Lidocaine Modulates Cytokine Production and Reprograms the Tumor Immune Microenvironment to Enhance Anti-Tumor Immune Responses in Gastric Cancer
Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and...
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| Published in | International journal of molecular sciences Vol. 26; no. 7; p. 3236 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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31.03.2025
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| Abstract | Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8+ PBMCs and IL-12 in CD14+ PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4+CD25+ and CD14+ cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8+ and CD14+ cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8+ TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14+ TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8+ TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. |
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| AbstractList | Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8+ PBMCs and IL-12 in CD14+ PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4+CD25+ and CD14+ cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8+ and CD14+ cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8+ TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14+ TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8+ TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer.Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8+ PBMCs and IL-12 in CD14+ PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4+CD25+ and CD14+ cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8+ and CD14+ cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8+ TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14+ TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8+ TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8+ PBMCs and IL-12 in CD14+ PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4+CD25+ and CD14+ cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8+ and CD14+ cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8+ TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14+ TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8+ TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8 PBMCs and IL-12 in CD14 PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4 CD25 and CD14 cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8 and CD14 cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8 TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14 TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8 TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8[sup.+] PBMCs and IL-12 in CD14[sup.+] PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4[sup.+]CD25[sup.+] and CD14[sup.+] cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8[sup.+] and CD14[sup.+] cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8[sup.+] TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14[sup.+] TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8[sup.+] TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood mononuclear cells (PBMCs) from healthy donors and tumor-infiltrating immune cells (TIICs) from gastric cancer patients. PBMCs from healthy donors and TIICs from gastric cancer patients were treated with lidocaine. Cytokine production was assessed using flow cytometry and cytokine assays, with a focus on IFN-γ, IL-12, IL-10, TGF-β, and IL-35 levels. Cytotoxicity against primary gastric cancer cells (PGCCs) was also evaluated. Lidocaine inhibited IFN-γ production in CD8 + PBMCs and IL-12 in CD14 + PBMCs while increasing anti-inflammatory cytokines (IL-10, TGF-β, IL-35) in CD4 + CD25 + and CD14 + cells. In TIICs, lidocaine enhanced IFN-γ and IL-12 production in CD8 + and CD14 + cells while reducing IL-10, TGF-β, and IL-35 levels, promoting an M1-like phenotype in macrophages. Mechanistically, lidocaine enhanced IFN-γ production in sorted CD8 + TIICs through G-protein-coupled receptor (GPCR) signaling and increased IL-12 production in sorted CD14 + TIICs via the toll-like receptor 4 (TLR4) signaling pathway. Lidocaine also increased IFN-γ production and cytotoxicity in CD8 + TIICs via NF-κB activation. Importantly, lidocaine did not affect the viability of PBMCs, TIICs, or PGCCs at concentrations up to 1.5 mM. Lidocaine reprogrammed the tumor immune microenvironment, enhancing anti-tumor immune responses, suggesting its potential to modulate immune functions in gastric cancer. |
| Audience | Academic |
| Author | Liu, Hung-Jen Chen, Ming-Shan Wu, Feng-Hsu Wu, Yi-Ying Wen, Hsiao-Wei Nielsen, Brent L. Liao, Tsai-Ling Chen, I-Chun |
| AuthorAffiliation | 10 Department of Medical Research, Taichung Veterans General Hospital, Taichung 407, Taiwan; tlliao@vghtc.gov.tw 12 Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA; brentnielsen@byu.edu 1 Institute of Molecular Biology, National Chung Hsing University, Taichung 402, Taiwan; yiying939@gmail.com 4 Department of Psychiatry, Taichung Veterans General Hospital, Taichung 407, Taiwan; ichun.chen@vghtc.gov.tw 13 Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung 402, Taiwan 14 Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan 5 Faculty of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan 11 Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan; hwwen@nchu.edu.tw 6 Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 402, Taiwan 8 Department of Critical Care, |
| AuthorAffiliation_xml | – name: 3 Department of Anesthesiology, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi City 600, Taiwan; 06590@cych.org.tw – name: 4 Department of Psychiatry, Taichung Veterans General Hospital, Taichung 407, Taiwan; ichun.chen@vghtc.gov.tw – name: 9 Department of Nursing, Hung Kuang University, Taichung 433, Taiwan – name: 7 Division of General Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung 407, Taiwan; b101091110@tmu.edu.tw – name: 12 Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA; brentnielsen@byu.edu – name: 5 Faculty of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan – name: 8 Department of Critical Care, Taichung Veterans General Hospital, Taichung 407, Taiwan – name: 2 The iEGG and Animal Biotechnology Center, National Chung Hsing University, Taichung 402, Taiwan – name: 6 Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 402, Taiwan – name: 14 Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan – name: 10 Department of Medical Research, Taichung Veterans General Hospital, Taichung 407, Taiwan; tlliao@vghtc.gov.tw – name: 13 Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung 402, Taiwan – name: 1 Institute of Molecular Biology, National Chung Hsing University, Taichung 402, Taiwan; yiying939@gmail.com – name: 11 Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan; hwwen@nchu.edu.tw |
| Author_xml | – sequence: 1 givenname: Yi-Ying orcidid: 0000-0002-3312-8938 surname: Wu fullname: Wu, Yi-Ying – sequence: 2 givenname: Ming-Shan orcidid: 0000-0003-2361-3195 surname: Chen fullname: Chen, Ming-Shan – sequence: 3 givenname: I-Chun surname: Chen fullname: Chen, I-Chun – sequence: 4 givenname: Feng-Hsu surname: Wu fullname: Wu, Feng-Hsu – sequence: 5 givenname: Tsai-Ling orcidid: 0000-0001-7059-4228 surname: Liao fullname: Liao, Tsai-Ling – sequence: 6 givenname: Hsiao-Wei orcidid: 0000-0003-3427-1768 surname: Wen fullname: Wen, Hsiao-Wei – sequence: 7 givenname: Brent L. orcidid: 0000-0001-6300-4816 surname: Nielsen fullname: Nielsen, Brent L. – sequence: 8 givenname: Hung-Jen orcidid: 0000-0002-1460-1494 surname: Liu fullname: Liu, Hung-Jen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40244064$$D View this record in MEDLINE/PubMed |
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| Snippet | Lidocaine, a local anesthetic, has been shown to modulate immune responses. This study examines its effects on cytokine production in peripheral blood... |
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| SubjectTerms | Cancer Care and treatment CD8-Positive T-Lymphocytes - drug effects CD8-Positive T-Lymphocytes - immunology Cell growth Cell Line, Tumor Cytokines Cytokines - metabolism Cytotoxicity Female Gastric cancer Humans Immune response Immune system Immunity (Disease) Immunotherapy Interferon-gamma - metabolism Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Lidocaine Lidocaine - pharmacology Lymphocytes Lymphocytes, Tumor-Infiltrating - drug effects Lymphocytes, Tumor-Infiltrating - immunology Lymphocytes, Tumor-Infiltrating - metabolism Macrophages Macrophages - drug effects Macrophages - immunology Macrophages - metabolism Male Middle Aged Stomach cancer Stomach Neoplasms - drug therapy Stomach Neoplasms - immunology Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Transforming growth factors Tumor Microenvironment - drug effects Tumor Microenvironment - immunology Tumors |
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| Title | Lidocaine Modulates Cytokine Production and Reprograms the Tumor Immune Microenvironment to Enhance Anti-Tumor Immune Responses in Gastric Cancer |
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