TY - JOUR
T1 - The induction of interferon production in fibroblasts by invasive bacteria
T2 - a comparison of Salmonella and Shigella species
AU - Hess, Cynthia B.
AU - Niesel, David W.
AU - Klimpel, Gary R.
N1 - Funding Information:
This work was supported by Public Health Service grants AI 24677 and Al 23731 from the National Institutes of Health, the John Sealy Memorial Endowment Fund, and the James W . McLaughlin Fellowship Fund .
PY - 1989/8
Y1 - 1989/8
N2 - As the role of interferon (IFN) in host defense against facultative intracellular bacterial infections continues to expand, it has become increasingly important to understand what cell types can produce IFN following infection and/or interaction with these invasive bacteria. We have demonstrated previously that Shigella flexneri was able to induce high levels of IFN in primary cultures of human and murine fibroblasts following bacterial invasion. In this study, we examined the ability of Salmonella typhimurium to induce IFN production in different cell lines. S. typhimurium-infected primary cell cultures of mouse embryo-fibroblasts (MEF) were shown to produce high levels of IFN following bacterial challenge. In contrast to Shigella, Salmonella required a much lower multiplicity of infection for optimal IFN induction. Examination at the RNA level of IFN production by MEF following challenge with either bacteria revealed that the IFN produced was a mixture of IFNα and IFNβ (IFN α β), with IFNβ1, as the predominant species. As previously demonstrated for Shigella, bacterial invasion of cells appeared to be required for the induction of IFN production by S. typhimurium. Salmonella rendered non-invasive by UV-treatment failed to induce IFN production in MEF. Furthermore, Salmonella LPS, when tested over a wide range of concentrations, was unable to induce IFN production in these cells. In contrast to MEF, human and murine continuous cell lines did not produce IFN following Salmonella challenge. These results taken together suggest that IFN may be a common factor involved in Salmonella and Shigella infections. Furthermore, IFN may play an important role in the front line host defense against these types of infections.
AB - As the role of interferon (IFN) in host defense against facultative intracellular bacterial infections continues to expand, it has become increasingly important to understand what cell types can produce IFN following infection and/or interaction with these invasive bacteria. We have demonstrated previously that Shigella flexneri was able to induce high levels of IFN in primary cultures of human and murine fibroblasts following bacterial invasion. In this study, we examined the ability of Salmonella typhimurium to induce IFN production in different cell lines. S. typhimurium-infected primary cell cultures of mouse embryo-fibroblasts (MEF) were shown to produce high levels of IFN following bacterial challenge. In contrast to Shigella, Salmonella required a much lower multiplicity of infection for optimal IFN induction. Examination at the RNA level of IFN production by MEF following challenge with either bacteria revealed that the IFN produced was a mixture of IFNα and IFNβ (IFN α β), with IFNβ1, as the predominant species. As previously demonstrated for Shigella, bacterial invasion of cells appeared to be required for the induction of IFN production by S. typhimurium. Salmonella rendered non-invasive by UV-treatment failed to induce IFN production in MEF. Furthermore, Salmonella LPS, when tested over a wide range of concentrations, was unable to induce IFN production in these cells. In contrast to MEF, human and murine continuous cell lines did not produce IFN following Salmonella challenge. These results taken together suggest that IFN may be a common factor involved in Salmonella and Shigella infections. Furthermore, IFN may play an important role in the front line host defense against these types of infections.
KW - Salmonella
KW - Shigella
KW - induction of interferon production
UR - http://www.scopus.com/inward/record.url?scp=0024404870&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0024404870&partnerID=8YFLogxK
U2 - 10.1016/0882-4010(89)90030-2
DO - 10.1016/0882-4010(89)90030-2
M3 - Article
C2 - 2687612
AN - SCOPUS:0024404870
SN - 0882-4010
VL - 7
SP - 111
EP - 120
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
IS - 2
ER -