title: Impaired antiviral activity of monocytes from patients on hemodiafiltration.
abstract: BACKGROUND
  The aim of our study was to determine whether intermittent hemodiafiltration (HDF) leads to an alteration in monocyte antiviral activity as well as in the in vitro release of cytokines such as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-alpha) and interferon-alpha (IFN-alpha) by the same cells.
  
  
  METHODS
  We enrolled 25 patients undergoing HDF for 3.5-4 hours 3 times a week (12 men, 13 women; mean age 58 +/- 6.7 years) and 25 healthy donors (ND) (12 men, 13 women; mean age 57 +/- 8 years). Monocytes from peripheral blood mononuclear cells were isolated with a Monocyte Isolation Kit II. Monocytic cells were infected with herpes simplex virus type 2 (HSV-2). Cytokines were assayed in supernatants.
  
  
  RESULTS
  The in vitro antiviral activity of monocytes from HDF patients was significantly impaired with respect to ND. Furthermore, monocytes from post-HDF patients were more prone to viral infection. Lipopolysaccharide (LPS) stimulation induced significant viral inhibition only in monocytes from NDs (p<0.05). The cytokine pattern (TNF-alpha, IFN-alpha and IL-12) in monocytes stimulated with LPS was markedly inhibited in HDF patients compared with ND (p<0.05). A basal production of TNF-alpha was found in monocytes from pre-HDF and post-HDF patients. No IFN-alpha production was found in LPS-stimulated and HSV-2-infected monocytes from pre-HDF and post-HDF patients. IL-12 production appeared significantly decreased after HDF in all experimental conditions (p<0.05).
  
  
  CONCLUSIONS
  The significant increase of viral replication in monocytes from HDF patients compared with healthy donors could be related to a significant reduction of cytokine production. Moreover, the dialytic session influenced the intrinsic antiviral activity of monocytes, favoring viral replication.
authors.affiliation: Unit of Microbiology, Department of Surgical Sciences, University of Messina, Messina - Italy.
authors.forename: Adriana
authors.initials: A
authors.lastname: Arena
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Coppolino
authors.forename: Lorena
authors.initials: L
authors.lastname: Nostro
authors.forename: Bernardette
authors.initials: B
authors.lastname: Pavone
authors.forename: Giulio
authors.initials: G
authors.lastname: Bonvissuto
authors.forename: Susanna
authors.initials: S
authors.lastname: Campo
authors.forename: Daniela
authors.initials: D
authors.lastname: Iannello
authors.forename: Letterio
authors.initials: L
authors.lastname: Bonina
authors.forename: Michele
authors.initials: M
authors.lastname: Buemi
mesh_terms: D016022:Case-Control Studies; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D015536:Down-Regulation; D005260:Female; D017583:Hemodiafiltration / Q000009:adverse effects*; D018258:Herpesvirus 2, Human / Q000187:drug effects; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D007674:Kidney Diseases / Q000097:blood / Q000628:therapy*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism / Q000821:virology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; C482199:lipopolysaccharide, E coli O55-B5; D018664:Interleukin-12; D007371:Interferon-gamma