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      Immunomodulatory activity of mefenamic acid in mice models of cell-mediated and humoral immunity

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          Abstract

          Objectives:

          Previously, different nonsteroidal anti-inflammatory drugs (NSAIDs) have been evaluated for their potential immunomodulatory activities. Mefenamic acid is a well-known NSAID and is used in the treatment of musculoskeletal disorders, inflammation, fever, and pain. To the best of our knowledge, promising data regarding the immunomodulatory activity of mefenamic acid is scarce. Current study investigates the immunomodulatory activity of mefenamic acid in different models of cell-mediated and humoral immunity.

          Materials and Methods:

          Immunomodulatory effects on cell-mediated immunity were evaluated using dinitrochlorobenzene-induced delayed type hypersensitivity (DTH) and cyclophosphamide-induce myelosuppression assays. While effects on humoral immunity were evaluated using hemagglutination assay and mice lethality test.

          Results:

          Hematological analysis showed that mefenamic acid significantly reduced white blood cell count, red blood cell (RBC) count, hemoglobin content, lymphocytes levels, and neutrophils levels in healthy mice as compared with control, suggesting the immunosuppressive activity of mefenamic acid. Treatment with mefenamic acid also significantly reduced all the hematological parameters in cyclophosphamide-induced neutropenic mice, as compared with positive control group. We found that treatment with mefenamic acid significantly suppressed DTH after 24 h, 48 h, and 72 h, as compared with positive control group. Mefenamic acid treated groups showed a significant reduction in antibody titer against sheep RBCs as compared to control group, similar to the effect of cyclophosphamide. We also found increased mice lethality rate in mefenamic acid treated groups, as compared with positive control group.

          Conclusions:

          The results provided basic information of immunosuppression of mefenamic acid on both cell-mediated and humoral immunity.

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          Most cited references25

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          Targeting natural killer cells and natural killer T cells in cancer.

          Eric Vivier, Sophie Ugolini, Didier Blaise … (2012)
          Natural killer (NK) cells and natural killer T (NKT) cells are subsets of lymphocytes that share some phenotypical and functional similarities. Both cell types can rapidly respond to the presence of tumour cells and participate in antitumour immune responses. This has prompted interest in the development of innovative cancer therapies that are based on the manipulation of NK and NKT cells. Recent studies have highlighted how the immune reactivity of NK and NKT cells is shaped by the environment in which they develop. The rational use of these cells in cancer immunotherapies awaits a better understanding of their effector functions, migratory patterns and survival properties in humans.
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            Immunopathogenesis of delayed-type hypersensitivity.

            K Kobayashi, K Kaneda, T. Kasama (2001)
            Cell-mediated immunity is defined as a beneficial host response characterized by an expanded population of specific T cells, which, in the presence of antigens, produce cytokines locally. The activation and recruitment of cells into an area of inflammation is a crucial step in the development of DTH responses. DTH is immunologically a process similar to cell-mediated immunity, involving T cells and cytokines. CD4 T helper (Th) 1 cells, differentiated from naive Th cells by IL-12 and IL-18 produced from macrophages, play a regulatory role in the expression of DTH and activation of macrophages via interferon gamma generated by Th1 and natural killer cells. Macrophages accumulate at the site of DTH and become activated through the CD4 Th1 cell-cytokine-macrophage axis. However, DTH leads to pathologic responses, such as granulomatous inflammation, calcification, caseation necrosis, and cavity formation. Granulomas usually form as a result of the persistence of a nondegradable product or as the result of DTH responses. DTH is also required for host defense against etiologic agents, such as Mycobacterium tuberculosis. The expression of cell-mediated immunity/DTH is a double-edged sword that may contribute to both clearance of the etiologic agent and tissue damage. Copyright 2001 Wiley-Liss, Inc.
            Article 0 comments Cited 39 times – based on 0 reviews     Review now
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              Anti-arthritic activity of N'-[(2,4-dihydroxyphenyl)methylidene]-2-(3,4-dimethyl-5,5-dioxidopyrazolo[4,3-c][1,2]benzothiazin-1(4H)-yl)acetohydrazide.

              Arham Shabbir, Muhammad Shahzad, Akbar Ali … (2014)
              Benzothiazine and pyrazole derivatives possess anti-inflammatory properties. Previously, synergism of both heterocyclic moieties into a single nucleus has shown to produce biologically active N'-arylmethylidene-2-(3,4-dimethyl-5,5-dioxidopyrazolo(4,3-c)(1,2)benzothiazin-2(4H)yl)acetohydrazides) compound. Present study investigates the anti-arthritic effect and possible mechanism of 2,4-dihydroxyphenyl derivative (DHP) in Freund's complete adjuvant-induced arthritic rat model. Ankle joint histopathology was performed with Hematoxylin & Eosin staining, while serum C-reactive protein (CRP) levels were measured by agglutination method. mRNA expression levels and protein levels of proinflammatory markers were measured by real time reverse transcription polymerase chain reaction and Enzyme linked immunosorbent assay (ELISA), respectively. in vitro Concanavalin A (ConA)-stimulated splenocyte proliferation was also measured by ELISA reader. DHP treatment reduced the macroscopic arthritic score, CRP levels, synovial inflammation, bone erosion and pannus formation. Levels of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), Prostaglandin-E2 (PGE2), and 5-lipoxygenase (5-LOX), were significantly attenuated by DHP. It also significantly decreased the levels of toll-like receptor 2, nuclear factor-kappaB (NF-ĸB), and tissue necrosis factor-α (TNF-α) and non-significantly elevated interleukin-4 (IL-4) levels. Piroxicam, used as reference drug, significantly reduced the levels of COX-1, COX-2, PGE2, NF-ĸB, and TNF-α, but did not show reduction in 5-LOX and toll-like receptor 2 levels. However piroxicam significantly enhanced the levels of IL-4. Both DHP and piroxicam suppressed ConA-stimulated splenocyte proliferation. DHP normalized all altered hematological markers and did not show any sign of hepatotoxicity or nephrotoxicity as determined by alanine transaminase, aspartate aminotransferase, urea, and creatinine levels. Results showed that DHP possesses significant anti-arthritic activity which may be attributed to its immunomodulatory and anti-inflammatory effects.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Pharmacol
                Journal ID (iso-abbrev): Indian J Pharmacol
                Journal ID (publisher-id): IJPharm
                Title: Indian Journal of Pharmacology
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0253-7613
                ISSN (Electronic): 1998-3751
                Publication date (Print): Mar-Apr 2016
                Volume: 48
                Issue: 2
                Pages: 172-178
                Affiliations
                [1]Pharmacology Section, Faculty of Pharmacy, The University of Lahore, Lahore, Pakistan
                [1 ]Department of Pharmacology, University of Health Sciences, Lahore, Pakistan
                Author notes
                Correspondence to: Dr. Arham Shabbir, E-mail: charham007@ 123456hotmail.com
                Article
                Publisher ID: IJPharm-48-172
                DOI: 10.4103/0253-7613.178837
                PMC ID: 4825435
                PubMed ID: 27127320
                SO-VID: 52df23bc-32ab-47aa-87de-50bf9bc6d98d
                Copyright © Copyright: © Indian Journal of Pharmacology
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                Date received : 02 November 2015
                Date revision received : 30 December 2015
                Date accepted : 17 February 2016
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cell-mediated immunity,humoral immunity,immunomodulation,mefenamic acid,nonsteroidal anti-inflammatory drugs
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cell-mediated immunity, humoral immunity, immunomodulation, mefenamic acid, nonsteroidal anti-inflammatory drugs

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