◀ Back to IL13

AHR — IL13

Text-mined interactions from Literome

Walter et al., J Immunol 2001 (Pulmonary Eosinophilia...) : These studies definitively demonstrate that IL-13 is necessary and sufficient for the induction of AHR and that eosinophilic airway inflammation in the absence of IL-13 is inadequate for the induction of AHR
Kibe et al., Am J Respir Crit Care Med 2003 (Eosinophilia...) : Treatment with dexamethasone inhibited eotaxin expression and completely abolished eosinophil accumulation, but it did not affect AHR , MUC5AC overexpression, or goblet cell hyperplasia induced by IL-13 ... The effects of tumor necrosis factor-alpha on IL-13 induced AHR were also examined ... These findings suggest that glucocorticoid is not sufficient to suppress IL-13 induced AHR or goblet cell hyperplasia and that eotaxin expression and eosinophilic inflammation do not have a causal relationship to the induction of AHR or goblet cell hyperplasia by IL-13
Yang et al., J Allergy Clin Immunol 2003 (Bronchial Hyperreactivity...) : AHR was dependent on IL-13 and signaling through the IL-4R alpha-chain and signal transducers and activators of transcription 6 pathways and the presence of eosinophils in the lung
Eum et al., Am J Physiol Lung Cell Mol Physiol 2005 (Bronchial Hyperreactivity...) : The aim of this study was to evaluate whether eotaxin and IL-5 were implicated in the effects of IL-13 on allergen induced AHR or whether IL-13 may exert its effects through direct actions on airway smooth muscle ( ASM ) ... These results suggest that IL-13 plays an important role in allergen induced AHR and is important in the early phases of the inflammatory process
Dakhama et al., J Immunol 2005 (Bronchial Hyperreactivity...) : Thus, neonatal RSV infection predisposes to the development of airway eosinophilia and enhanced AHR via an IL-13 dependent mechanism during reinfection, whereas infection at a later age protects against the development of these altered airway responses after reinfection
Park et al., Chest 2005 (Asthma...) : Experimental studies on asthma have indicated that interleukin (IL)-13 induces airway hyperreactivity (AHR) ... However, it remains unproven that IL-13 is responsible for AHR in asthmatic patients ... Comparisons between asthma and EB would clarify the role of IL-13 in AHR
Perkins et al., J Allergy Clin Immunol 2006 (Bronchial Hyperreactivity...) : IL-4 promotes T ( H ) 2 response induction, and IL-13 is necessary and sufficient to induce airways hyperresponsiveness (AHR) and goblet cell hyperplasia in some mouse models of asthma
Yang et al., J Immunol 2006 (Asthma...) : Expression of arginase I, but not eosinophilia or mucus hypersecretion, temporally correlated with the development, persistence, and resolution of IL-13 induced AHR ... Pharmacological supplementation with l-arginine or with NO donors amplified or attenuated IL-13 induced AHR , respectively ... Moreover, inducing loss of function of arginase I specifically in the lung by using RNA interference abrogated the development of IL-13 induced AHR ... These data suggest an important role for metabolism of l-arginine by arginase I in the modulation of IL-13 induced AHR and identify a potential pathway distal to cytokine receptor interactions for the control of IL-13 mediated bronchoconstriction in asthma
Nath et al., Clin Exp Allergy 2007 (Asthma...) : IL-13 is mainly responsible for AHR , ASM hyperplasia and increases in IgE, while IL-4, -5 and -9 may contribute to goblet cell hyperplasia and eosinophilic inflammation induced by chronic allergen exposure in a murine model
Akbari et al., J Immunol 2008 (Asthma...) : The failure of ICOS ( -/- ) iNKT cells to induce AHR was due in part to an inability of the ICOS ( -/- ) iNKT cells to produce IL-4 and IL-13 on activation
Moynihan et al., Am J Physiol Lung Cell Mol Physiol 2008 (Asthma...) : Interleukin-13 (IL-13) has been strongly implicated in the pathogenesis of allergic asthma through animal models that have shown that IL-13 is both necessary and sufficient to cause airway hyperresponsiveness (AHR) ... Airway smooth muscle ( ASM ) is a primary effector of AHR , and IL-13 increases the responsiveness of ASM, by increasing Ca ( 2+ ) release intracellularly, to bronchoconstrictors such as histamine
Kirstein et al., Infect Immun 2010 (Bronchial Hyperreactivity) : Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent ... Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-gamma
Perkins et al., J Exp Med 2011 (Bronchial Hyperreactivity) : Furthermore, differences in mouse versus human airway anatomy and observations that selective IL-13 stimulation of Stat6 in airway epithelium induces murine AHR raise questions about the importance of direct IL-4R effects on smooth muscle in murine asthma models and the relevance of these models to human asthma
Barlow et al., J Allergy Clin Immunol 2012 (Asthma...) : These findings identify nuocytes as a novel cell type in allergic lung inflammation and an innate source of IL-13 that can directly induce AHR in the absence of IL-13 producing CD4 ( + ) T cells
Crapster-Pregont et al., J Allergy Clin Immunol 2012 (Inflammation) : In either case mice were not protected from IL-13 induced AHR and mucus metaplasia
Jiang et al., J Pharmacol Exp Ther 2012 (Asthma...) : This report is the first to demonstrate that PI3K? in ASM cells is important for IL-13 induced AHR and that acute treatment with a PI3K? inhibitor can ameliorate AHR in a murine model of asthma
Starkey et al., Mucosal Immunol 2013 (Chlamydial Pneumonia...) : We investigated the role of interleukin-13 (IL-13) in promoting early-life Chlamydia respiratory infection, infection induced airway hyperresponsiveness (AHR) , and severe allergic airway disease ( AAD ) ... Thus, early-life Chlamydia respiratory infection reduces IL-13Ra2 production, which may enhance the effects of constitutive IL-13 and promote more severe infection, persistent AHR , and AAD
Sullo et al., Am J Physiol Lung Cell Mol Physiol 2013 (Bronchial Hyperreactivity) : In a separate set of experiments cell proliferation in lymphocytes, cytokine levels, IgE serum levels, and the effect of UFP-112 on IL-13 induced AHR were evaluated ... No effect on allergen induced AHR was observed when the treatment was performed at the end of sensitization process, on tissues harvested from OVA sensitized mice and on IL-13 induced AHR