scholarly journals Supplementation of antioxidants glutathione and α-lipoic acid attenuates oxidative stress and Th2 response in allergic airway inflammation

2013 ◽  
Vol 27 (1) ◽  
pp. 19 ◽  
Author(s):  
Naveen Arora ◽  
Smitha Nair ◽  
Prabhanshu Tripathi
Keyword(s):  
Oxidative Stress ◽  
Airway Inflammation ◽  
Lipoic Acid ◽  
Allergic Airway Inflammation ◽  
Th2 Response

scholarly journals Protective effects of combined Mycobacterium bovis BCG and interleukin-12 vaccination on airway inflammation in a murine model of allergic asthma

2010 ◽  
Vol 33 (3) ◽  
pp. 196 ◽  
Author(s):  
Xia Ke ◽  
Jiangju Huang ◽  
Quan Chen ◽  
Suling Hong ◽  
Daoyin Zhu
Keyword(s):  
Airway Inflammation ◽  
Allergic Asthma ◽  
Mycobacterium Bovis ◽  
Immunoglobulin E ◽  
Allergic Airway Inflammation ◽  
Interleukin 12 ◽  
Protective Effects ◽  
Th2 Response ◽  
Bcg Vaccination ◽  
Th2 Responses

Purpose. Allergic asthma is characterized by chronic airway inflammation and airway hyperresponsiveness driven by allergen-specific T helper (Th)2 cells. Mycobacterium bovis bacillus Calmette-Guérin (BCG) vaccination has been documented to suppress Th2 responses and allergic airway inflammation in animal models. Since interleukin (IL)-12 is capable of inhibiting Th2 responses, we sought to investigate whether IL-12 could function as an adjuvant to increase the efficacy of BCG vaccination against allergic asthma. Methods. BALB/c neonatal mice (24 mice, 48-72 h old) were randomly divided into 3 subgroups (n = 8 for each group) to be immunized with PBS (control) or BCG with or without DNA plasmid-expressing IL-12. All of the mice were then sensitized and provoked with ovalbumin (OVA) to establish a model of allergic asthma. Results. Mice vaccinated with BCG alone showed a significant reduction in airway inflammation, percentage of eosinophils in bronchoalveolar lavage (BAL) fluid, and serum OVA-specific immunoglobulin E (IgE) levels in comparison with control animals. The suppressive effects of BCG were substantially augmented by the combination with IL-12. Furthermore, a decreased IL-4 and increased interferon-gamma (IFN-γ) production in BAL fluid were observed in animals inoculated with BCG alone or with IL-12 relative to control animals. Conclusion. Our data indicate that the combined vaccination with BCG and IL-12 yields a favorable outcome in prevention of experimental allergic airway inflammation, which is likely mediated through triggering a shift from a Th2 response to a Th1 response.

Antagonism of mmu-mir-106a attenuates asthma features in allergic murine model

2012 ◽  
Vol 113 (3) ◽  
pp. 459-464 ◽  
Author(s):  
Amit Sharma ◽  
Manish Kumar ◽  
Tanveer Ahmad ◽  
Ulaganathan Mabalirajan ◽  
Jyotirmoi Aich ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Diseases ◽  
Allergic Airway Inflammation ◽  
Interleukin 10 ◽  
Dependent Manner ◽  
Th2 Response ◽  
Lung Histology ◽  
Health And Disease

MicroRNAs (miRs) regulate immunological pathways in health and disease, and a number of miRs have been shown to be altered in mouse models of asthma. The secretion of interleukin-10 (IL-10), an anti-inflammatory cytokine, has been shown to be defective in many inflammatory diseases including asthma. We recently demonstrated that miR-106a inhibits IL-10 in a post-transcriptional manner. In this study, we investigated the effect of inhibition of mmu-miR106a in asthmatic condition to find its possible role as a therapeutic target. Our in vitro experiments with mouse macrophage, RAW264.7, revealed that mmu-miR-106a potentially decreased IL-10 along with increase in proinflammatory cytokine. Furthermore, administration of mmu-miR-106a to naive mice reduced IL-10 levels in lungs in a dose-dependent manner without altering lung histology. Most interestingly, knockdown of mmu-miR-106a in an established allergic airway inflammation has significantly alleviated most of the features of asthma such as airway hyperresponsiveness, airway inflammation, increased Th2 response, goblet cell metaplasia, and subepithelial fibrosis along with increase in IL-10 levels in lung. This represents the first in vivo proof of a miRNA-mediated regulation of IL-10 with a potential to reverse an established asthmatic condition.

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