<p>The formation of tongue coating is closely related with the differentiation of the lingual dorsal mucosa, and a great deal of evidence shows that the variation of tongue coating reflects the pathological and physiological state of the gastric mucosa. However, the detailed mechanism remains elusive. This study established a rat model of gastric intestinal metaplasia (GIM) with 2% sodium salicylate and 20 mmol/L of deoxycholate sodium, and used single-cell RNA sequencing (scRNA-seq) to reveal the cell landscape of tongue dorsal mucosa. In comparison to the control group, the tongue dorsal mucosa of GIM rats became grayish-white, and the histologic characteristics presented an uneven distribution of tongue papilla with many immune cells in the submucosal layer. The expressive levels of pro-inflammatory factors (IL-1β, IL-6, and IL-17) were significantly higher in GIM rats than in the control group. Stratified analysis revealed the significant downregulation of autophagy marker gene <i>Map1lc3a</i> in neutrophils and T cells, and the significant downregulation of cuproptosis marker gene <i>Dlst</i> in fibroblasts of the tongue dorsal mucosa in GIM rats. These changes were closely related to mucosal inflammation and impaired tissue barrier integrity. Significantly, the expression of several keratin genes (<i>Krt7</i>, <i>Krt8</i>, <i>Krt13</i>, <i>Krt16</i>, and <i>Krt76</i>) was significantly downregulated, as well as the expression of the bitter taste receptor gene <i>Rtp4</i> and the sweet taste receptor gene <i>Tas1r2</i> in the GIM rats. The data indicated that fewer cells entered regulated cell death in immune cells of tongue mucosa, a more active inflammatory response occurred, the keratinization of tongue dorsal mucosal cells was inhibited, and the taste perception function was weakened. The results bring new perspectives on tongue coating in the application of gastric disorders.</p><p></p>