BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a chemokine locally and systemically augmented in psoriasis. A single nucleotide polymorphism in MCP-1 promoter region -2518A→G is associated with higher gene expression. OBJECTIVE: The aim was to evaluate MCP-1 plasma level in psoriatic patients and to relate any association in plasmatic and cutaneous MCP-1 with clinical improvement due to biological drugs. METHODS: Blood samples were obtained from: (i) 30 Caucasian patients with psoriasis and 10 controls, for determining MCP-1 plasma concentrations and -2518A→G polymorphism occurrence, (ii) 16 psoriatic patients treated by anti-tumor necrosis factor-α (TNF-α) adalimumab/etanercept or by anti-CD-11 efalizumab, before and after 2 months of treatment. Moreover, biopsies were performed on lesional skin of five patients treated with anti-TNF-α. MCP-1 plasma concentration and cutaneous expression were determined by ELISA and qRT-PCR. RESULTS: MCP-1 plasma level was significantly increased in psoriatic patients. -2518A→G polymorphism was similarly distributed in patients and controls and unrelated to MCP-1 plasma level or to Psoriasis Area and Severity Index. All patients receiving biological drugs showed significant clinical improvement. Anti-TNF-α therapy moderately reduced MCP-1 plasma concentration and robustly decremented MCP-1 expression in lesional skin. CONCLUSION: MCP-1 should be a potential local inflammatory marker in psoriatic patients to assess disease severity and anti-TNF-α treatment efficacy.
BACKGROUND:Monocyte chemoattractant protein-1 (MCP-1) is a chemokine locally and systemically augmented in psoriasis. A single nucleotide polymorphism in MCP-1 promoter region -2518A→G is associated with higher gene expression. OBJECTIVE: The aim was to evaluate MCP-1 plasma level in psoriaticpatients and to relate any association in plasmatic and cutaneous MCP-1 with clinical improvement due to biological drugs. METHODS: Blood samples were obtained from: (i) 30 Caucasian patients with psoriasis and 10 controls, for determining MCP-1 plasma concentrations and -2518A→G polymorphism occurrence, (ii) 16 psoriaticpatients treated by anti-tumornecrosis factor-α (TNF-α) adalimumab/etanercept or by anti-CD-11 efalizumab, before and after 2 months of treatment. Moreover, biopsies were performed on lesional skin of five patients treated with anti-TNF-α. MCP-1 plasma concentration and cutaneous expression were determined by ELISA and qRT-PCR. RESULTS:MCP-1 plasma level was significantly increased in psoriaticpatients. -2518A→G polymorphism was similarly distributed in patients and controls and unrelated to MCP-1 plasma level or to Psoriasis Area and Severity Index. All patients receiving biological drugs showed significant clinical improvement. Anti-TNF-α therapy moderately reduced MCP-1 plasma concentration and robustly decremented MCP-1 expression in lesional skin. CONCLUSION:MCP-1 should be a potential local inflammatory marker in psoriaticpatients to assess disease severity and anti-TNF-α treatment efficacy.
Authors: Lenka Hasikova; Marketa Pavlikova; Hana Hulejova; Petr Kozlik; Kveta Kalikova; Aparna Mahajan; Martin Herrmann; Blanka Stiburkova; Jakub Zavada Journal: Rheumatol Int Date: 2019-07-31 Impact factor: 2.631
Authors: Farah Asa'ad; Marco Fiore; Aniello Alfieri; Paolo Daniele Maria Pigatto; Chiara Franchi; Emilio Berti; Carlo Maiorana; Giovanni Damiani Journal: Biomed Res Int Date: 2018-05-20 Impact factor: 3.411