We examined the remnant bacteria in the brain after E. coli
RS218 infection, which increased up to (2.4 0.2) 107 at
24 hours after infection and up to (6.0 0.3) 107 at 36
hours after infection (Table 1); the mice died within 36
hours of intracerebral E. coli RS218 infection. In addition,
for mice infected with E. coli RS218 premixed with recombinant
OmpA fragments L1e2, L1e4, and L3e4, the
remnant bacteria in the brains increased up to
(4.0 0.2) 106, (4.5 0.4) 106, and (5.0 0.3) 106 at
24 hours after infection, respectively, and up to
(8.6 0.1) 107, (9.2 0.0) 107, and (8.8 0.1) 107 at
60 hours after infection, respectively (Table 1); all mice
died within 72 hours after bacterial infection. By contrast,
the remnant bacteria in the brains infected with E. coli
RS218 premixed with recombinant OmpA fragments L1e3,
L2e3, and L2e4 were (5.4 0.4) 105, (3.2 0.1) 105,
and (5.5 0.4) 105 at 24 hours after infection, respectively,
and were undetectable at 60 hours after infection
(Table 1). This indicates that these specific recombinant
OmpA fragments protected the mice against E. coli infection
and that this protection correlated with bacterial
clearance.