Serum concentration of IL-6, IL-2, TNF-α, and IFNγ in Vitiligo patients

Background:

Vitiligo is an acquired depigmenting disorder characterized by the loss of functional melanocytes from the epidermis. Although the etiology of vitiligo is unknown, over the last few years, substantial data from clinical research has greatly supported the ‘Autoimmune theory’ and this is supported by the frequent association of vitiligo with disorders that have an autoimmune origin, including Hashimoto''s thyroiditis, Graves disease, type 1 insulin-dependent diabetes mellitus, and Addison''s disease. As cytokines are important mediators of immunity, there is evidence to suggest that they play a major role in the pathogenesis of autoimmune diseases.

Aim:

Keeping this in view we have assayed sera for cytokine IL-6, IL-2, Tumor necrosis factor (TNF)-α, and IFNγ in 80 cases of vitiligo and compared it with healthy subjects, in order to find out whether they play a role in the pathogenesis of vitiligo or not.

Materials and Methods:

Serum IL-6, IL-2, TNF-α, and IFNγ were done by the indirect enzyme linked immunosorbent assay (ELISA).

Results:

The mean serum IL-6 and IL-2 levels in the patient group were significantly higher when compared with those of the normal controls. The mean serum IFNγ level in patients with vitiligo was significantly lower than that in the control group. There was no significant difference in the serum level of TNF-α between vitiligo and healthy controls.

Conclusion:

An increase in the production of proinflammatory cytokines such as IL-6 and IL-2 in vitiligo patients may play an important role in melanocytic cytotoxicity. Thus, we speculate that the cytokine production of epidermal microenvironment may be involved in vitiligo.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Elevated levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TNF-α and IL-1β

Background The pathogenesis of hidradenitis suppurativa (HS) is largely unknown and the disease is difficult to treat. Patients are in high need of an effective treatment. Although it is not known whether the levels of tumour necrosis factor (TNF)‐α are aberrant in HS skin, anti‐TNF‐α biologics are used, with variable clinical efficacy. Objectives To determine the cytokine profile in lesional and perilesional HS skin. Methods We cultured 20 lesional and 10 normal‐appearing perilesional HS skin samples, seven psoriasis and six healthy control skin samples in a transwell culture system. Two distinct cytokine bead arrays were used to measure the spectrum of inflammatory cytokines in the culture supernatant. Results from HS skin samples were compared with those of healthy and psoriasis skin. Results The proinflammatory cytokines interleukin (IL)‐1β and TNF‐α as well as the anti‐inflammatory cytokine IL‐10 were significantly elevated in HS skin. Elevated levels of these cytokines were also found in perilesional HS skin. Fold increases relative to control skin of IL‐1β, TNF‐α and IL‐10 in HS were 31, 5 and 34, compared with psoriasis: 4, 1 and 2, respectively. Levels of all three cytokines showed a trend towards a positive correlation with disease severity. IL‐2, IL‐4, IL‐5 and interferon‐γ were hardly detectable in HS or healthy control skin. Conclusions This study shows for the first time that IL‐1β, TNF‐α and IL‐10 levels are elevated in HS skin. These data provide a rationale for therapies with biologics targeting cytokines such as TNF‐α and IL‐1.     

Comparative effects of polyphenols from green tea (EGCG) and soybean (genistein) on VEGF and IL-8 release from normal human keratinocytes stimulated with the proinflammatory cytokine TNFα

In skin inflammation, vascular endothelial growth factor (VEGF) and IL-8 play an important role and are produced by activated keratinocytes. Recently, some polyphenols have been reported to exhibit antiinflammatory and antiangiogenic properties. We therefore evaluated the effects of green tea, its major component epigallocatechin-3-gallate (EGCG) and an isoflavone derived from soybean (genistein) on the release of VEGF and IL-8 by activated normal human keratinocytes (NHK). NHK cultured in defined medium were stimulated for 48 h with the proinflammatory cytokine TNF with the addition or not of different concentrations of polyphenols. Levels of VEGF and IL-8 were measured in cell supernatants by enzyme-linked immunosorbent assays. The different constituents tested inhibited keratinocyte proliferation without inducing apoptosis. They reduced in a dose-dependent manner the basal release and the upregulation of VEGF in NHK. Green tea and EGCG were also potent inhibitors of IL-8 release by TNF-stimulated NHK, whereas genistein exerted only minor effects. These results underline the divergent pathways involved in the downregulation of VEGF and IL-8 by polyphenols in activated keratinocytes. They also suggest that polyphenols may contribute to moderate inflammatory processes in skin diseases associated with angiogenesis.