In summary, this study found that in experimental airway allergy, NKCC1 is upregulated and KCC2 is downregulated in airway vagal centers, leading to augmented excitatory response of putative AVPNs to GABA; and all of the changes induced by airway allergy, including brainstem neurochemical, airway vagal functional, pulmonary functional and pulmonary inflammatory changes, were prevented or attenuated by inhibition of microglia activation with not only, intraperitoneal but also, intracerebroventricular minocycline. The gene discussed is SLC12A2; the disease is allergic respiratory disease.