title: Increased percentages of tumor necrosis factor-alpha+/interferon-gamma+ T [corrected] lymphocytes and calprotectin+/tumor necrosis factor-alpha+ monocytes in patients with acute Kawasaki disease.
abstract: In vivo exposure to microorganisms resident in the oral cavity is considered as a possible cause of Kawasaki disease (KD), and some epitopes derived from streptococci display homology with Factor H of Complement. Additionally, calprotectin, a major calcium binding protein released by neutrophils and activated monocytes, could be directly involved in endothelial damage occurring in KD. The aim of our study is to evaluate the percentages of IFN-gamma+ and/or  TNF-alpha+ lymphocytes and double  positive calprotectin/TNF-alpha  monocytes (CD14+) after in vitro  stimulation with streptococcal- and/or Factor H-derived peptides, in patients with acute KD. Peripheral Blood Mononuclear Cells (PBMCs) obtained from KD patients and febrile controls were stimulated in vitro with peptides. After culture, cells were collected, stained with fluorochrome-labelled monoclonal antibodies against CD3, CD14, calprotectin, IFN-gamma and TNF-alpha, and cytofluorimetric analyses were performed. Our results showed increased percentages of TNF-alpha+/IFN-gamma+ lymphocytes in KD patients in  respect  to  controls  when  PBMCs  were  stimulated  with  streptococcal  or  Factor  H-derived  epitopes. In addition, also calprotectin+/TNF-alpha+ monocytes from KD patients were activated after PBMC  in vitro stimulation. These findings lead us to speculate that some peptides, derived from oral streptococci and cross-reactive with the human Factor H of Complement, could induce lymphocyte and monocyte activation potentially involved in the pathogenesis of KD. Our results should be confirmed by further studies enrolling more patients and controls than those analyzed in our study.
authors.affiliation: Department of Medical and Phorensic Biopathology and Biotechnology, University of Palermo,  Italy.
authors.forename: G
authors.initials: G
authors.lastname: Guggino
authors.forename: R
authors.initials: R
authors.lastname: Cimaz
authors.forename: S
authors.initials: S
authors.lastname: Accomando
authors.forename: I
authors.initials: I
authors.lastname: Pagnini
authors.forename: G
authors.initials: G
authors.lastname: Simonini
authors.forename: D
authors.initials: D
authors.lastname: Di Liberto
authors.forename: M
authors.initials: M
authors.lastname: De Martino
authors.forename: F
authors.initials: F
authors.lastname: Dieli
authors.forename: G
authors.initials: G
authors.lastname: Sireci
mesh_terms: D000208:Acute Disease; D002478:Cells, Cultured; D002648:Child; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000097:blood*; D039841:Leukocyte L1 Antigen Complex / Q000097:blood*; D018950:Lipopolysaccharide Receptors / Q000502:physiology; D008297:Male; D009000:Monocytes / Q000737:chemistry*; D009080:Mucocutaneous Lymph Node Syndrome / Q000276:immunology*; D013601:T-Lymphocytes / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D039841:Leukocyte L1 Antigen Complex; D018950:Lipopolysaccharide Receptors; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma