Mouse model of allergic airway inflammation is a well-established model using BALB/c mice sensitized with intraperitoneal OVA/Alum and challenged intranasal nebulized OVA. This model stays as a gold standard model for studying the pathophysiology of lung during allergic airway inflammation. Growing evidences suggest an increased intestinal permeability and intestinal inflammation as one of the significant causes for the development of allergic airway diseases including asthma. Studies have observed the gut inflammation and barrier dysfunction in mouse model of allergic asthma highlighting the lung to gut axis.  However, the characterization of gut inflammation and leakage in the mouse model of OVA induced allergic airway inflammation in context of gut to lung axis is not yet studied.  In the current study, we have observed an intestinal barrier damage and type 2 inflammation marked with increased eosinophils, enhanced expression of type 2 cytokines (IL-4 and IL-13) and transcriptional factor STAT6 in the gut before and after intranasal OVA challenge associated with development of allergic airway inflammation. In addition, we also observed a dysregulated alveolar barrier function, reduced tight junction protein expression levels before intranasal OVA challenge. Our data demonstrates that, intraperitoneal OVA sensitization initiates a primary type 2 inflammation and leakage in gut that orchestrate the development of allergic airway responses in mouse model of allergic airway inflammation in vivo, adding evidences to gut to lung axis.