2007a; Levy et al., 2007b).
McSorley et al. found that HES products inhibit the allergic reaction in the ovalbumin (OVA -induced mOVA -inducedmouse by suppressing the releasthma IL-33 and inhibiting the activation of ILC2s (modelley et al., 2014; McSorley et al., 2015).
The mouse asthma model was established as previously described [ 25] with some modifications.
Our preliminary data shows that activin A immunolocalization in airway epithelium is decreased in asthmatics (Fig. 1), akin to the situation in the mouse asthma model [ 18].
To conduct the study, human lung specimens and peripheral blood mononuclear cells (PBMCs) and a HDM-based mouse asthma model were used.
7– 11 Indeed in the mouse asthma model, mice treated with an H4R antagonist only during the sensitisation phase of the model, where T cell responses are initiated, exhibit reduced disease.
