Abstract

Salmonella enterica serovar Pullorum (S. pullorum) causes pullorum disease in poultry and results in great economic losses to the poultry industry. Although an eradication program has been successfully performed in some countries, it remains a major threat to countries with poor poultry disease surveillance. Currently there are no effective control measures for pullorum disease except eradication. In particular, the pathogenesis of S. pullorum infection is still largely unknown. Here we identified bacterioferritin (Bfr) as a major antigen of S. pullorum to elicit a humoral immune response. Furthermore, we demonstrate that Bfr induces activation of IFN-β promoter and mRNA expression in DF-1 cells, and that the amino acids 1–50 form a critical domain involved in IFN-β expression. Moreover, we found that the p38 MAPK signaling pathway was essential for Bfr-induced IFN-β expression. Importantly, S. pullorum-induced IFN-β expression was totally abolished by deficiency of Bfr in the bacteria, indicating that Bfr plays a critical role in S. pullorum induced IFN-β expression in DF-1 cells. Our findings provide new insights into the molecular mechanisms of the host response to S. pullorum infection.

Highlights

  • IntroductionAn acute systemic disease commonly seen in young birds, is caused by Salmonella enterica serovar Pullorum

  • Pullorum disease, an acute systemic disease commonly seen in young birds, is caused by Salmonella enterica serovar Pullorum

  • Since S. pullorum infection elicits a robust humoral immune response in chickens, we wanted to determine the major antigens of S. pullorum responsible for the induction of specific antibodies

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Summary

Introduction

An acute systemic disease commonly seen in young birds, is caused by Salmonella enterica serovar Pullorum. The clinical signs of pullorum disease are characterized by anorexia, diarrhea, dehydration, weakness and high mortality in young chicks, but this disease usually shows a persistent infection and causes decreased egg production and diarrhea in adult fowls (Shivaprasad, 2000). S. pullorum, currently belonging to biovars of serovar Gallinarum within serogroup D, has identical somatic antigens (O1, O9, O12) and no flagella due to mutations in flagellar genes while its pathogenicity is restricted only to avian species (Barrow and Freitas, 2011). The relatively high rate of accumulation of mutations in the genome of S. pullorum suggests a rapid rate of evolution associated with the host adaptation, in the development of S. pullorum (Barrow and Freitas, 2011).

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