title: Borrelia burgdorferi NapA-driven Th17 cell inflammation in lyme arthritis.
abstract: OBJECTIVE
  Human Lyme arthritis caused by Borrelia burgdorferi is characterized by an inflammatory infiltrate that consists mainly of neutrophils and T cells. This study was undertaken to evaluate the role of the innate and acquired immune responses elicited by the neutrophil-activating protein A (NapA) of B burgdorferi in patients with Lyme arthritis.
  
  
  METHODS
  Serum anti-NapA antibodies were measured in 27 patients with Lyme arthritis and 30 healthy control subjects. The cytokine profile of synovial fluid T cells specific for NapA was investigated in 5 patients with Lyme arthritis. The cytokine profile induced by NapA in neutrophils and monocytes was also investigated.
  
  
  RESULTS
  Serum anti-NapA antibodies were found in 48% of the patients with Lyme arthritis but were undetectable in the healthy controls. T cells from the synovial fluid of patients with Lyme arthritis produced interleukin-17 (IL-17) in response to NapA. Moreover, NapA was able to induce the expression of IL-23 in neutrophils and monocytes, as well as the expression of IL-6, IL-1beta, and transforming growth factor beta (TGFbeta) in monocytes, via Toll-like receptor 2.
  
  
  CONCLUSIONS
  These findings indicate that NapA of B burgdorferi is able to drive the expression of IL-6, IL-1beta, IL-23, and TGFbeta by cells of the innate immune system and to elicit a synovial fluid Th17 cell response that might play a crucial role in the pathogenesis of Lyme arthritis.
authors.affiliation: Venetian Institute of Molecular Medicine, and University of Padua, Padua, Italy.
authors.forename: Gaia
authors.initials: G
authors.lastname: Codolo
authors.forename: Amedeo
authors.initials: A
authors.lastname: Amedei
authors.forename: Allen C
authors.initials: AC
authors.lastname: Steere
authors.forename: Elena
authors.initials: E
authors.lastname: Papinutto
authors.forename: Andrea
authors.initials: A
authors.lastname: Cappon
authors.forename: Alessandra
authors.initials: A
authors.lastname: Polenghi
authors.forename: Marisa
authors.initials: M
authors.lastname: Benagiano
authors.forename: Silvia Rossi
authors.initials: SR
authors.lastname: Paccani
authors.forename: Vittorio
authors.initials: V
authors.lastname: Sambri
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Del Prete
authors.forename: Cosima Tatiana
authors.initials: CT
authors.lastname: Baldari
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Zanotti
authors.forename: Cesare
authors.initials: C
authors.lastname: Montecucco
authors.forename: Mario Milco
authors.initials: MM
authors.lastname: D'Elios
authors.forename: Marina
authors.initials: M
authors.lastname: de Bernard
mesh_terms: D000293:Adolescent; D000328:Adult; D000907:Antibodies, Bacterial / Q000032:analysis; D001426:Bacterial Proteins / Q000276:immunology*; D025065:Borrelia burgdorferi / Q000276:immunology*; D019743:Chemokines, CXC / Q000276:immunology*; D002648:Child; D005260:Female; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D053759:Interleukin-23 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008193:Lyme Disease / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D013582:Synovial Fluid / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000096:biosynthesis
chemical_list: D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; D019743:Chemokines, CXC; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; C534091:NapA protein, Borrelia burgdorferi; D016212:Transforming Growth Factor beta