Induction of oral tolerance (OT) is known to prevent allergic inflammation in models of asthma.
Bice, D. E., Seagrave, J. & Green, F. H. Animal models of asthma: potential usefulness for studying health effects of inhaled particles.
Our findings suggest that TAS2R agonists mitigate allergen-induced airway inflammation, remodeling, mucus secretion and AHR in murine models of asthma.
AHR has been shown recently in animal models of asthma to require the presence of CD1d-restricted, invariant T cell receptor-positive, natural killer T (iNKT) cells.
Retrieved literature data demonstrates that the aqueous fraction of the ethanolic extract from the leaves exerts an immunomodulatory activity in different animal models of asthma.
There were fourteen preclinical studies describing multiple effects of NS in animal or cellular models of asthma including bronchodilation, anti-histaminic, anti-inflammatory, anti-leukotrienes and immunomodulatory effects.
Impaired surfactant function, attributable to increased plasma protein leakage, has been demonstrated in animal models of asthma and in BAL fluid of asthmatic patients.
We aimed to systematically review the literature regarding the potential benefits of stem cell therapy in animal models of asthma to determine whether a human trial is warranted.
More importantly our studies using both animal models of asthma, and mechanistic studies in humans in vitro clearly demonstrate that TAS2R agonists dampen global allergen-induced airway inflammation and have broader application in terms of reducing dependence on inhaled steroids, mainstay maintenance therapy for asthma.
The new models of asthma and COPD described herein demonstrate that improved clinical understanding of the diseases and better preclinical models is an iterative process that will hopefully lead to therapies that can effectively manage severe asthma and COPD.
We showed that knocking down Cav1.2 and/or Cav1.3 subunits impairs the functions of Th2 lymphocytes and is beneficial in experimental models of asthma, while it has no effect on Th1 cell functions.
