title: MCP-1 in psoriatic patients: effect of biological therapy.
abstract: 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.
  
  
  CONCLUSIONS
  MCP-1 should be a potential local inflammatory marker in psoriatic patients to assess disease severity and anti-TNF-α treatment efficacy.
authors.affiliation: Department of Systematic Pathology, Section of Clinical, Allergological and Venereological Dermatology, University of Naples "Federico II" , Italy.
authors.forename: Serena
authors.initials: S
authors.lastname: Lembo
authors.forename: Rosanna
authors.initials: R
authors.lastname: Capasso
authors.forename: Anna
authors.initials: A
authors.lastname: Balato
authors.forename: Teresa
authors.initials: T
authors.lastname: Cirillo
authors.forename: Filomena
authors.initials: F
authors.lastname: Flora
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Zappia
authors.forename: Nicola
authors.initials: N
authors.lastname: Balato
authors.forename: Diego
authors.initials: D
authors.lastname: Ingrosso
authors.forename: Fabio
authors.initials: F
authors.lastname: Ayala
mesh_terms: D000068879:Adalimumab; D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D002648:Child; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007155:Immunologic Factors / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011565:Psoriasis / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012074:Remission Induction; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D055815:Young Adult
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D015415:Biomarkers; D018932:Chemokine CCL2; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000068879:Adalimumab; D000068800:Etanercept; C472181:efalizumab