Gastric cancer peritoneal metastasis (GCPM) carries a poor prognosis, and the local immune microenvironment is central to disease progression and treatment response. Here, we analyzed paired peritoneal lavage samples collected before and after intraperitoneal chemotherapy (IPC) using bulk RNA sequencing (bulk RNA−seq) and single−cell RNA sequencing (scRNA−seq) to characterize IPC associated immune changes. Bulk RNA−seq showed post−IPC upregulation of immune−related genes, including IL1B, IRAK2, ICAM1, and NLRP3. Pathway enrichment of differentially expressed genes indicated that immune/inflammatory programs—chemokine signaling, and Toll−like receptor signaling—were enriched after IPC, whereas pre−treatment samples were relatively enriched for stromal−remodeling processes, including epithelial−mesenchymal transition (EMT), complement and coagulation cascades, and angiogenesis. CIBERSORT deconvolution further suggested an increase in CD8⁺T cells and a decrease in Treg cells and overall myeloid proportions after IPC. Consistently, scRNA−seq showed higher T/NK−cell proportions and lower myeloid proportions post−treatment. Cell−cell communication analysis further revealed strengthened interactions between CD8_CTL cells and myeloid subsets, most notably along the CCL4−CCR5 and NECTIN2−CD226 axes—consistent with enhanced recruitment and activation of effector lymphocytes. Overall, IPC was associated with increased effector T−cell activity and attenuation of myeloid suppressive features, indicating partial remodeling of the peritoneal immune microenvironment. These findings provide a transcriptomic basis for optimizing local therapeutic strategies in GCPM.