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Infect. Immun., Apr 1996, 1369-1372, Vol 64, No. 4
W Hopkins, A Gendron-Fitzpatrick, DO McCarthy, JE Haine and DT Uehling
Host defense against bacterial urinary tract infections (UTI) includes both
inflammatory and immune responses to infecting bacteria. The cellular
events leading up to local inflammation are thought to be under genetic
control and initiated by lipopolysaccharides (LPS) of gram-negative
bacteria such as Escherichia coli. It has been previously reported that
mice which lack functional Lps genes are more susceptible to induced E.
coli UTI than mice with normal mitogenic responses to LPS. In contrast to
these findings, data in this report demonstrate that LPS-responder and
nonresponder C3H mouse strains are equally susceptible to E. coli UTI. When
C3H/OuJ (Lps(n)/Lps(n)) and C3H/HeJ (Lps(d)/Lps(d)) were intravesically
inoculated with equal numbers of uropathogenic E. coli organisms, neither
strain was able to effectively resolve the induced UTI. The inability of
C3H/OuJ mice to combat the infection was not due to an impaired response to
LPS, nor could defect in the local inflammatory response be identified. The
results indicate that factors other than LPS responsiveness are also
important in determining hose resistance to UTI.
Copyright © 1996, American Society for Microbiology
Lipopolysaccharide-responder and nonresponder C3H mouse strains are equally susceptible to an induced Escherichia coli urinary tract infection
Medical School, University of Wisconsin, Madison, USA.
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