Although bacteria and/or bacterial products have been shown to induce interferon (IFN) production in cells of the immune system, the ability of non-lymphoid cells to produce IFN in response to bacterial products and/or bacterial invasion is currently unknown. In this study we examined murine and human fibroblasts for their ability to produce IFN in response to challenge with the invasive bacteria Shigella flexneri and enteroinvasive Escherichia coli. Both human and murine primary cell cultures produced high levels (500 to 1000 U/ml) of IFN-β within 12 hr after Shigella invasion. The production of IFN appeared to be dependent upon bacterial invasion because no IFN was produced by cells pretreated with a non-invasive isogenic variant of S. flexneri. Furthermore, UV treated invasive S. flexneri, which lose the ability to invade cells, failed to induce IFN production in fibroblasts after bacterial challenge. In contrast to primary cells, most human and murine continuous cell lines did not produce IFN in response to Shigella invasion. The above results demonstrate that bacterial invasion of primary cultures of fibroblasts can induce IFN production. Taken together with previous findings, these results suggest that IFN may play an important front line host defense against invasive bacterial infections.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1987|
ASJC Scopus subject areas
- Immunology and Allergy