title: Differential effects of Sendai virus infection on mediator synthesis by mesangial cells from two mouse strains.
abstract: BACKGROUND
  Recently, we observed that the severity of glomerulonephritis in an experimental model of immunoglobulin A nephropathy (IgAN) induced by Sendai virus differs between C57BL/6 and BALB/c mouse strains. The determinants of differing renal insufficiency are not understood. In the present study, we examine the capacity for mesangial cells to support Sendai viral replication and assess the direct effects of Sendai virus on the production of selected cytokines, chemokines, and eicosanoids by mesangial cells, comparing C57BL/6 to BALB/c mouse strains.
  
  
  METHODS
  Sendai virus replication was measured by viral plaque assay using LLCMK2 cells. Production of cytokines [interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)], chemokines (JE and KC), and eicosanoids [prostaglandin E2 (PGE2) and thromboxane B2 (TxB2)] in culture medium was evaluated by sandwich enzyme-linked immunosorbent assay (ELISA) or competitive enzyme immunoassay (EIA) after 48 hours' incubation with infectious or inactivated Sendai virus.
  
  
  RESULTS
  Sendai virus replicates equally well in mesangial cells from both strains, and infection evokes increased IL-6, JE, KC, and PGE2 production in relation to viral dose. BALB/c mesangial cells produce significantly more IL-6 and JE than those from C57BL/6, and the dose response for KC is steeper in BALB/c mesangial cells than those from C57BL/6. Synthesis of PGE2 in BALB/c mesangial cells is higher than that of C57BL/6 mesangial cells, both under basal conditions and in response to infectious Sendai virus, again in a dose-dependent manner. There is no TNF-alpha or thromboxane response to viral stimulation.
  
  
  CONCLUSIONS
  We conclude that different mesangial cell responses to this common mucosal viral pathogen might influence the severity of IgAN in our model system.
authors.affiliation: Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
authors.forename: Noriyoshi
authors.initials: N
authors.lastname: Kobayashi
authors.forename: Nayer
authors.initials: N
authors.lastname: Bagheri
authors.forename: John G
authors.initials: JG
authors.lastname: Nedrud
authors.forename: Robert M
authors.initials: RM
authors.lastname: Strieter
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Tomino
authors.forename: Michael E
authors.initials: ME
authors.lastname: Lamm
authors.forename: Steven N
authors.initials: SN
authors.lastname: Emancipator
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D003470:Culture Media; D016207:Cytokines / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D005920:Glomerular Mesangium / Q000166:cytology / Q000276:immunology / Q000821:virology*; D005922:Glomerulonephritis, IGA / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D000882:Haplorhini; D018836:Inflammation Mediators / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D010253:Respirovirus Infections / Q000276:immunology* / Q000378:metabolism; D029082:Sendai virus; D013045:Species Specificity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D003470:Culture Media; C475895:Cxcl1 protein, mouse; D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C074302:keratinocyte-derived chemokines; D015232:Dinoprostone