Unfulfilled Inflammatory Resolution: A Key Factor in the Pathogenesis of Psoriasis
Abstract
Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psoriasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic strategies.
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2. Šahmatova L, Sügis E, Šunina M, Hermann H, Prans E, Pihlap M, et al. Signs of innate immune activation and premature immunosenescence in psoriasis patients. Sci Rep.2017;7(1):7553.
3. Jadali Z, Eslami MB. T cell immune responses in psoriasis. Iran J Allergy Asthma Immunol. 2014;13(4):220-30.
4. Doria A, Zen M, Bettio S, Gatto M, Bassi N, Nalotto L, et al. Autoinflammation and autoimmunity: Bridging the divide. Autoimmun Rev. 2012;12(1):22-30.
5. Deng Y, Chang C, Lu Q. The inflammatory response in psoriasis: a comprehensive review. Clin Rev Allergy Immunol.2016;50(3):377-89.
6. Krejsek J. Defensive and damaging inflammation: basic characteristics. Vnitr Lek 2019 Winter;65(2):76-80.
7. Sugimoto MA, Vago JP, Perretti M, Teixeira MM. Mediators of the resolution of the Inflammatory Response. Trends Immunol. 2019;40(3):212-27.
8. Germolec DR, Shipkowski KA, Frawley RP, Evans E.Markers of inflammation. Methods Mol Biol. 2018;1803:57-79.
9. Sugimoto MA, Sousa LP, Pinho V, Perretti M, Teixeira MM.Resolution of inflammation: what controls its onset? Front Immunol. 2016;7:160.
10. Schett G, Neurath MF. Resolution of chronic inflammatory disease: universal and tissue-specific concepts. Nat Commun.2018;9(1):3261.
11. Nathan C, Ding A. Nonresolving inflammation. Cell. 2010;140(6):871-82.
12. Saqib U, Sarkar S, Suk K, Mohammad O, Baig MS, Savai R. Phytochemicals as modulators of M1-M2 macrophages in inflammation. Oncotarget. 2018;9(25):17937-50.
13. Wang N, Liang H, Zen K. Molecular mechanisms that influence the macrophage M1-M2 polarization balance. Front Immunol. 2014;5:614.
14. Hume DA. The many alternative faces of macrophage activation. Front Immunol. 2015;6:370.
15. Glanz V, Myasoedova VA, Sukhorukov V, Grechko A, Zhang D, Romaneneko EB, et al. Transcriptional characteristics of activated macrophages. Curr Pharm Des. 2019;25(3):213-17.
16. Siouti E, Andreakos E. The many facets of macrophages in rheumatoid arthritis. Biochem Pharmacol. 2019 l;165:152-69.
17. Lu CH, Lai CY, Yeh DW, Liu YL, Su YW, Hsu LC, et al. Involvement of M1 macrophage polarization in endosomal toll-like receptors activated psoriatic inflammation. Mediators Inflamm. 2018;2018:3523642.
18. Zhang J, Lin Y, Li C, Zhang X, Cheng L, Dai L, et al. IL-35 decelerates the inflammatory process by regulating inflammatory cytokine secretion and M1/M2 macrophage ratio in psoriasis. J Immunol. 2016;197(6):2131-44.
19. Lin SH, Chuang HY, Ho JC, Lee CH, Hsiao CC. Treatment with TNF-α inhibitor rectifies M1 macrophage polarization from blood CD14+ monocytes in patients with psoriasis independent of STAT1 and IRF-1 activation. Dermatol Sci. 2018;91(3):276-84.
20. Tang MM, Spanou Z, Tang H, Schibler F, Pelivani N, Yawalkar N.Rapid downregulation of innate immune cells, interleukin-12 and interleukin-23 in generalized pustular psoriasis with infliximab in combination with acitretin. Dermatology. 2012;225(4):338-43.
21. Hou Y, Zhu L, Tian H, Sun HX, Wang R, Zhang L, et al. IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis. Protein Cell. 2018;9(12):1027-38.
22. Senra L, Stalder R, Alvarez Martinez D, Chizzolini C, Boehncke WH, Brembilla NC. Keratinocyte-derived IL-17E contributes to inflammation in psoriasis. J Invest Dermatol. 2016;136(10):1970-80.
23. Katayama H. Development of psoriasis by continuous neutrophil infiltration into the epidermis. Exp Dermatol. 2018;27(10):1084-91.
24. Fräki JE, Jakoi L, Davies AO, Lefkowitz RJ, Snyderman R, Lazarus GS. Polymorphonuclear leukocyte function in psoriasis: chemotaxis, chemokinesis, beta-adrenergic receptors, and proteolytic enzymes of polymorphonuclear leukocytes in the peripheral blood from psoriatic patients. J Invest Dermatol. 1983;81(3):254-7.
25. Shao S, Fang H, Dang E, Xue K, Zhang J, Li B, et al. Neutrophil extracellular traps promote inflammatory responses in psoriasis via activating epidermal TLR4/IL-36R crosstalk. Front Immunol. 2019;10:746.
26. Schön M, Denzer D, Kubitza RC, Ruzicka T, Schön MP. Critical role of neutrophils for the generation of psoriasiform skin lesions in flaky skin mice. J Invest Dermatol. 2000;114(5):976-83.
27. Ikeda S, Takahashi H, Suga Y, Eto H, Etoh T, Okuma K, et al.Therapeutic depletion of myeloid lineage leukocytes in patients with generalized pustular psoriasis indicates a major role for neutrophils in the immunopathogenesis of psoriasis. J Am Acad Dermatol. 2013;68(4):609-17.
28. Steffen S, Abraham S, Herbig M, Schmidt F, Blau K, Meisterfeld S, et al. Toll-like receptor-mediated upregulation of CXCL16 in psoriasis orchestrates neutrophil activation. J Invest Dermatol. 2018;138(2):344-54.
29. Morriello F.Neutrophils and inflammation: unraveling a new connection. Biol Med. (Aligarh) 2016, 8(6):1-3.
30. Fox S, Leitch AE, Duffin R, Haslett C, Rossi AG. Neutrophil apoptosis: relevance to the innate immune response and inflammatory disease. J Innate Immun. 2010;2(3):216-27.
31. El Kebir D, Filep JG. Modulation of neutrophil apoptosis and the resolution of inflammation through β2 integrins. Front Immunol. 2013;4(60):1-15.
32. Brach MA, deVos S, Gruss HJ, Herrmann F. Prolongation of survival of human polymorphonuclear neutrophils by granulocyte-macrophage colony-stimulating factor is caused by inhibition of programmed cell death. Blood.1992;80(11):2920-4.
33. Cox G, Gauldie J, Jordana M. Bronchial epithelial cell-derived cytokines (G‐CSF and GM-CSF) promote the survival of peripheral blood neutrophils in vitro. Am J Respir Cell Mol Biol. 1992;7(5):507-13.
34. Bonifati C,Carducci M,Cordiali Fei P,Trento E,Sacerdoti G,Fazio M,et al. Correlated increases of tumour necrosis factor-alpha, interleukin-6 and granulocyte monocyte-colony stimulating factor levels in suction blister fluids and sera of psoriatic patients--relationships with disease severity. Clin Exp Dermatol. 1994;19(5):383-7.
35. Takematsu H, Tagami H. Granulocyte-macrophage colony-stimulating factor in psoriasis. Dermatologica. 1990;181(1):16-20.
36. Alvarez-Ruiz S, Peñas PF, Fernández-Herrera J, Sánchez-Pérez J, Fraga J, García-Díez A. Maculopapular eruption with enlarged macrophages in eight patients receiving G-CSF or GM-CSF. J Eur Acad Dermatol Venereol. 2004;18(3):310-3.
37. Jacob SE, Nassiri M, Kerdel FA, Vincek V. Simultaneous measurement of multiple Th1 and Th2 serum cytokines in psoriasis and correlation with disease severity. Mediators Inflamm. 2003;12(5):309-13.
38. Lorthois I, Asselineau D, Seyler N, Pouliot R. Contribution of in vivo and organotypic 3D models to understanding the role of macrophages and neutrophils in the pathogenesis of psoriasis. Mediators Inflamm. 2017;2017:7215072.
39. Liu ZG, Hsu H, Goeddel DV, Karin M.Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-kappaB activation prevents cell death.Cell. 1996;87(3):565-76.
40. Colotta F, Re F, Polentarutti N, Sozzani S, Mantovani A. Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products. Blood. 1992;80(8):2012-20.
41. Chiricozzi A, Romanelli P, Volpe E, Borsellino G, Romanelli M. Scanning the immunopathogenesis of psoriasis. Int J Mol Sci. 2018;19(1).
42. Opal SM, DePalo VA. Anti-inflammatory cytokines. Chest 2000;117(4):1162-72.
43.Kelly A, Houston SA, Sherwood E, Casulli J, Travis MA. Regulation of innate and adaptive immunity by TGFβ. Adv Immunol. 2017;134:137-233.
44. Shull MM, Ormsby I, Kier AB, Pawlowski S, Diebold RJ, Yin M, et al. Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease. Nature. 1992;359(6397):693-9.
45. Hahm KB, Im YH, Lee C, Parks WT, Bang YJ, Green JE, et al. Loss of TGF-β signaling contributes to autoimmune pancreatitis. J Clin Invest.2000;105:1057–65.
46. Sanjabi S, Oh SA, Li MO. Regulation of the immune response by TGF-β: from conception to autoimmunity and infection. Cold Spring Harb Perspect Biol. 2017;9(6):a022236.
47. Yoshimura A, Wakabayashi Y, Mori T. Cellular and molecular basis for the regulation of inflammation by TGF-beta.J Biochem. 2010;147(6):781-92.
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| Files | ||
| Issue | Vol 19 No 4 (2020) | |
| Section | Review Article(s) | |
| DOI | https://doi.org/10.18502/ijaai.v19i4.4130 | |
| PMID | 33463101 | |
| Keywords | ||
| Autoimmunity Inflammation Psoriasis Skin | ||
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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
How to Cite
1.
Jadali Z. Unfulfilled Inflammatory Resolution: A Key Factor in the Pathogenesis of Psoriasis. Iran J Allergy Asthma Immunol. 2020;19(4):337-347.
