Attenuated Escherichia coli ameliorates airway hyper responsiveness in a mouse model of ovalbumin induced asthma: Role of TNF-α, IL's, IgE and IgG

Allergic asthma is a chronic inflammatory airway disease that is characterized by airway hyperresponsiveness (AHR), accumulation of eosinophils and goblet cell hyperplasia. The efficacy of attenuated E. coli (AEC) strain has been reported in various disease. To evaluate the effect of AEC in mice model of Ovalbumin (OVA)-induced AHR. Materials and method: AHR was induced in Female BALB/c mice (18-20 g) by intraperitoneal injection of OVA (50 μL, emulsified in 0.8 mg aluminium hydroxide) on day 7, 8, 9 and 20 followed by intranasal challenges of OVA on days 20, 23, 27, 30 and 34. OVA control mice will receive an equal volume of saline. Mice were treated with either AEC (10 CFU/ml) or montelukast (10 mg/kg) or vehicle on day 0, 7, 20 and 27 immediately before administration of OVA. AHR to methacholine were assessed on day 35, 24 h after the last pulmonary challenge. Treatment with AEC caused significant restoration in OVA-induced alteration in the cellular count of bronchoalveolar lavage fluid, hematological count, and pulmonary function test. Elevated levels of OVA-induced oxido-nitrosative stress was significantly decreased by AEC treatment. Total IgE, OVA-specific IgE and IgG1 in serum as well as lung TNF-α, IL-4, IL-5, IL-8 and IL-10 levels was significantly reduced by AEC. Histological aberration induced by OVA was reduced by AEC treatment. AEC inhibits OVA-induced AHR in mice via down-regulation of nitroso-oxidative stress, cytokine, and chemokine, as well as IgE and IgG, releases supporting its anti-inflammatory and bronchodilator role during the allergic response.