Induction of an atypical interferon by bacteroides fragilis and Escherichia coli in experimental infections and in leukocyte cultures.

Previous reports have shown that Bacteroides fragilis may enhance the pathogenicity of coinfecting enterobacteriaceae by interfering with the host's immune response. With the present study, we have investigated the possible role of interferons (IFN) in mediating these effects. Mice injected with B. fragilis developed moderate serum levels of IFN that appeared just prior to alterations of the animals' immunity described earlier. The IFN was neutralized by treatment with anti-IFN-alpha/beta-antibodies or hydrochloric acid; hence it displayed the same "atypical" characteristics as IFN found in patients with immuno-compromising diseases such as AIDS, systemic lupus erythematosus or rheumatoid arthritis. Escherichia coli displayed the same induction patterns as B. fragilis, while gram-positive bacteria induced "regular" IFN alpha/beta and gamma. Spleen cells, peritoneal macrophages, or liver leukocytes taken from B. fragilis or E. coli-injected animals 6 h post infection were refractory to IFN induction by E. coli lipopolysaccharide in vitro; cells from mice infected with gram-positive organisms showed normal or enhanced responsiveness.