Background and Purpose Emerging evidence has suggested that somatic stimulation, including electroacupuncture (EA), could produce autonomic reflexes to modulate visceral functions. However, the efficacy and underlying mechanisms for EA on allergic pulmonary inflammation (API) remain elusive. Experimental Approach Papain-induced API mice were treated with distinct current-intensity EA at the back BL13, hindlimb ST36, and forelimb LU5 acupoints. The change in API was determined by whole-body plethysmograph (WBP), immunohistochemistry, flow cytometry, and HE staining. We employed lung functional testing combined with pharmacological inhibition and optogenetic activation approaches to examine the underlying mechanisms for EA effects on API. Key Results EA at the back BL13 region, but not limb regions, via a current-intensity-dependent manner, exacerbated the API. Pharmacological blocking of the local thoracic sensory or the lung-innervated autonomic nerve eliminates the EA-produced detrimental effects. Chemical pulmonary sympathectomy was further enhanced, but inhibition of the upregulated muscarinic M3 acetylcholine receptor within the pulmonary was sufficient to protect from the inflammation-exacerbation effect of EA. Conclusions and Implications Our findings suggest that BL13 EA evokes a somatic-autonomic-pulmonary M3 pathway to enhance API. The revelation of somatotopic organization and intensity-dependency in driving the pulmonary autonomic pathways could help optimize stimulation parameters to improve both efficacy and safety in various forms of physical therapy, including bioelectronic medicine and traditional as well as modern forms of moxibustion and EA, to modulate API.