INFECTION OF HUMAN LUNG FIBROBLASTS WITH EPSTEIN-BARR VIRUS CAUSES INCREASED IL-1ß AND bFGF PRODUCTION

Abstract

An association between Epstein-Barr virus (EBV) infection and fibroblast proliferation in the interstitial spaces of the lung has been suggested in idiopathic interstitial pneumonia. In this study we show that EBV can infect human lung fibroblasts in vitro. A primary-cultured human lung fibroblast cell line, designated CCD-32Lu, expressed EBV nuclear antigen 1 after coculture with lethally irradiated EBV producing cells. The infection further induced CCD-32Lu cells to produce the fibrogenic cytokines basic fibroblast growth factor (bFGF) and interleukin-1beta. These findings indicate that lung fibroblasts may be a target for EBV infection and suggest that EBV may play a role in increased production of these cytokines and induce fibroblast proliferation in idiopathic interstitial pneumonia.

Sulfatide inhibits fibroblast growth, activation and oxidative stress induced by ectopic insulin

“…This, however, does not rule out sulfatide and GalCer from exhibiting similar effects on cellular growth, as was observed in this study. Whether cytokines produced by fibroblasts are implicated in diabetes pathogenesis is unknown, but they do have a role in other diseases such as liver and renal fibrosis, systemic sclerosis and rheumatoid arthritis 53‐55 . To what extent sulfatide, GalCer or other glycolipids may influence the cytokine‐induced pathology in these diseases is currently unknown.…”