andin Prophage phiv142-3 Enhance the Iron-Acquisition Ability and Resistance of Avian PathogenicStrain DE142 to Serum.

Abstract

Avian pathogenic(APEC), an extraintestinal pathogenic(ExPEC), is the causative agent of avian colibacillosis, a disease that causes huge economic losses in the poultry industry and is characterized by infection through respiratory tract colonization followed by bacteraemia. A previous study in our lab demonstrated that phiv142-3 enhanced the survival ability of APEC strain DE142 in chickens serum. However, the mechanism of this affect has not been completely revealed. Here, we analyzed the transcriptional level of the prophage phiv142-3 region in DE142 when grown in chicken serum. Several upregulated genes attracted our attention, and a series of mutants were constructed. Deletion oforfrom phiv142-3 led to lower yields compared with WT after cultivation in serum for 10 h (< 0.05). Furthermore, avian infection assays showed that compared with WT, the bacterial loads in blood and heart tissue of chickens challenged with DE142&#x394;were decreased to 3.9 and 13%, while the bacterial burden in blood and heart from chickens infected with DE142&#x394;was decreased to 7.2 and 8%, respectively (< 0.05). DE142&#x394;showed an obviously attenuated growth rate in the logarithmic phase when cultured in iron-deficient medium, and the transcription level of thegene decreased to 43% (< 0.05). The bactericidal assays showed that the survival of the mutant DE142&#x394;was ~60% compared with WT in 50% chicken serum. The K1 capsule-related genes (, and) were down-regulated nearly 2-fold in DE142&#x394;(< 0.01). Together, these results suggested thataffects growth by contributing to the uptake ability of iron, whileincreases resistance to serum by upregulating K1 capsule-related genes.