Fig. 3

Gene expression. The gene expressions of Akt, PI3k, NLR3, MyD88, NF-κB, TLR4, CCL24, CCL11, Eotaxin, MUC5a, IL-8, and IL-38 were assessed in all groups. GAPDH was used as reference gene. It was observed that the expression levels of Akt, PI3K, NF-kB, and TLR4 significantly (p < 0.05) increased in the OVA-LPS group. The administration of probiotics and prebiotics dramatically attenuated the expression of Akt. Administration of probiotics and prebiotics remarkably inhibited the gene expressions of NF‐κB as compared to the asthma control group (p < 0.05). Treatment with probiotics could control TLR4 expression and prebiotics remarkably inhibited PI3K expressions. In our study, MyD88, MUC5a and NLR3 were up-regulated in the airways of OVA-LPS mice. However, MyD88, NLR3 and MUC5a expression significantly reduced (p < 0.05) in the animals treated with pro-/pre-biotics. The eotaxin gene expression increased in OVA-LPS sensitization/challenge animals. After treatment with probiotics and prebiotics; however, the level of eotaxin reduced (but it was not statistically significant; p > 0.05). On the other hand, the expressions of CCL11 and CCL24 were reduced in the pro- and pre-biotics treated mice, while there was a significant reduction in only CCL11 in the probiotics treated mice (p < 0.05). Also, the up-regulation of IL-8 gene was considerably inhibited following the treatment of OVA-LPS-sensitized mice with probiotics (but not statistically significant; p > 0.05). Allergen exposure significantly (p < 0.05) disturbed the expression of IL-38. Probiotics and prebiotics treatment increased IL-38 gene expression, but only probiotics treatment had significant effect (p < 0.05). The significant difference (p < 0.05) between treated groups and non-treated OVA-LPS group was shown with symbols that include: * for MyD88, # for NLR3, & for PI3k, @ for TLR4, $ for Akt, % for CCL11, Σ for NF-κB, Ω for IL-38 and φ for MUC5a