title: The effect of viable Chlamydia pneumoniae on serum cytokines and adhesion molecules in hemodialysis patients.
abstract: BACKGROUND
  Chlamydia pneumoniae (Cp) induces the production of cytokines and adhesion molecules in infected host eukaryotic cells. The causes for pro-inflammatory cytokine and adhesion molecule increase in hemodialysis (HD) patients have not been fully elucidated. The possibility that, in this particularly atherosclerotic population, Cp, a microorganism implicated in the infectious-based inflammatory hypothesis of atherosclerosis' is also responsible for these molecules' increase is assessed in this study.
  
  
  METHODS
  In 130 stable HD patients, serum interleukin-1 beta (IL-1), interleukin-6, tumor necrosis factor alpha, interleukin-10, L-selectin, E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 (VCAM-1) levels were determined. Cp presence was identified by inoculation of the patient's peripheral blood mononuclear cells (PBMCs) in Hep-2 cell lines and subsequent polymerase chain reaction (PCR) in DNA extracted from cell cultures, as well as by determination of serum IgG antibodies against Cp (IgGCp).
  
  
  RESULTS
  Patients, positive or negative for IgGCp, had no statistically significant differences in all molecules measured. Patients with viable Cp in PBMCs had higher serum levels of IL-1 and soluble VCAM-1 than negative ones for IgGCp (IL-1 6.87 +/- 7.35 vs. 2.34 +/- 1.47 pg/mL; P = 0.0009 and VCAM-1 1647.16 +/- 513.64 vs. 1162.14 +/- 546.83 ng/mL; P = 0.0115, respectively). Viable Cp in PBMCs remained a significant predictor factor for IL-1 and VCAM-1 in statistical analysis, when patients' characteristics and dialysis conditions were also evaluated.
  
  
  CONCLUSIONS
  Our results showed that some serum cytokine and adhesion molecule increase in HD patients could be attributed to viable Cp presence in PBMCs. These findings support the Cp-based inflammatory atherogenous hypothesis and add a better understanding of these molecules' increase in HD patients.
authors.affiliation: Renal Unit, Alexandra General Hospital, Athens, Greece. tsipg@hellsnet.gr
authors.forename: George
authors.initials: G
authors.lastname: Tsirpanlis
authors.forename: Stylianos
authors.initials: S
authors.lastname: Chatzipanagiotou
authors.forename: Anastasios
authors.initials: A
authors.lastname: Ioannidis
authors.forename: Kostantina
authors.initials: K
authors.lastname: Ifanti
authors.forename: Pantelis
authors.initials: P
authors.lastname: Bagos
authors.forename: Antonis
authors.initials: A
authors.lastname: Lagouranis
authors.forename: Cornelia
authors.initials: C
authors.lastname: Poulopoulou
authors.forename: Chrysoula
authors.initials: C
authors.lastname: Nicolaou
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000276:immunology / Q000382:microbiology; D002690:Chlamydia Infections / Q000276:immunology*; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000097:blood* / Q000276:immunology; D016753:Interleukin-10 / Q000097:blood / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000276:immunology*; D019041:L-Selectin / Q000097:blood; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D019040:E-Selectin; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D019041:L-Selectin; D016753:Interleukin-10