Spleen-based proteogenomics reveals that Escherichia coli infection induces activation of phagosome maturation pathway in chicken

Avian pathogenic Escherichia coli (APEC) leads to economic losses in poultry industry and is also a threat to human health. Various strategies were used for searching virulence factors, while little is known about the mechanism by which APEC survives in host or is eliminated by host. Thus, chicken colibacillosis model was constructed by intraperitoneally injecting E. coli O78 in this study, then the protein dynamic expression of spleen was characterized at different post-infection times by quantitative proteome. Comparative analysis showed that E. coli induced significant dysregulation at 72 h post infection in spleen tissue. Transcriptomic method was further used to assess the changes of dysregulated proteins at 72 h post infection at the mRNA level. Total 278 protein groups (5.7%) and 2,443 genes (24.4%) were dysregulated, respectively. The upregulated proteins and genes were consistently enriched in phagosome and lysosome pathways, indicating E. coli infection activates phagosome maturation pathway. The matured phagolysosome might kill the invasive E. coli. This study illuminated the genetic dysregulation in chicken spleen at the protein and mRNA levels after E. coli infecting and identified candidate genes for host response to APEC infection.

Automated summary

In this study, a chicken colibacillosis model was constructed by injecting E. coli O78 into the chicken's peritoneal cavity. The protein expression in the spleen at different time points post-infection was analyzed using quantitative proteomics. Dysregulation of proteins at 72 hours post-infection was observed, and transcriptomics was used to assess the changes at the mRNA level. The dysregulated proteins and genes were found to be enriched in phagosome and lysosome pathways. This study provides insights into the genetic dysregulation in the chicken spleen after E. coli infection and identifies candidate genes involved in the host response.