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1 ting microglial activation in response to C. koseri.
2 r regulation of one such gene in Citrobacter koseri.
3 wth of Escherichia coli K1/r and Citrobacter koseri.
4 15.8] vs 3.0 [3.0-5.3]; p<0.0001) than did C koseri.
5                                  Citrobacter koseri (22 [46%] of 48) and C freundii (20 [42%]) were t
6 escens, 12 Proteus mirabilis, 10 Citrobacter koseri, 9 Citrobacter freundii, 8 Klebsiella oxytoca, 5
7 in UTI89 and by enteric bacteria Citrobacter koseri and Salmonella enterica serovar typhimurium.
8  serovars, Escherichia coli, and Citrobacter koseri are rapidly attracted toward sources of human ser
9 nce was 97.8% similar to that of Citrobacter koseri but 97.0% similar to that of Enterobacter cloacae
10             In this study, we showed that C. koseri causes meningitis and brain abscesses in the neon
11  pneumoniae, Klebsiella oxytoca, Citrobacter koseri, Citrobacter freundii group, Enterobacter spp., a
12 f a novel bacterial homolog from Citrobacter koseri, CLC-ck2, has yielded surprising discoveries abou
13 ues, including Escherichia coli, Citrobacter koseri, Enterobacter cloacae, and clinical isolates of n
14 4 mutant and MyD88 KO microglia following C. koseri exposure, indicating a contribution of TLR4- and
15                   Gut-associated Citrobacter koseri genomes harbored 47 polymorphic sites that we use
16 brain parenchyma, microglial responses to C. koseri have not yet been examined.
17 n macrophages in vitro and that uptake of C. koseri increases in the presence of human pooled serum i
18 ng exposure to either live or heat-killed C. koseri, indicating a critical role for both TLR4- and My
19 ns) were the primary target for long-term C. koseri infection.
20 marily facilitates the entry of opsonized C. koseri into macrophages.
21                                  Citrobacter koseri is a Gram-negative bacterium that can cause a hig
22              A unique feature of Citrobacter koseri is the extremely high propensity to initiate brai
23 n and that more than 90% of intracellular C. koseri organisms are colocalized within phagolysosomes.
24                      To better understand C. koseri pathogenesis, we have characterized the interacti
25     These lesions were caused by Citrobacter koseri septicaemia, identified by transfontanelle ultras
26 n macrophages may be a mechanism by which C. koseri subverts the host response and elicits chronic in
27                             We found that C. koseri survives and replicates within macrophages in vit
28 fluorescence microscopy demonstrates that C. koseri survives phagolysosomal fusion and that more than
29 range from 0.4-log reduction for Citrobacter koseri to > 8 log reduction for Kocuria rhizophila.
30                            The ability of C. koseri to survive phagolysosome fusion and replicate wit
31 udies lend support to the hypothesis that C. koseri uses morphologically different methods of uptake
32                            Interestingly, C. koseri was capable of surviving intracellularly in both
33 entration [IC(50)], approximately 10 nM), C. koseri was intermediate (IC(50), approximately 1,000 nM)
34  Salmonella typhimurium LT2, and Citrobacter koseri were able to cross-seed in vitro.
35 we have characterized the interactions of C. koseri with human macrophages.
36 lts demonstrate that microglia respond to C. koseri with the robust expression of proinflammatory mol