Cytokine gene expression of peritoneal tissues in response to mixed infection of Bacteroides fragilis and Escherichia coli.
- Author:
Jung Mogg KIM
1
;
Young Jeon KIM
;
Hwon Kyum PARK
;
Yang Ja CHO
Author Information
1. Department of Microbiology, Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, South Korea.
- Publication Type:Original Article
- MeSH:
Abscess;
Animals;
Bacteria;
Bacteroides fragilis*;
Bacteroides*;
Coinfection*;
Colon;
Cytokines;
Enterobacteriaceae;
Enzyme-Linked Immunosorbent Assay;
Escherichia coli*;
Escherichia*;
Gene Expression*;
Interleukins;
Mice;
Peritoneal Cavity;
RNA;
RNA, Messenger;
Tumor Necrosis Factor-alpha
- From:Journal of the Korean Society for Microbiology
2000;35(1):41-48
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Bacteroides fragilis and Escherichia coli, normal colonic inhabitants, are the most frequently isolated bacteria in infected tissues, particularly in intraabdominal abscesses. This study was designed to determine whether enteric bacteria may alter the B. fragilis-induced expression of proinflammatory cytokines in mouse peritoneal tissue (MPT). After C57BL/6 mice were inoculated with abscess-forming mixture containing B. fragilis in the presence or absence of E. coli, RNA was extracted from MPT. Expression of interleukin (IL)-1alpha and tumor necrosis factor (TNF)alpha mRNA was assessed using RT-PCR and standard RNA. Each cytokine protein was also measured by ELISA. The co-inoculation of E. coli into mouse peritoneal cavity advanced the onset of abscess development by B. fragilis infection. When mouse was co-infected with E. coli and B. fragilis intraperitoneally, there was a synergistic increase in the expression of IL-1alpha and TNFalpha mRNA in MPT and this was paralleled by increased cytokine protein secretion. Mixed inoculation of heat-killed E. coli and B. fragilis did not cause a synergistic increase in those cytokine mRNA expression. These results suggest that enteric bacteria may significantly affect proinflammatory cytokine signal produced by host peritoneal cavity in response to B. fragilis infection.
