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Alterations of voluntary behavior in the course of disease progress and pharmacotherapy in mice with collagen-induced arthritis

大藤, 洋介 東京慈恵会医科大学 DOI:info:doi/10.1186/s13075-019-2071-z

2021.10.22

概要

Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis and bone destruction at the joints, causing pain and motor disturbance. Despite the better control of inflammation and joint deformity afforded by modern disease-modifying anti-rheumatic drugs, many patients with RA remain dissatisfied with their treatment, primarily because of sensory-emotional distress. Pre-clinical tests that can evaluate not only the symptoms of arthritis but also the associated pain as sensory-emotional experience are urgently needed.

Methods: Here, we introduce two types of novel methods for evaluation of voluntary behavior in a commonly used model of RA (collagen-induced arthritis; CIA) in male mice. First, spontaneous motor activity was assessed with a running wheel placed in home cages and the number of rotations was continuously recorded in a 12:12-h light environment. Second, temperature preference was assessed by measuring the time spent in either of the floor plates with augmenting (25 to 49 °C) or fixed temperature (25 °C). We also evaluated the effects of tofacitinib on CIA-associated changes in voluntary wheel running and temperature preference.

Results: We detected a significant decrease in voluntary wheel running, a significant shift in the distribution of movement in the dark phase, and a significant increase in the time spent in warmer environments than the room temperature in the mice with CIA. These alterations in voluntary behavior have never been described with conventional methods. We also revealed tofacitinib-resistant significant changes in the voluntary behavior and choice of temperature despite significant mitigation of the symptoms of arthritis.

Conclusions: We described for the first time significant alterations of the voluntary behavior of the mice with CIA during the clinical periods, indicating that the overall physical/motivational states and its circadian variation, as well as the specific preference to a certain environmental temperature, are modified in the mice with CIA, as observed in human patients. Some of these did not parallel with the conventional arthritis scores, particularly during the pharmacotherapy suggesting that mice with CIA show not only the peripheral symptoms but also the central consequences. The use of these approaches would also help clarify the biological mechanisms underlying physician-patient discordance in the assessment of RA.

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参考文献

1. Studenic P, Radner H, Smolen JS, Aletaha D. Discrepancies between patients and physicians in their perceptions of rheumatoid arthritis disease activity. Arthritis Rheum. 2012;64:2814–23.

2. Kaneko Y, Kuwana M, Kondo H, Takeuchi T. Discordance in global assessments between patient and estimator in patients with newly diagnosed rheumatoid arthritis: associations with progressive joint destruction and functional impairment. J Rheumatol. 2014;41:1061–6.

3. Desthieux C, Hermet A, Granger B, Fautrel B, Gossec L. Patient-physician discordance in global assessment in rheumatoid arthritis: a systematic literature review with meta-analysis. Arthritis Care Res. 2016;68:1767–73.

4. Michelsen B, Kristianslund EK, Hammer HB, Fagerli KM, Lie E, Wierød A, et al. Discordance between tender and swollen joint count as well as patient’s and evaluator’s global assessment may reduce likelihood of remission in patients with rheumatoid arthritis and psoriatic arthritis: data from the prospective multicentre NOR-DMARD stu. Ann Rheum Dis. 2017;76:708–11.

5. Walsh DA, McWilliams DF. Mechanisms, impact and management of pain in rheumatoid arthritis. Nat Rev Rheumatol. 2014;10:581–92.

6. IASP. Pain terms: a list with definitions and notes on usage: recommended by the IASP Subcommittee on Taxonomy. Pain. 1979;6:249.

7. Inglis JJ, Notley CA, Essex D, Wilson AW, Feldmann M, Anand P, et al. Collagen-induced arthritis as a model of hyperalgesia: functional and cellular analysis of the analgesic actions of tumor necrosis factor blockade. Arthritis Rheum. 2007;56:4015–23.

8. Nieto FR, Clark AK, Grist J, Hathway GJ, Chapman V, Malcangio M. Neuron- immune mechanisms contribute to pain in early stages of arthritis. J Neuroinflammation. 2016;13:96.

9. Clark AK, Grist J, Al-Kashi A, Perretti M, Malcangio M. Spinal cathepsin S and fractalkine contribute to chronic pain in the collagen-induced arthritis model. Arthritis Rheum. 2012;64:2038–47.

10. Straub RH, Kalden JR. Stress of different types increases the proinflammatory load in rheumatoid arthritis. Arthritis Res Ther. 2009;11:114.

11. Luo JG, Zhao XL, Xu WC, Zhao XJ, Wang JN, Lin XW, et al. Activation of spinal NF-κB/p65 contributes to peripheral inflammation and hyperalgesia in rat adjuvant-induced arthritis. Arthritis Rheumatol. 2014;66:896–906.

12. Ito H, Noda K, Yoshida K, Otani K, Yoshiga M, Oto Y, et al. Prokineticin 2 antagonist, PKRA7 suppresses arthritis in mice with collagen-induced arthritis. BMC Musculoskelet Disord. 2016;17:1–7.

13. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔCT method. Methods. 2001;25: 402–8.

14. Milici AJ, Kudlacz EM, Audoly L, Zwillich S, Changelian P. Cartilage preservation by inhibition of Janus kinase 3 in two rodent models of rheumatoid arthritis. Arthritis Res Ther. 2008;10:R14.

15. Lu H, Howatt DA, Balakrishnan A, Moorleghen JJ, Rateri DL, Cassis LA, et al. Subcutaneous angiotensin II infusion using osmotic pumps induces aortic aneurysms in mice. J Vis Exp. 2015;103:e53191.

16. Kanda Y. Investigation of the freely available easy-to-use software “EZR” for medical statistics. Bone Marrow Transplant. 2013;48:452–8.

17. Walker DA. Converting Kendall ’ s tau for correlational or meta-analytic analyses. J Mod Appl Stat Methods. 2003;2:525–30.

18. Zhou LL, Zhu YM, Qian FY, Yuan CC, Yuan DP, Zhou XP. MicroRNA-143-3p contributes to the regulation of pain responses in collagen-induced arthritis. Mol Med Rep. 2018;18:3219–28.

19. Chagas PM, Fulco BCW, Sari MHM, Roehrs JA, Nogueira CW. Bis (phenylimidazoselenazolyl) diselenide elicits antinociceptive effect by modulating myeloperoxidase activity, NOx and NFkB levels in the collagen- induced arthritis mouse model. J Pharm Pharmacol. 2017;69:1022–32.

20. Gao X, Gao R, Tian Y, McGonigle P, Barrett J, Dai Y, et al. A store-operated calcium channel inhibitor attenuates collagen-induced arthritis. Br J Pharmacol. 2015;172:2991–3002.

21. Tanimoto A, Shinozaki Y, Nozawa K, Kimoto Y, Amano W, Matsuo A, et al. Improvement of spontaneous locomotor activity with JAK inhibition by JTE- 052 in rat adjuvant-induced arthritis. BMC Musculoskelet Disord. 2015;16:339.

22. Sasakawa T, Sasakawa Y, Ohkubo Y, Mutoh S. FK506 ameliorates spontaneous locomotor activity in collagen-induced arthritis: implication of distinct effect from suppression of inflammation. Int Immunopharmacol. 2005;5:1762–72.

23. Kandasamy R, Lee AT, Morgan MM. Depression of home cage wheel running: a reliable and clinically relevant method to assess migraine pain in rats. J Headache Pain. 2017;18:5.

24. Grace PM, Loram LC, Christianson JP, Strand KA, Flyer-Adams JG, Penzkover KR, et al. Behavioral assessment of neuropathic pain, fatigue, and anxiety in experimental autoimmune encephalomyelitis (EAE) and attenuation by interleukin-10 gene therapy. Brain Behav Immun. 2017;59:49–54.

25. Grace PM, Strand KA, Maier SF, Watkins LR. Suppression of voluntary wheel running in rats is dependent on the site of inflammation: evidence for voluntary running as a measure of hind paw-evoked pain. J Pain. 2014;15:121–8.

26. Cutolo M, Straub RH. Circadian rhythms in arthritis: hormonal effects on the immune/inflammatory reaction. Autoimmun Rev. 2008;7:223–8.

27. Arvidson NG, Gudbjornsson B, Elfman L, Ryden A-C, Totterman TH, Hallgren R. Circadian rhythm of serum interleukin-6 in rheumatoid arthritis. Ann Rheum Dis. 1994;53:521–4.

28. Zoli A, Lizzio MM, Ferlisi EM, Massafra V, Mirone L, Barini A, et al. ACTH, cortisol and prolactin in active rheumatoid arthritis. Clin Rheumatol. 2002;21:289–93.

29. Louati K, Berenbaum F. Fatigue in chronic inflammation - a link to pain pathways. Arthritis Res Ther. 2015;17:254.

30. To H, Irie S, Tomonari M, Watanabe Y, Kitahara T, Sasaki H. Therapeutic index of methotrexate depends on circadian cycling of tumour necrosis factor-alpha in collagen-induced arthritic rats and mice. J Pharm Pharmacol. 2009;61:1333–8.

31. Jordt SE, McKemy DD, Julius D. Lessons from peppers and peppermint: the molecular logic of thermosensation. Curr Opin Neurobiol. 2003;13:487–92.

32. Fioravanti A, Cantarini L, Guidelli GM, Galeazzi M. Mechanisms of action of spa therapies in rheumatic diseases: what scientific evidence is there? Rheumatol Int. 2011;31:1–8.

33. Karagülle M, Kardeş S, Dişçi R, Karagülle MZ. Spa therapy adjunct to pharmacotherapy is beneficial in rheumatoid arthritis: a crossover randomized controlled trial. Int J Biometeorol. 2018;62:195–205.

34. Yahiro T, Kataoka N, Nakamura Y, Nakamura K. The lateral parabrachial nucleus, but not the thalamus, mediates thermosensory pathways for behavioural thermoregulation. Sci Rep. 2017;7:1–10.

35. Todd AJ. Neuronal circuitry for pain processing in the dorsal horn. Nat Rev Neurosci. 2010;11:823–36.

36. Engblom D, Ek M, Ericsson-Dahlstrand A, Blomqvist A. Activation of prostanoid EP (3) and EP (4) receptor mRNA-expressing neurons in the rat parabrachial nucleus by intravenous injection of bacterial wall lipopolysaccharide. J Comp Neurol. 2001;440:378–86.

37. Borbély É, Kiss T, Szabadfi K, Pintér E, Szolcsányi J, Helyes Z, et al. Complex role of capsaicin-sensitive afferents in the collagen antibody-induced autoimmune arthritis of the mouse. Sci Rep. 2018;8:2–9.

38. Christianson CA, Corr M, Firestein GS, Mobargha A, Yaksh TL, Svensson CI. Characterization of the acute and persistent pain state present in K/BxN serum transfer arthritis. Pain. 2010;151:394–403.

39. McWilliams DF, Ferguson E, Young A, Kiely PDW, Walsh DA. Discordant inflammation and pain in early and established rheumatoid arthritis: latent class analysis of Early Rheumatoid Arthritis Network and British Society for Rheumatology Biologics Register data. Arthritis Res. Ther. 2016;18:1–12.

40. Karpouzas GA, Ramadan SN, Cost CE, Draper TL, Hernandez E, Strand V, et al. Discordant patient-physician assessments of disease activity and its persistence adversely impact quality of life and work productivity in US Hispanics with rheumatoid arthritis. RMD Open. 2017;3:1–9.

41. Smolen JS, Strand V, Koenig AS, Szumski A, Kotak S, Jones TV. Discordance between patient and physician assessments of global disease activity in rheumatoid arthritis and association with work productivity. Arthritis Res Ther. 2016;18:1–11.

42. Sneddon LU, Elwood RW, Adamo SA, Leach MC. Defining and assessing animal pain. Anim Behav. 2014;97:201–12.

43. Cohen M, Quintner J, van Rysewyk S. Reconsidering the International Association for the Study of Pain definition of pain. PAIN Reports. 2018;3:e634.

44. Percie Du Sert N, Rice A. Improving the translation of analgesic drugs to the clinic: animal models of neuropathic pain. Br J Pharmacol. 2014;171:2951–63.

45. Nieto FR, Clark AK, Grist J, Chapman V, Malcangio M. Calcitonin gene-related peptide-expressing sensory neurons and spinal microglial reactivity contribute to pain states in collagen-induced arthritis. Arthritis Rheumatol. 2015;67:1668–77.

46. Kami K, Tajima F, Senba E. Activation of mesolimbic reward system via laterodorsal tegmental nucleus and hypothalamus in exercise-induced hypoalgesia. Sci Rep. 2018;8:1–14.

47. Jeon S, Caterina MJ. Molecular basis of peripheral innocuous warmth sensitivity. Handb Clin Neurol. 2018;156:69–82.

48. Sorge RE, Mapplebeck JCS, Rosen S, Beggs S, Taves S, Alexander JK, et al. Different immune cells mediate mechanical pain hypersensitivity in male and female mice. Nat Neurosci. 2015;18:1081–3.

49. Bushnell MC, Ceko M, Low L. Cognitive and emotional control of pain and its disruption in chronic pain. Nat Rev Neurosci. 2013;14:502–11.

50. Kato F, Sugimura YK, Takahashi Y. Pain-associated neural plasticity in the parabrachial to central amygdala circuit pain changes the brain, the brain changes the pain. Adv Exp Med Biol. 2018;1099:157–66.

51. Tsuda M, Kohro Y, Yano T, Tsujikawa T, Kitano J, Tozaki-Saitoh H, et al. JAK- STAT3 pathway regulates spinal astrocyte proliferation and neuropathic pain maintenance in rats. Brain. 2011;134:1127–39.

52. Kohro Y, Sakaguchi E, Tashima R, Tozaki-Saitoh H, Okano H, Inoue K, et al. A new minimally-invasive method for microinjection into the mouse spinal dorsal horn. Sci Rep. 2015;5:14306.

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