-, no lesions; +, mild lesions; ++, Selleckchem AZD4547 moderate lesions; +++, severe lesions. Figure 3 Heart sections of chickens infected via air sac inoculation with virulent wild-type strains or iron acquisition mutants. Magnification,×400. Heart sections of chickens infected with E058 (A), E058Δ chuT (B), E058Δ iroD (C), E058Δ iucD (D), E058Δ chuT Δ iroD Δ iucD (E), U17 (F), U17Δ chuT (G), U17Δ iroD (H), U17Δ iucD (I), U17Δ chuT Δ iroD Δ iucD (J). Heart section of a mock bird (K). Figure 4 Liver sections of chickens infected via air sac inoculation with virulent wild-type strains or iron acquisition mutants.

Magnification,×400. Liver sections of chickens infected with E058 (A), E058Δ chuT (B), E058Δ iroD (C), E058Δ iucD (D), E058Δ chuT Δ iroD Δ iucD (E), U17 (F), U17Δ chuT (G), U17Δ iroD (H), U17Δ iucD (I), U17Δ chuT Δ iroD Δ iucD (J). Liver section of a mock bird (K). Discussion APEC and UPEC Nutlin-3 datasheet are the two main subsets of ExPEC bacteria, causing diseases outside the gastrointestinal tract. Previous studies have investigated the similarities of APEC and UPEC strains by determining serogroups,

virulence genotypes, and assignments to phylogenetic groups [27–30]. It has been proposed that poultry may be a candidate vehicle for E. coli capable of causing human urinary tract disease, based on the possible transmission of avian E. coli from poultry to humans, and similarities between APEC and UPEC [31–34]. Interestingly, the human UPEC isolate CFT073 was shown to be virulent in an avian respiratory Suplatast tosilate infection model, but APEC isolates have not yet been found

to cause disease in humans [35]. Although previous studies have been devoted to the contribution of iron uptake systems to pathogenesis of APEC or UPEC individually, the contribution of these systems to the virulence of APEC and UPEC has not been clarified simultaneously in a chicken challenge model. In this study, the roles of heme, salmochelin and aerobactin systems in the virulence of APEC E058 and UPEC U17 were assessed. Results indicated that the contribution of these three distinct iron acquisition systems to APEC E058 pathogenesis was quite similar to that of UPEC U17 when assessed simultaneously in chickens. Drawing conclusions from this study, ChuT-mediated heme transport system was generally redundant both in APEC E058 and UPEC U17 colonization and histopathological lesion formation in chickens. The IucD- mediated aerobactin synthsis played an important role in the pathogenesis of both E058 and U17, while the IroD-dependent salmochelin system provided a more critical contribution to the virulence of APEC E058 and UPEC U17. Heme is the most abundant iron source in vivo, and can be utilized by certain bacterial pathogens.