Inflammatory pain is a common type of pathological pain. Although the dorsal root ganglion (DRG) is key to pathogenesis of inflammatory pain, the underlying specific molecular and cellular mechanisms remain unclear. In this study, we used mouse models of acute or chronic inflammatory pain, induced by formalin or complete Freund' s adjuvant (CFA), respectively, to explore whether tyrosine kinase receptor ErbB4 participates in the pathogenesis of inflammatory pain. Firstly, we found that both the expression of Neuregulin 1 (Nrg1) and phosphorylation of ErbB4 receptor were upregulated in DRG after inflammatory pain, implying the activation of ErbB4 in DRG. Using ErbB4-mutant mice, we found reduced pain sensitivity of mice when ErbB4 gene expression was largely ablated; furthermore, ErbB4 deletion decreased the inflammatory pain hypersensitivity of either formalin- or CFA-induced mouse models. Moreover, the pain sensitivity was reduced in mice with specific deletion of ErbB4 on advillin-positive neurons within DRG. Importantly, pain hypersensitivity also decreased in Advillin-Cre;ErbB4-/- cKO mice after formalin- or CFA-induced inflammatory pain. Finally, gene quantification differential expression analysis, using RNAseq technology in combination with GO and KEGG enrichment analysis, suggested that calcium signaling pathway possibly mediated the roles of ErbB4 on DRG sensory neurons in inflammatory pain models. Together, these results indicate that ErbB4 on advillin-positive sensory neurons enhances inflammatory pain sensitivity, providing new clues towards the pathogenic mechanisms of inflammatory pain.