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      Anti-inflammatory effects of zinc in PMA-treated human gingival fibroblast cells

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          Abstract

          Objectives: Abnormal cellular immune response has been considered to be responsible for oral lesions in recurrent aphthous stomatitis. Zinc has been known to be an essential nutrient metal that is necessary for a broad range of biological activities including antioxidant, immune mediator, and anti-inflammatory drugs in oral mucosal disease. The objective of this study was to investigate the effects of zinc in a phorbol-12-myristate-13-acetate (PMA)-treated inflammatory model on human gingival fibroblast cells (hGFs). Study Design: Cells were pre-treated with zinc chloride, followed by PMA in hGFs. The effects were assessed on cell viability, cyclooxygenease-1,2(COX-1/2) protein expression, PGE2 release, ROS production and cytokine release, Results: The effects were assessed on cell viability, COX1/2 protein expression, PGE2 release, ROS production, cytokine release. The results showed that, in the presence of PMA, zinc treatment leads to reduce the production of ROS, which results in decrease of COX-2 expression and PGE2 release. Conclusions: Thus, we suggest that zinc treatment leads to the mitigation of oral inflammation and may prove to be an alternative treatment for recurrent aphthous stomatitis.

          Key words:Zinc, inflammatory response, cytokines, phorbol-12-myristate-13-acetate, gingival fibroblasts cells.

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          Zinc: role in immunity, oxidative stress and chronic inflammation.

          S. Prasad (2009)
          Zinc is essential for multiple cellular functions including immunity. Many investigators have used zinc supplementation in an attempt to affect the outcome of various diseases. These efforts were aimed at either supporting immunity by zinc administration or correcting the zinc dependent immune functions in zinc deficient individuals. In this review, recent findings of zinc supplementation in various diseases have been presented. Beneficial therapeutic response of zinc supplementation has been observed in the diarrhea of children, chronic hepatitis C, shigellosis, leprosy, tuberculosis, pneumonia, acute lower respiratory tract infection, common cold, and leishmaniasis. Zinc supplementation was effective in decreasing incidences of infections in the elderly, in patients with sickle cell disease (SCD) and decreasing incidences of respiratory tract infections in children. Zinc supplementation has prevented blindness in 25% of the elderly individuals with dry type of AMD. Zinc supplementation was effective in decreasing oxidative stress and generation of inflammatory cytokines such as TNF-alpha and IL-1beta in elderly individuals and patients with SCD. Zinc supplementation has been successfully used as a therapeutic and preventive agent for many conditions. Zinc functions as an intracellular signal molecule for immune cells.
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            NALPs: a novel protein family involved in inflammation.

            Jurg Tschopp, Fabio Martinon, Kimberly Burns (2003)
            A newly discovered family of cytoplasmic proteins--the NALPs--has been implicated in the activation of caspase-1 by the Toll-like receptors (TLRs) during the cell's response to microbial infection. Like the structurally related apoptotic protease-activating factor-1 (APAF-1), which is responsible for the activation of caspase-9, the NALP1 protein forms a large, signal-induced multiprotein complex, the inflammasome, resulting in the activation of pro-inflammatory caspases.
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              Tumor-derived chemokine CCL5 enhances TGF-β-mediated killing of CD8(+) T cells in colon cancer by T-regulatory cells.

              Hui Peng, Ming-Hsien Chiang, Chau-Ting Yeh … (2012)
              Chemokine CCL5/RANTES is highly expressed in cancer where it contributes to inflammation and malignant progression. In this study, we show that CCL5 plays a critical role in immune escape in colorectal cancer. We found that higher levels of CCL5 expression in human and murine colon tumor cells correlated with higher levels of apoptosis of CD8+ T cells and infiltration of T-regulatory cells (T(reg)). In mouse cells, RNA interference (RNAi)-mediated knockdown of CCL5 delayed tumor growth in immunocompetent syngeneic hosts but had no effect on tumor growth in immunodeficient hosts. Reduced tumor growth was correlated with a reduction in T(reg) infiltration and CD8(+) T-cell apoptosis in tumors. Notably, we found that CCL5 enhanced the cytotoxicity of T(reg) against CD8(+) T cells. We also found tumor growth to be diminished in mice lacking CCR5, a CCL5 receptor, where a similar decrease in both T(reg) cell infiltration and CD8(+) T-cell apoptosis was noted. TGF-β signaling blockade diminished apoptosis of CD8(+) T cells, implicating TGF-β as an effector of CCL5 action. In support of this concept, CCL5 failed to enhance the production of TGF-β by CCR5-deficient T(reg) or to enhance their cytotoxic effects against CD8(+) T cells. CCR5 signaling blockade also diminished the in vivo suppressive capacity of T(reg) in inhibiting the antitumor responses of CD8(+) T cells, in the same way as CCL5 signaling blockade. Together, our findings establish that CCL5/CCR5 signaling recruits T(reg) to tumors and enhances their ability to kill antitumor CD8(+) T cells, thereby defining a novel mechanism of immune escape in colorectal cancer.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Med Oral Patol Oral Cir Bucal
                Journal ID (iso-abbrev): Med Oral Patol Oral Cir Bucal
                Journal ID (publisher-id): Medicina Oral S.L.
                Title: Medicina Oral, Patología Oral y Cirugía Bucal
                Publisher: Medicina Oral S.L.
                ISSN (Print): 1698-4447
                ISSN (Electronic): 1698-6946
                Publication date (Print): March 2015
                Publication date (Electronic): 7 February 2015
                Volume: 20
                Issue: 2
                Pages: e180-e187
                Affiliations
                [1 ]Department of Oral Pathology, Dental Science Research Institute and Medical Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University, Bug-Gu, Gwangju, Korea
                [2 ]Department of Oral Pathology, Chonnam National University hospital, Bug-Gu, Gwangju, Korea
                [3 ]Department of oral medicine, School of Dentistry, Chonnam National University, Gwangju, Republic of Korea
                [4 ]Su Dental Clinical Research Center, Yeoksam-dong, Gangnam-gu, Seoul, Korea
                Author notes
                Department of Oral Pathology Dental Science Research Institute and Medical Research Center for Biomineralization Disorders School of Dentistry, Chonnam National University Bug-Gu, Gwangju, 500-757, Korea , E-mail: js3894@ 123456chonnam.ac.kr

                Conflict of interest statement: The authors have declared that no conflict of interest exist.

                Article
                Publisher ID: 19896
                DOI: 10.4317/medoral.19896
                PMC ID: 4393980
                PubMed ID: 25662537
                SO-VID: 5ec35147-e7ed-4b30-93e8-44b3a09f457c
                Copyright © Copyright: © 2015 Medicina Oral S.L.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 23 October 2014
                Date received : 21 February 2014
                Categories
                Subject: Research
                Subject: Oral Medicine and Pathology

                ScienceOpen disciplines: Surgery
                Data availability:
                ScienceOpen disciplines: Surgery

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