Abstract
Interactions between the gut microbiota and the immune system may be involved in vaccine and infection responses. In the present study, we studied the interactions between caecal microbiota composition and parameters describing the immune response in six experimental inbred chicken lines harboring different MHC haplotypes. Animals were challenge-infected with the infectious bronchitis virus (IBV), and half of them were previously vaccinated against this pathogen. We explored to what extent the gut microbiota composition and the genetic line could be related to the immune response, evaluated through flow cytometry. To do so, we characterized the caecal bacterial communities with a 16S rRNA gene amplicon sequencing approach performed one week after the IBV infectious challenge. We observed significant effects of both the vaccination and the genetic line on the microbiota after the challenge infection with IBV, with a lower bacterial richness in vaccinated chickens. We also observed dissimilar caecal community profiles among the different lines, and between the vaccinated and non-vaccinated animals. The effect of vaccination was similar in all the lines, with a reduced abundance of OTU from the Ruminococcacea UCG-014 and Faecalibacterium genera, and an increased abundance of OTU from the Eisenbergiella genus. The main association between the caecal microbiota and the immune phenotypes involved TCR(ϒδ) expression on TCR(ϒδ)(+) T cells. This phenotype was negatively associated with OTU from the Escherichia-Shigella genus that were also less abundant in the lines with the highest responses to the vaccine. We proved that the caecal microbiota composition is associated with the IBV vaccine response level in inbred chicken lines, and that the TCR(ϒδ)(+) T cells (judged by TCR(ϒδ) expression) may be an important component involved in this interaction, especially with bacteria from the Escherichia-Shigella genus. We hypothesized that bacteria from the Escherichia-Shigella genus increased the systemic level of bacterial lipid antigens, which subsequently mitigated poultry γδ T cells.