Volume 9, Issue 5 (September & October 2018 2018)
BCN 2018, 9(5): 325-336 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Shadnoush M, Nazemian V, Manaheji H, Zaringhalam J. The Effect of Orally Administered Probiotics on the Behavioral, Cellular, and Molecular Aspects of Adjuvant-Induced Arthritis. BCN 2018; 9 (5) :325-336
URL: http://bcn.iums.ac.ir/article-1-977-en.html
URL: http://bcn.iums.ac.ir/article-1-977-en.html
1- Department of Clinical Nutrition & Dietetics, School of Nutrition Sciences & Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- Neurophysiology Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- Neurophysiology Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Introduction: Rheumatoid Arthritis (RA) is a chronic autoimmune disease, which is accompanied with pain, hyperalgesia, and edema. Overproduction of pro-inflammatory cytokines and activation of intracellular signaling pathways sustain the RA symptoms considerably. There is a strong correlation between the expression of cytokines and opioid receptors in the arthritis process. Studies have shown that probiotics via different pathways such as reducing the levels of pro-inflammatory cytokines can alleviate inflammatory symptoms. Therefore, based on the crucial role of cellular and humoral immunity in induction of RA symptoms and potency of probiotics in modulation of immune responses, the purpose of this study was to investigate the effect of orally administered probiotics on the behavioral, cellular and molecular aspects of adjuvant-induced arthritis in male Wistar rats.
Methods: Complete Freund’s Adjuvant (CFA)-induced arthritis was caused by single subcutaneous injection of CFA into the rat’s hind paw on day 0. Different doses of probiotics (1/250, 1/500 and 1/1000 [109 CFU/g]) were administered daily (gavage) after CFA injection. Hyperalgesia, edema, serum IL-1β levels, μ-Opioid Receptor (MOR) expression, and p38MAPK (Mitogen-Activated Protein Kinase) activities were assessed on days 0, 7, 14 and 21 of the study.
Results: The results of this study indicated the efficacy of probiotics in reducing hyperalgesia, edema, serum levels of Interleukin-1β, and p38MAPK pathway activity during different phases of arthritis as well as increasing the expression of MORs during chronic phase of CFA-induced arthritis.
Conclusion: It seems that probiotics can effectively reduce inflammatory symptoms by inhibiting the intracellular signaling pathway and cytokine production.
Keywords: Probiotics, Hyperalgesia, Edema, Interleukin-1β (IL-1β), p38 Mitogen-Activated Protein Kinase (MAPK), μ-Opioid Receptor (MOR)
Type of Study: Original |
Subject:
Behavioral Neuroscience
Received: 2017/07/10 | Accepted: 2018/03/6 | Published: 2018/09/1
Received: 2017/07/10 | Accepted: 2018/03/6 | Published: 2018/09/1
References
1. Akhtari, Z., Zaringhalam, J., Rohani, A. H., & Tekieh, E. (2013). [Role of increasing serum tumor necrosis factor on hyperalgesia and edema variation during different stages of adjuvant-induced arthritis in male rats (Persian)]. Koomesh, 14(3), 357-66.
2. Bressan, E., Cunha, F., & Tonussi, C. (2006). Contribution of TNFα, IL-1β and CINC-1 for articular incapacitation, edema and cell migration in a model of LPS-induced reactive arthritis. Cytokine, 36(1), 83-8. [DOI:10.1016/j.cyto.2006.11.007] [DOI:10.1016/j.cyto.2006.11.007]
3. Cantagrel, A., Navaux, F., Loubet-Lescoulié, P., Nourhashemi, F., Enault, G., Abbal, M., et al. (1999). Interleukin-1β, interleukin-1 receptor antagonist, interleukin-4, and interleukin-10 gene polymorphisms: Relationship to occurrence and severity of rheumatoid arthritis. Arthritis & Rheumatology, 42(6), 1093-100. [DOI:10.1002/1529-0131(199906)42:6≤1093::AID-ANR5>3.0.CO;2-P] [PMID]
https://doi.org/10.1002/1529-0131(199906)42:6<1093::AID-ANR5>3.0.CO;2-P [DOI:10.1002/1529-0131(199906)42:63.0.CO;2-P]
4. De Jongh, R. F., Vissers, K. C., Meert, T. F., Ooij, L. H. D. J., Catharina, S., & Heylen René, J. (2003). The role of interleukin-6 in nociception and pain. Anesthesia & Analgesia, 96(4), 1096-103. [PMID] [DOI:10.1213/01.ANE.0000055362.56604.78]
5. De schepper, H., Cremonini, F., Park, M., & Camilleri, M. (2004). Opioids and the gut: Pharmacology and current clinical experience. Neurogastroenterology & Motility, 16(4), 383-94. [DOI:10.1111/j.1365-2982.2004.00513.x] [PMID] [DOI:10.1111/j.1365-2982.2004.00513.x]
6. Dinarello, C. (2009). Immunological and inflammatory functions of the interleukin-1 family. Annual Review of Immunology, 27, 519-50. [DOI: 10.1146/annurev.immunol.021908.132612] [PMID] [DOI:10.1146/annurev.immunol.021908.132612]
7. Goldsmith, J., Uronis, J., & Jobin, C. (2011). Mu opioid signaling protects against acute murine intestinal injury in a manner involving Stat3 signaling. The American Journal of Pathology, 179(2), 673-83. [DOI:10.1016/j.ajpath.2011.04.032] [PMCID] [PMID] [DOI:10.1016/j.ajpath.2011.04.032]
8. Korb, A., Tohidast Akrad, M., Cetin, E., Axmann, R., Smolen, J., & Schett, G. (2006). Differential tissue expression and activation of p38 MAPK α, β, γ, and δ isoforms in rheumatoid arthritis. Arthritis & Rheumatism, 54(9), 2745-56. [DOI: 10.1002/art.22080] [PMID] [DOI:10.1002/art.22080]
9. Möller, B., & Villiger, P. (2006). Inhibition of IL-1, IL-6, and TNF-α in immune-mediated inflammatory diseases. Seminars in Immunopathology, 27(4), 391-408. [DOI:10.1007/s00281-006-0012-9] [DOI:10.1007/s00281-006-0012-9]
10. Moradi, J., Abbasipour, F., Zaringhalam, J., Maleki, B., Ziaee, N., Khodadoustan, A., et al. (2014). Anethole, a medicinal plant compound, decreases the production of pro-inflammatory TNF-α and IL-1β in a Rat model of LPS-induced periodontitis. Iranian Journal of Pharmaceutical Research, 13(4), 1319-25. [PMID] [PMCID]
11. Nasseri, B., Nazemian, V., Manaheji, H., & Zaringhalam, J. (2016). Microglia are involved in pain related behaviors during the acute and chronic phases of arthritis inflammation. Cellular and Molecular Anesthesia, 1(4), 137-45.
12. Nazemian, V., Nasseri, B., Manaheji, H., & Zaringhalam, J. (2016). Effects of mesenchymal stem cells conditioned medium on behavioral aspects of inflammatory arthritic pain induced by complete freund's adjuvant. Journal of Cellular & Molecular Anesthesia, 1(2), 47-55.
13. Philippe, D., Chakass, D., Thuru, X., Zerbib, P., Tsicopoulos, A., Geboes, K., et al. (2006). Mu opioid receptor expression is increased in inflammatory bowel diseases: implications for homeostatic intestinal inflammation. Gut, 55(6), 815-23. [Doi:10.1136/gut.2005.080887] [PMID] [DOI:10.1136/gut.2005.080887]
14. Rodriguez-vita, J., & Lawrence, T. (2010). The resolution of inflammation and cancer. Cytokine & Growth Factor Reviews, 21(1), 61-65. [DOI:10.1016/j.cytogfr.2009.11.006] [DOI:10.1016/j.cytogfr.2009.11.006]
15. Samuel, B., Shaito, A., Motoike, T., Rey, F., Backhed, F., & Manchester, J., et al. (2008). Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41. Proceedings of the National Academy of Sciences of the United States of America, 105(43), 16767-72. [DOI:10.1073/pnas.0808567105] [PMCID] [PMID] [DOI:10.1073/pnas.0808567105]
16. Shadnoush, M., Shaker Hosseini, R., Mehrabi, Y., Delpisheh, A., Alipoor, E., Faghfoori, Z., et al. (2013). Probiotic yogurt affects pro-inflammatory and anti-inflammatory factors inpatients with inflammatory bowl diseases. Iranian Journal of Pharmaceutical Research, 12(4), 929-36. [PMID] [PMCID] [PMID] [PMCID]
17. Suzuki, M., Tetsuka, T., Yoshida, S., Watanabe, N., Kobayashi, M., Matsui, N., et al. (2000). The role of p38 mitogen-activated protein kinase in IL-6 and IL-8 production from the TNF-α-or IL-1β-stimulated rheumatoid synovial fibroblasts. FEBS Letters, 465(1), 23-27. [DOI:10.1016/S0014-5793(99)01717-2] [DOI:10.1016/S0014-5793(99)01717-2]
18. Tekieh, E., Zaringhalam, J., & Akhtari, Z. (2014). Relationship between cytokines and spinal mu opioid receptor expression during adjuvant-induced arthritis in rats. Annual Review & Research in Biology, 4(11), 1854. [DOI:10.9734/ARRB/2014/8512]
19. Thomas, C. M., & Versalovic, J. (2010). Probiotics-host communication: Modulation of signaling pathways in the intestine. Gut Microbes, 1(3), 148-63. [doi:10.4161/gmic.1.3.11712] [DOI:10.4161/gmic.1.3.11712]
20. Treede, R., Meyer, R., Raja, S., & Campbell, J. (1992). Peripheral and central mechanisms of cutaneous hyperalgesia. Progress in Neurobiology, 38(4), 397-421. [PMID] [DOI:10.1016/0301-0082(92)90027-C]
21. Vaghef Mehrabany, E., Alipour, B., Homayouni Rad, A., Sharif, S. K., Asghari Jafarabadi, M., & Zavvari, S. (2014). Probiotic supplementation improves inflammatory status in patients with rheumatoid arthritis. Nutrition, 30(4), 430-5. [DOI: 10.1016/j.nut.2013.09.007] [PMID] [DOI:10.1016/j.nut.2013.09.007]
22. Vanderpool, C., Yan, F., & Polk, D. (2008). Mechanisms of probiotic action: Implications for therapeutic applications in inflammatory bowel diseases. Inflammatory Bowel Diseases, 14(11), 1585-96. [DOI: 10.1002/ibd.20525] [PMID] [DOI:10.1002/ibd.20525]
23. Zamani, B., Golkar, H. R., Farshbaf, S., Emadi-Baygi, M., Tajabadi-Ebrahimi, M., Jafari, P., et al. (2016). Clinical and metabolic response to probiotic supplementation in patients with rheumatoid arthritis: A randomized, double-blind, placebo-controlled trial. International Journal of Rheumatic Diseases, 19(9), 869-79. [DOI:10.1111/1756-185X.12888] [DOI:10.1111/1756-185X.12888]
24. Zaringhalam, J., Akbari, A., Zali, A., Manaheji, H., Nazemian, V., Shadnoush, M., et al. (2016). Long-term treatment by vitamin b1 and reduction of serum proinflammatory cytokines, hyperalgesia, and paw edema in adjuvant-induced arthritis. Basic and Clinical Neuroscience, 7(4), 331-40. [DOI: 10.15412/J.BCN.03070406] [PMID] [PMCID] [DOI:10.15412/J.BCN.03070406]
25. Zaringhalam, J., Akhtari, Z., Eidi, A., Ruhani, A., & Tekieh, E. (2014). Relationship between serum IL10 level and p38MAPK enzyme activity on behavioral and cellular aspects of variation of hyperalgesia during different stages of arthritis in rats. Inflammopharmacology, 22(1), 37-44. [DOI: 10.1007/s10787-013-0174-8] [PMID] [DOI:10.1007/s10787-013-0174-8]
26. Zaringhalam, J., Manaheji, H., Mghsoodi, N., Farokhi, B., & Mirzaiee, V. (2008). Spinal µ-opioid receptor expression and hyperalgesia with dexamethasone in chronic adjuvant-induced arthritis in rats. Clinical and Experimental Pharmacology and Physiology, 35(11), 1309-15. [PMID] [PMCID] [DOI:10.1111/j.1440-1681.2008.05009.x] [PMID]
27. Zaringhalam, J., Tekieh, E., Manaheji, H., & Akhtari, Z. (2013). Cellular events during arthritis-induced hyperalgesia are mediated by Interleukin-6 and p38 MAPK and their effects on the expression of spinal mu-opioid receptors. Rheumatology International, 33(9), 2291-9. [DOI: 10.1007/s00296-013-2715-2] [PMID] [DOI:10.1007/s00296-013-2715-2]
28. Zimmermann, M. (1983). Ethical guidelines for investigations of experimental pain in conscious animals. Pain, 16(2), 109-10. [PMID] [DOI:10.1016/0304-3959(83)90201-4]
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
Copyright © The Author(s);
This is an open access article distributed under the terms of the Creative Commons Attribution License (CC-By-NC), which permits use, distribution, and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Contact Information
