Serum soluble endoglin, IL-13, and IL-23 in psoriatic patients in Basra, Iraq

A. N. Abbas; A. A. Al-Shakour; S. A. Dhaher

doi:10.15421/0225061

A. N. Abbas University of Basrah
A. A. Al-Shakour University of Basrah
S. A. Dhaher University of Basrah

Keywords: serum soluble endoglin, interleukin-13, interleukin-23, inflammatory biomarkers.

Abstract

Psoriasis (PsO) is a persistent inflammatory skin condition. PsO exhibits similar immunologic and genetic characteristics to other autoimmune inflammatory disorders, including rheumatoid arthritis and multiple sclerosis. Endoglin (ENG), a 180 kDa pr o tein is located on the cells ’ surface and acts as a co-receptor for the Transforming Growth Factor (TGF)-β superfamily. Interleukin-13 (IL-13) is known for its importance as a modulator of Th2 immune responses. It was discovered that Th17 cells express the IL-13 receptor, and it has been observed that IL-13 inhibits the production of IL-17 in these cells. IL-23 promotes survival and prolif e ration of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. The aim of the study was to evaluate serum level of ENG, IL-13, and IL-23 in PsO patients compared to the control group. We conducted a case control study in which 80 patients with Ps O and 80 age and sex-matched apparently healthy controls were recruited. The s erum level of the aforeme n tioned markers was measured by ELISA. All the measured markers showed significant difference in patients with PsO when co m pared to control group. A positive significant correlation was observed between IL-13 and IL-23. sENG showed significant diffe r ence with treatment type, IL-13 and IL-23 showed significant difference with PASI score and treatment type. IL-23 also showed significant difference with PsO duration. The study suggested that ENG may have a potential role in the pathophysiology of PsO. IL-13 and IL-23 have significant relation with PsO; however, they did not have a correlation with ENG.

References

Al Samarai, A. G. M. (2009). Prevalence of skin diseases in Iraq: A community-based study. International Journal of Dermatology, 48(7), 734–739.

Altomonte, M., Montagner, R., Fonsatti, E., Colizzi, F., Cattarossi, I., Brasoveanu, L. I., Nicotra, M. R., Cattelan, A., Natali, P. G., & Maio, M. (1996). Expression and structural features of endoglin (CD105), a transforming growth factor β1 and β3 binding protein, in human melanoma. British Journal of Cancer, 74(10), 1586–1591.

Armstrong, A. W., Mehta, M. D., Schupp, C. W., Gondo, G. C., Bell, S. J., & Griffiths, C. E. M. (2021). Psoriasis prevalence in adults in the United States. JAMA Dermatology, 157(8), 940–946.

Bettelli, E., Carrier, Y., Gao, W., Korn, T., Strom, T. B., Oukka, M., Weiner, H. L., & Kuchroo, V. K. (2006). Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature, 441(7090), 235–238.

Blauvelt, A. (2007). New concepts in the pathogenesis and treatment of psoriasis: Key roles for IL-23, IL-17A and TGF-β1. Expert Review of Dermatology, 2(1), 69–78.

Coimbra, S., Oliveira, H., Reis, F., Belo, L., Rocha, S., Quintanilha, A., Figueiredo, A., Teixeira, F., Castro, E., Rocha-Pereira, P., & Santos-Silva, A. (2010). Interleukin (IL)-22, IL-17, IL-23, IL-8, vascular endothelial growth factor and tumour necrosis factor-α levels in patients with psoriasis before, during and after psoralen-ultraviolet A and narrowband ultraviolet B therapy. British Journal of Dermatology, 163(6), 1282–1290.

Ferber, I. A., Brocke, S., Taylor-Edwards, C., Ridgway, W., Dinisco, C., Steinman, L., Dalton, D., & Fathman, C. G. (1996). Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). Journal of Immunology, 156(1), 5–7.

Flisiak, I., Chodynicka, B., Porebski, P., & Flisiak, R. (2002). Association between psoriasis severity and transforming growth factor β1 and β2 in plasma and scales from psoriatic lesions. Cytokine, 19(3), 121–125.

Fotiadou, C., Lazaridou, E., Sotiriou, E., Gerou, S., Kyrgidis, A., Vakirlis, E., & Ioannides, D. (2015). IL-17A, IL-22, and IL-23 as markers of psoriasis activity. Journal of Cutaneous Medicine and Surgery, 19(6), 555–560.

González Muñoz, T., Amaral, A. T., Puerto-Camacho, P., Peinado, H., & de Álava, E. (2021). Endoglin in the spotlight to treat cancer. International Journal of Molecular Sciences, 22(6), 3186.

Hamad, A. A., Mustafa, H. M., & Mohsein, O. A. (2024). Detection of the levels of immune cytokines (IL4, IL5, TNF-α) in school-age and preschoolers with an Ascaris lumbricoides infection. Journal of Parasitic Diseases, 48(4), 782–787. ‏

Hijnen, D., Knol, E. F., Gent, Y. Y., Giovannone, B., Beijn, S. J. P., Kupper, T. S., Bruijnzeel-Koomen, C. A. F. M., & Clark, R. A. (2013). CD8+ T cells in the lesional skin of atopic dermatitis and psoriasis patients are an important source of IFN-γ, IL-13, IL-17, and IL-22. Journal of Investigative Dermatology, 133(4), 973–979.

Hsieh, C.-L., Yu, S.-J., Lai, K.-L., Chao, W.-T., & Yen, C.-Y. (2024). IFN-γ, IL-17A, IL-4, and IL-13: Potential biomarkers for prediction of the effectiveness of biologics in psoriasis patients. Biomedicines, 12(5), 1115.

Ibrahim, M. A., Akl, E. M., Abdul-Hafeez, N. A., & El-Shebl, S. Z. (2020). Evalution of serum level of endoglin in psoriatic pateints. Benha Journal of Applied Sciences, 5(1), 1–6.

Lateef, D., Nasser, N., & Mohsein, O. (2024). The relationships between aplein, vaspin and thyroid hormone levels in obese diabetic and non-diabetic women. Journal of Experimental and Clinical Medicine, 41(2), 239–245. ‏

Li, A. G., Wang, D., Feng, X., & Wang, X. (2004). Latent TGFβ1 overexpression in keratinocytes results in a severe psoriasis-like skin disorder. The EMBO Journal, 23(8), 1770–1781.

Mangan, P. R., Harrington, L. E., O’Quinn, D. B., Helms, W. S., Bullard, D. C., Elson, C. O., Hatton, R. D., Wahl, S. M., Schoeb, T. R., & Weaver, C. T. (2006). Transforming growth factor-β induces development of the TH17 lineage. Nature, 441(7090), 231–234.

Maul, J.-T., Navarini, A. A., Sommer, R., Anzengruber, F., Sorbe, C., Mrowietz, U., Drach, M., Blome, C., Boehncke, W.-H., Thaci, D., Reich, K., von Kiedrowski, R., Körber, A., Yawalkar, N., Mainetti, C., Laffitte, E., Streit, M., Rustenbach, S., Conrad, C., … Augustin, M. (2019). Gender and age significantly determine patient needs and treatment goals in psoriasis – a lesson for practice. Journal of the European Academy of Dermatology and Venereology, 33(4), 700–708.

Michalek, I. M., Loring, B., & John, S. M. (2017). A systematic review of worldwide epidemiology of psoriasis. Journal of the European Academy of Dermatology and Venereology, 31(2), 205–212.

Nickoloff, B. J., & Naidu, Y. (1994). Perturbation of epidermal barrier function correlates with initiation of cytokine cascade in human skin. Journal of the American Academy of Dermatology, 30(4), 535–546.

Raychaudhuri, S. K., Maverakis, E., & Raychaudhuri, S. P. (2014). Diagnosis and classification of psoriasis. Autoimmunity Reviews, 13(4–5), 490–495.

Rulo, H. F. C., Westphal, J. R., van de Kerkhof, P. C. M., de Waal, R. M. W., van Vlijmen, I. M. J. J., & Ruiter, D. J. (1995). Expression of endoglin in psoriatic involved and uninvolved skin. Journal of Dermatological Science, 10(2), 103–109.

Schoonderwoerd, M. J. A., Goumans, M.-J. T. H., & Hawinkels, L. J. A. C. (2020). Endoglin: Beyond the endothelium. Biomolecules, 10(2), 289.

Stockinger, B., & Veldhoen, M. (2007). Differentiation and function of Th17 T cells. Current Opinion in Immunology, 19(3), 281–286.

Vermeire, K., Heremans, H., Vandeputte, M., Huang, S., Billiau, A., & Matthys, P. (1997). Accelerated collagen-induced arthritis in IFN-gamma receptor-deficient mice. Journal of Immunology, 158(11), 5507–5513.

Wilson, F. C., Icen, M., Crowson, C. S., McEvoy, M. T., Gabriel, S. E., & Kremers, H. M. (2009). Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: A population-based study. Arthritis Care and Research, 61(2), 233–239.

Wu, M., Dai, C., & Zeng, F. (2023). Cellular mechanisms of psoriasis pathogenesis: A systemic review. Clinical, Cosmetic and Investigational Dermatology, 16, 2503–2515.