Lung infection of avian pathogenic Escherichia coli co-upregulates the expression of cSP-A and cLL in chickens.

The host innate defense-pathogen interaction in the lung has always been a topic of concern. The respiratory tract is a common entry route for Avian pathogenic Escherichia coli (APEC). Chicken surfactant protein A (cSP-A) and chicken lung lectin (cLL) can bind to the carbohydrate moieties of various microorganisms. Despite their detection in chickens, their role in the innate immune response is largely unknown. This study aimed to examine whether the expression levels of cSP-A and cLL in the chicken respiratory system were affected by APEC infection. A lung colonization model was established in vivo using 5-day-old specific-pathogen-free chickens infected intratracheally with APEC. The chickens were euthanized 12 h post-infection (hpi) and 1-3 days post-infection (dpi) to detect various indicators. The results of quantitative reverse transcription-polymerase chain reaction and fluorescence multiplex immunohistochemical staining showed that the mRNA and protein expression levels of cSP-A and cLL in the lung and trachea were significantly co-upregulated at 2dpi.Transcriptome RNA-sequencing analysis indicated that the inoculation with APEC AE17 at 2 dpi resulted in differential gene expression of approximately 810 genes compared with control birds, but only a few genes were expressed with astatistically significant ≧2-fold difference. cLL and cSP-A were among the significantly upregulated genes involved in innate immunity. These findings indicated that cSP-A and cLL might play an important role in lung innate host defense against APEC infection at the early stage.