Abstract
Avian pathogenic Escherichia coli (APEC) is the etiologic agent of colibacillosis, an important cause of morbidity and mortality in poultry. Though, many virulence factors associated with APEC pathogenicity are known, their regulation remains unclear. FNR (fumarate and nitrate reduction) is a well-known global regulator that works as an oxygen sensor and has previously been described as a virulence regulator in bacterial pathogens. The goal of this study was to examine the role of FNR in the regulation of APEC virulence factors, such as Type I fimbriae, and processes such as adherence and invasion, type VI secretion, survival during oxidative stress, and growth in iron-restricted environments. To accomplish this goal, APEC O1, a well-characterized, highly virulent, and fully sequenced strain of APEC harboring multiple virulence mechanisms, some of which are plasmid-linked, was compared to its FNR mutant for expression of various virulence traits. Deletion of FNR was found to affect APEC O1's adherence, invasion and expression of ompT, a plasmid-encoded outer membrane protein, type I fimbriae, and aatA, encoding an autotransporter. Indeed, the fnr− mutant showed an 8-fold reduction in expression of type I fimbriae and a highly significant (P < 0.0001) reduction in expression of fimA, ompT (plasmid-borne), and aatA. FNR was also found to regulate expression of the type VI secretion system, affecting the expression of vgrG. Further, FNR was found to be important to APEC O1's growth in iron-deficient media and survival during oxidative stress with the mutant showing a 4-fold decrease in tolerance to oxidative stress, as compared to the wild type. Thus, our results suggest that FNR functions as an important regulator of APEC virulence.
Highlights
Escherichia coli is an important gastrointestinal inhabitant
FNR is related to transcriptional activators that control the expression of networks of E. coli genes in response to oxygen starvation, as observed in non-pathogenic E. coli strains such as E. coli K-12 (MG 1655; Guest et al, 1996)
Under anaerobic conditions, FNR was able to bind to specific DNA targets at promoter sites and modulate transcription (Kiley and Beinert, 2003; Kang et al, 2005; Salmon et al, 2005; Anjum et al, 2016), here we found that FNR were able to regulate Avian Pathogenic Escherichia coli (APEC) virulence genes under aerobic conditions
Summary
Escherichia coli is an important gastrointestinal inhabitant. Virulence factors confer on bacteria the ability to adapt to new niches, exploit resources available there and cause disease. E. coli (ExPEC) strains may exist in the gut without causing disease, they have the capacity to disseminate and colonize host niches beyond the gut such as the urinary tract, bloodstream, and central nervous system, resulting in localized or systemic infection and disease, depending on the panoply of virulence mechanisms they possess and express during infection (Wiles et al, 2008). The ExPEC of poultry, Avian Pathogenic Escherichia coli (APEC), causes colibacillosis, a disease which is a significant economic burden on all facets of the poultry industry (Nolan et al, 2013). The most common virulence traits among APEC include the ability to adhere to host tissues, survive within host fluids, and resist the host immune defenses (Ewers et al, 2007; Johnson and Nolan, 2009)
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