IL-17A is a critical proinflammatory cytokine for the pathogenesis of asthma including neutrophilic pulmonary inflammation and airway hyperresponsiveness.
While the contribution of IL-17/Th17 responses to both physiological and pathological lung inflammation is now well established, the cellular interactions, soluble factors, and signalling pathways that determine Th17 cell responses to fungal infection remain unclear.
Importantly, we demonstrate that PI3K inhibitor significantly suppressed IL-17 production and lung inflammation caused by HP-PRRSV <i>in vivo</i>, implicating that higher IL-17 level induced by HP-PRRSV might be associated with severe lung inflammation.
The present review is an insight into the involvement and contributions of the proinflammatory cytokine IL-17A in chronic respiratory diseases like Idiopathic Pulmonary Fibrosis (IPF), Chronic Obstructive Pulmonary Distress (COPD), asthma, pneumonia, obliterative bronchiolitis, lung cancer and many others.
Monotherapy of IL-17A mAb partially attenuated lung inflammation in OVA-challenged and ozone-exposed mice, while the combination treatment of Dex and IL-17A mAb effectively reduced lung inflammation, inactivated p38 MAPK and up regulated GR in lung tissue.
Here, we report that MLN4924 can markedly reduce the expression of proinflammatory cytokines and chemokines such as IL-1β, IL-6, and CXCL-1 and neutrophilia in a mouse model of IL-17A adenovirus-induced pulmonary inflammation.
This suggests that antioxidant NAC attenuates IL-17A-induced pulmonary inflammation by restoring oxidant-antioxidant balance and attenuation of IL-6 in the lung.
<b>Objective:</b> To study the effects of an anti-IL17 neutralizing antibody and ROCK inhibitor treatments, separately and in combination, in a murine model of chronic allergy-induced lung inflammation.
In every aspect of pulmonary inflammation investigated, dexmedetomidine significantly and dose-dependently attenuated the inflammatory effects of IL-17.
We report that allergic lung inflammation is attenuated in absence of either IL-17A or IL-17F with reduced airway hyperreactivity, eosinophilic inflammation, goblet cell hyperplasia, cytokine and chemokine production as found in absence of IL-17RA.
Altogether, PTX3 deficiency results in augmented airway hyperresponsiveness, mucus production, and IL-17A-dominant pulmonary inflammation, suggesting a regulatory role of PTX3 in the development of allergic inflammation.
Administration of these two chemical inhibitors similarly inhibited the AHR, the BAL IFN-γ and IL-6 production, the perivascular lung inflammation and the lung IL-17 mRNA expression of OVA-O3 model.
Delayed clearance of the bacteria and stronger lung inflammation observed in infected CS-exposed mice were associated with an altered production of IL-17 and IL-22 by innate immune cells.