title: Synergy of Bacteroides fragilis and Escherichia coli in the induction of KC gene expression in mouse peritoneal tissues.
abstract: B. fragilis induces cytokine expression, which can serve as a host signal leading to inflammatory reaction and abscess formation in the peritoneal cavity. We assessed the hypothesis that enteric bacteria may alter the B. fragilis-induced expression of KC genes in mouse peritoneal tissues (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 KC mRNA was quantified using reverse-transcription polymerase chain reaction and standard RNA. KC and TNFalpha proteins were measured by enzyme-linked immunosorbent assay. KC mRNA in MPT was upregulated following inoculation of B. fragilis and this was paralleled by increased KC protein secretion. When the mice were co-infected with E. coli and B. fragilis intraperitoneally, there was a synergistic increase in the expression of KC of MPT. Co-infection with L. acidophilus and B. fragilis downregulated KC mRNA expression, but co-infection with E. faecalis and B. fragilis synergistically increased KC expression in the infected MPT. Inhibition of TNFalpha production could downregulate KC expression in mixed infected MPT. These results suggest that enteric bacteria may significantly affect the KC signal produced by the host peritoneal cavity in response to B. fragilis infection.
authors.affiliation: Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
authors.forename: J M
authors.initials: JM
authors.lastname: Kim
authors.forename: Y J
authors.initials: YJ
authors.lastname: Kim
authors.forename: Y J
authors.initials: YJ
authors.lastname: Cho
mesh_terms: D000038:Abscess / Q000382:microbiology; D000818:Animals; D001442:Bacteroides Infections / Q000150:complications*; D001441:Bacteroides fragilis / Q000235:genetics*; D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004926:Escherichia coli / Q000235:genetics*; D004927:Escherichia coli Infections / Q000150:complications*; D015964:Gene Expression Regulation, Bacterial; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D010538:Peritonitis / Q000382:microbiology*; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D015854:Up-Regulation
chemical_list: D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; C475895:Cxcl1 protein, mouse; D016207:Cytokines; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C074302:keratinocyte-derived chemokines