Acta Med. 2021, 64: 204-212

https://doi.org/10.14712/18059694.2022.3

Goeckerman Regimen Reduces Alarmin Levels and PASI Score in Paediatric Patients with Psoriasis

Drahomíra Holmannováa, Barbora Císařováa, Pavel Borskýa,b, Zdeněk Fialaa, Ctirad Andrýsc, Květoslava Hamákovád, Tereza Švadlákováa,c, Jan Krejsekc, Vladimír Paličkae, Lenka Kotingováa, Lenka Borskáa

aInstitute of Preventive Medicine, Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
bInstitute of Pathological Physiology, Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
cInstitute of Clinical Immunology and Allergology, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
dClinic of Dermal and Venereal Diseases, University Hospital, Hradec Králové, Czech Republic
eInstitute of Clinical Biochemistry and Diagnostics, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic

Received August 31, 2021
Accepted December 20, 2021

References

1. Schön MP, Boehncke W-H. Psoriasis. N Engl J Med 2005; 352(18): 1899–912. <https://doi.org/10.1056/NEJMra041320>
2. Oppenheim JJ, Tewary P, De La Rosa G, Yang D. Alarmins initiate host defense. In: Advances in Experimental Medicine and Biology. Vol 601. Adv Exp Med Biol; 2007: 185–94. <https://doi.org/10.1007/978-0-387-72005-0_19>
3. Rider P, Voronov E, Dinarello CA, Apte RN, Cohen I. Alarmins: Feel the Stress. J Immunol 2017; 198(4): 1395–402. <https://doi.org/10.4049/jimmunol.1601342>
4. Lowes MA, Suárez-Fariñas M, Krueger JG. Immunology of psoriasis. Annu Rev Immunol 2014; 32: 227–55. <https://doi.org/10.1146/annurev-immunol-032713-120225> <PubMed>
5. Nie Y, Yang D, Oppenheim JJ. Alarmins and Antitumor Immunity. Clin Ther 2016; 38(5): 1042–53. <https://doi.org/10.1016/j.clinthera.2016.03.021> <PubMed>
6. Zaba LC, Fuentes-Duculan J, Eungdamrong NJ, et al. Psoriasis is characterized by accumulation of immunostimulatory and Th1/Th17 cell-polarizing myeloid dendritic cells. J Invest Dermatol 2009; 129(1): 79–88. <https://doi.org/10.1038/jid.2008.194> <PubMed>
7. Andersson U, Tracey KJ. HMGB1 is a therapeutic target for sterile inflammation and infection. Annu Rev Immunol 2011; 29: 139–62. <https://doi.org/10.1146/annurev-immunol-030409-101323> <PubMed>
8. Murugesapillai D, McCauley MJ, Maher LJ, Williams MC. Single-molecule studies of high-mobility group B architectural DNA bending proteins. Biophys Rev 2017; 9(1): 17–40. <https://doi.org/10.1007/s12551-016-0236-4> <PubMed>
9. Klune JR, Dhupar R, Cardinal J, Billiar TR, Tsung A. HMGB1: Endo­genous danger signaling. Mol Med 2008; 14(7–8): 476–84. <https://doi.org/10.2119/2008-00034.Klune> <PubMed>
10. Bianchi ME, Manfredi AA. High-mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity. Immunol Rev 2007; 220(1): 35–46. <https://doi.org/10.1111/j.1600-065X.2007.00574.x>
11. Sabat R, Ouyang W, Wolk K. Therapeutic opportunities of the IL-22-IL-22R1 system. Nat Rev Drug Discov 2014; 13(1): 21–38. <https://doi.org/10.1038/nrd4176>
12. Zhuang L, Ma W, Yan J, Zhong H. Evaluation of the effects of IL-22 on the proliferation and differentiation of keratinocytes in vitro. Mol Med Rep 2020; 22(4): 2715–22.
13. Cayrol C, Girard JP. IL-33: An alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. Curr Opin Immunol 2014; 31: 31–7. <https://doi.org/10.1016/j.coi.2014.09.004>
14. Kunes P, Holubcova Z, Kolackova M, Krejsek J. Interleukin-33, a novel member of the IL-1/IL-18 cytokine family, in cardiology and cardiac surgery. Thorac Cardiovasc Surg 2010; 58(8): 443–9. <https://doi.org/10.1055/s-0030-1250436>
15. Woodrick J, Gupta S, Camacho S, et al. A new sub‐pathway of long‐patch base excision repair involving 5́ gap formation. EMBO J 2017; 36(11): 1605–22. <https://doi.org/10.15252/embj.201694920> <PubMed>
16. Theoharides TC, Petra AI, Taracanova A, Panagiotidou S, Conti P. Targeting IL-33 in autoimmunity and inflammation. J Pharmacol Exp Ther 2015; 354(1): 24–31. <https://doi.org/10.1124/jpet.114.222505>
17. Xu H, Turnquist HR, Hoffman R, Billiar TR. Role of the IL-33-ST2 axis in sepsis. Mil Med Res 2017; 4(3).
18. Kim MH, Jin SP, Jang S, et al. IL-17A–Producing Innate Lymphoid Cells Promote Skin Inflammation by Inducing IL-33–Driven Type 2 Immune Responses. J Invest Dermatol 2020; 140(4): 827–837.e9. <https://doi.org/10.1016/j.jid.2019.08.447>
19. Zenobia C, Hajishengallis G. Basic biology and role of interleukin-17 in immunity and inflammation. Periodontol 2000 2015; 69(1): 142–59. <https://doi.org/10.1111/prd.12083> <PubMed>
20. Jin W, Dong C. IL-17 cytokines in immunity and inflammation. Emerg Microbes Infect 2013; 2(9): e60. <https://doi.org/10.1038/emi.2013.58> <PubMed>
21. Watson PH, Leygue ER, Murphy LC. Psoriasin (S100A7). Int J Biochem Cell Biol 1998; 30(5): 567–71. <https://doi.org/10.1016/S1357-2725(97)00066-6>
22. Granata M, Skarmoutsou E, Mazzarino MC, D’Amico F. S100A7 in psoriasis: Immunodetection and activation by CRISPR technology. In: Methods in Molecular Biology. Vol 1929. Humana Press Inc.; 2019: 729–38.
23. Vogl T, Stratis A, Wixler V, et al. Autoinhibitory regulation of S100A8/S100A9 alarmin activity locally restricts sterile inflammation. J Clin Invest 2018; 128(5): 1852–66. <https://doi.org/10.1172/JCI89867> <PubMed>
24. Wang S, Song R, Wang Z, Jing Z, Wang S, Ma J. S100A8/A9 in inflammation. Front Immunol 2018; 9(JUN): 1298. <https://doi.org/10.3389/fimmu.2018.01298> <PubMed>
25. Pietzsch J, Hoppmann S. Human S100A12: A novel key player in inflammation? Amino Acids 2009; 36(3): 381–9. <https://doi.org/10.1007/s00726-008-0097-7>
26. Foell D, Roth J. Proinflammatory S100 proteins in arthritis and autoimmune disease. Arthritis Rheum 2004; 50(12): 3762–71. <https://doi.org/10.1002/art.20631>
27. Wilsmann‐Theis D, Wagenpfeil J, Holzinger D, et al. Among the S100 proteins, S100A12 is the most significant marker for psoriasis disease activity. J Eur Acad Dermatology Venereol 2016; 30(7): 1165–70. <https://doi.org/10.1111/jdv.13269>
28. Moscaliuc ML, Heller MM, Lee ES, Koo J. Goeckerman therapy: A very effective, yet often forgotten treatment for severe generalized psoriasis. J Dermatolog Treat 2013; 24(1): 34–7. <https://doi.org/10.3109/09546634.2012.658014>
29. Zhu TH, Nakamura M, Farahnik B, et al. The Patient’s Guide to Psoriasis Treatment. Part 4: Goeckerman Therapy. Dermatol Ther (Heidelb) 2016; 6(3): 333–9. <https://doi.org/10.1007/s13555-016-0132-7> <PubMed>
30. Borska L, Andrys C, Krejsek J, et al. Genotoxic hazard and cellular stress in pediatric patients treated for psoriasis with the Goeckerman regimen. Pediatr Dermatol 2009; 26(1): 23–7. <https://doi.org/10.1111/j.1525-1470.2008.00774.x>
31. Sekhon S, Jeon C, Nakamura M, et al. Review of the mechanism of action of coal tar in psoriasis. J Dermatolog Treat 2018; 29(3): 230–2. <https://doi.org/10.1080/09546634.2017.1369494>
32. DesGroseilliers JP, Cullen AE, Rouleau GA. Ambulatory Goeckerman treatment of psoriasis: Experience with 200 patients. Can Med Assoc J 1981; 124(8): 1018–20. https://pubmed.ncbi.nlm.nih .gov/7260786/. Accessed January 8, 2021.
33. Kortuem KR, Davis MDP, Witman PM, McEvoy MT, Farmer SA. Results of Goeckerman treatment for psoriasis in children: A 21-year retrospective review. Pediatr Dermatol 2010; 27(5): 518–24. <https://doi.org/10.1111/j.1525-1470.2010.01124.x>
34. Petrozzi JW. Goeckerman regimen for psoriatic patients refractory to biologic therapy. J Am Acad Dermatol 2014; 71(1): 195. <https://doi.org/10.1016/j.jaad.2013.10.069>
35. Fitzmaurice S, Bhutani T, Koo J. Goeckerman regimen for management of psoriasis refractory to biologic therapy: The University of California San Francisco experience. J Am Acad Dermatol 2013; 69(4): 648–9. <https://doi.org/10.1016/j.jaad.2010.08.030>
36. Archid R, Duerr HP, Patzelt A, et al. Relationship between Histological and Clinical Course of Psoriasis: A Pilot Investigation by Reflectance Confocal Microscopy during Goeckerman Treatment. Skin Pharmacol Physiol 2016; 29(1): 47–54. <https://doi.org/10.1159/000443211>
37. Ekman AK, Bivik Eding C, Rundquist I, Enerbäck C. IL-17 and IL-22 Promote Keratinocyte Stemness in the Germinative Compartment in Psoriasis. J Invest Dermatol 2019; 139(7): 1564–73.e8. <https://doi.org/10.1016/j.jid.2019.01.014>
38. Soubry A, Murphy SK, Wang F, et al. Newborns of obese parents have altered DNA methylation patterns at imprinted genes. Int J Obes 2015; 39(4): 650–7. <https://doi.org/10.1038/ijo.2013.193> <PubMed>
39. Fotiadou C, Lazaridou E, Sotiriou E, et al. IL-17A, IL-22, and IL-23 as markers of psoriasis activity: A cross-sectional, hospital-based study. J Cutan Med Surg 2015; 19(6): 555–60. <https://doi.org/10.1177/1203475415584503>
40. Olejniczak-Staruch I, Narbutt J, Ceryn J, et al. AntiTNF-alpha therapy normalizes levels of lipids and adipokines in psoriatic patients in the real-life settings. Sci Rep 2021 Apr 29; 11(1): 9289. <https://doi.org/10.1038/s41598-021-88552-6> <PubMed>
41. Gkalpakiotis S, Cetkovska P, Arenberger P, Dolezal T, Arenbergerova M, Velackova B, Fialova J, Kojanova M; BIOREP study group. Risankizumab for the Treatment of Moderate-to-Severe Psoriasis: Real-Life Multicenter Experience from the Czech Republic. Dermatol Ther (Heidelb) 2021 Aug; 11(4): 1345–55. <https://doi.org/10.1007/s13555-021-00556-2> <PubMed>
42. Sobhan MR, Farshchian M, Hoseinzadeh A, Ghasemibasir HR, Solgi G. Serum levels of IL-10 and IL-22 cytokines in patients with psoriasis. Iran J Immunol 2016; 13(4): 317–23.
43. Elela MA, Hegazy RA, Fawzy MM, Rashed LA, Rasheed H. Interleukin 17, interleukin 22 and FoxP3 expression in tissue and serum of non-segmental vitiligo: A case- controlled study on eighty-four patients. Eur J Dermatology 2013; 23(3): 350–5.
44. Kim JC, Kim SM, Soh BW, Lee ES. Comparison of cytokine expression in paediatric and adult psoriatic skin. Acta Derm Venereol 2020; 100(4): 1–2.
45. Michalak-Stoma A, Bartosińska J, Kowal M, Raczkiewicz D, Krasowska D, Chodorowska G. IL-17A in the Psoriatic Patients’ Serum and Plaque Scales as Potential Marker of the Diseases Severity and Obesity. Mediators Inflamm 2020; 2020: 7420823. <https://doi.org/10.1155/2020/7420823> <PubMed>
46. Borska L, Fiala Z, Krejsek J, et al. Immunologic changes in TNF-alpha, sE-selectin, sP-selectin, sICAM-1, and IL-8 in pediatric patients treated for psoriasis with the Goeckerman regimen. Pediatr Dermatol 2007; 24(6): 607–12. <https://doi.org/10.1111/j.1525-1470.2007.00548.x>
47. Benham H, Norris P, Goodall J, et al. Th17 and Th22 cells in psoriatic arthritis and psoriasis. Arthritis Res Ther 2013; 15(5): R136. <https://doi.org/10.1186/ar4317> <PubMed>
48. Dyring-Andersen B, Honoré T V., Madelung A, et al. Interleukin (IL)-17A and IL-22-producing neutrophils in psoriatic skin. Br J Dermatol 2017; 177(6): e321–e322. <https://doi.org/10.1111/bjd.15533> <PubMed>
49. Ward NL, Umetsu DT. A new player on the psoriasis block: IL-17A- and IL-22-producing innate lymphoid cells. J Invest Dermatol 2014; 134(9): 2305–7. <https://doi.org/10.1038/jid.2014.216> <PubMed>
50. Tardif MR, Chapeton-Montes JA, Posvandzic A, Pagé N, Gilbert C, Tessier PA. Secretion of S100A8, S100A9, and S100A12 by Neutrophils Involves Reactive Oxygen Species and Potassium Efflux. J Immunol Res 2015; 2015: 1–16. <https://doi.org/10.1155/2015/296149> <PubMed>
51. Borsky P, Fiala Z, Andrys C, et al. Alarmins HMGB1, IL-33, S100A7, and S100A12 in Psoriasis Vulgaris. Mediators Inflamm 2020; 2020: 8465083. <https://doi.org/10.1155/2020/8465083> <PubMed>
52. D’Amico F, Trovato C, Skarmoutsou E, et al. Effects of adalimumab, etanercept and ustekinumab on the expression of psoriasin (S100A7) in psoriatic skin. J Dermatol Sci. 2015; 80(1): 38–44. <https://doi.org/10.1016/j.jdermsci.2015.07.009>
53. Defrêne J, Berrazouane S, Esparza N, et al. Deletion of S100a8 and S100a9 Enhances Skin Hyperplasia and Promotes the Th17 Response in Imiquimod-Induced Psoriasis. J Immunol 2020; 206(3): ji2000087.
54. Valiathan R, Ashman M, Asthana D. Effects of Ageing on the Immune System: Infants to Elderly. Scand J Immunol 2016; 83(4): 255–66. <https://doi.org/10.1111/sji.12413>
55. Walscheid K, Heiligenhaus A, Holzinger D, et al. Elevated S100A8/A9 and S100A12 serum levels reflect intraocular inflammation in juvenile idiopathic arthritis- associated uveitis: Results from a pilot study. Investig Ophthalmol Vis Sci 2015; 56(13): 7653–60. <https://doi.org/10.1167/iovs.15-17066>
56. Behnsen J, Jellbauer S, Wong CP, et al. The Cytokine IL-22 Promotes Pathogen Colonization by Suppressing Related Commensal Bacteria. Immunity 2014; 40(2): 262–73. <https://doi.org/10.1016/j.immuni.2014.01.003> <PubMed>
57. Zeng F, Chen H, Chen L, et al. An Autocrine Circuit of IL-33 in Keratinocytes is Involved in the Progression of Psoriasis. J Invest Dermatol. August 2020.
58. Mitsui A, Tada Y, Takahashi T, et al. Serum IL-33 levels are increased in patients with psoriasis. Clin Exp Dermatol 2016; 41(2): 183–9. <https://doi.org/10.1111/ced.12670>
59. Zhang W, Guo S, Li B, et al. Proinflammatory effect of high-mobility group protein B1 on keratinocytes: an autocrine mechanism underlying psoriasis development. J Pathol 2017; 241(3): 392–404. <https://doi.org/10.1002/path.4848>
60. Watanabe T, Yamaguchi Y, Watanabe Y, Takamura N, Aihara M. Increased level of high mobility group box 1 in the serum and skin in patients with generalized pustular psoriasis. J Dermatol 2020; 47(9): 1033–6. <https://doi.org/10.1111/1346-8138.15467>
61. Kamel M, Hassan E, Sobhy M, El Sayes MI. Role of high-mobility group box-1 as a marker of disease severity and diagnosis of metabolic syndrome in psoriatic patients. Egypt J Dermatology Venerol 2017; 37(2): 69.
62. Bergmann C, Strohbuecker L, Lotfi R, et al. High mobility group box 1 is increased in the sera of psoriatic patients with disease progression. J Eur Acad Dermatology Venereol 2016; 30(3): 435–41. <https://doi.org/10.1111/jdv.13564>
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