Signaling via dopamine receptors affect IL-17 secretion from Th17 cells, as shown in our previous studies. Tannic acid (TA) is a herbal polyphenol containing a galloyl group with anti-inflammatory and anti-viral properties. In our recent previous study, we found that i) TA is an agonist of the dopamine D2L receptor (D2LR); ii) TA enhances IL-10 secretion from lipopolysaccharide (LPS)-stimulated mouse splenocytes; iii) TA also enhances IL-10 but reduces IL-17 secretion from anti-CD3/CD28 antibody-stimulated splenocytes. In addition, iv) administration of TA to mice with experimentally induced neutrophilic colitis strikingly suppresses weight loss, colon shrinkage, and IL-17 secretion from mesenteric lymph node lymphocytes. Because IL-17 is one of the essential cytokines to induce neutrophilic inflammation, we in this study tested the effect of TA on other neutrophilic inflammation models in rodents, such as carrageenan-induced periodontitis, 2,4,6-trinitrochlorobenzene-induced atopic dermatitis, and imiquimod-induced psoriasis. We successfully showed that i) TA is effective in reducing the resorption of the alveolar bone in periodontitis model and in atopic dermatitis model; ii) TA and gallic acid are effective in easing psoriasis model as well as neutrophilic inflammation; and iii) not only TA but also related compounds such as gallic acid, epicatechin gallate, and epigallocatechin gallate are D2LR agonists. Therefore, TA and related compounds are effective in in vivo animal models for neutrophilic inflammation.