Abundance of single filamentous bacteria and expression of differentiated Th17 cells, cytokines IL-17A and IL-22, and retinoic acid receptor are significantly high in infants with abysmal oral rotavirus vaccine replication

Abstract

<title>Abstract</title> Single filamentous bacteria (SFB) have been shown to prevent murine rotavirus (RV) and other mammalian enteric infections, independent of type I and II interferons, by promoting the adaptive and innate immunity through differentiation of intestinal Th17 cells, production of immunoglobulin A and retinoic acid receptor (RAR) signalling. Here, we assessed whether the abundance of the bacterium at the time of oral RV vaccination would impede the vaccine performance. Stool samples were collected from infants a week after RV vaccination to decide vaccine shedders (n = 20) and non-shedders (n = 20). The abundance of SFB and expression of cathepsin L (CTSL, a biomarker for differentiated Th17 cells), cytokines 17A and IL-22, and retinoic acid receptor (RAR) were assayed using quantitative PCR. Infants who did not shed the vaccine in stool samples had a significantly high abundance of SFB compared to vaccine shedders, <italic>p</italic> = 0.042, and the abundance correlated negatively with vaccine virus shedding load (R = − 0.69). The expression of CTSL was increased 3.5-fold in non-shedders compared to vaccine shedders, <italic>p</italic> = 0.035. Similarly, the expression of IL-17A and IL-22 was increased 8.5- and 12-fold, respectively, in non-shedders versus shedders. The expression of RAR was also increased 5.9-fold in non-shedders compared to vaccine shedders, <italic>p</italic> = 0.034. Infants possessing elevated abundance of SFB were less likely to shed the vaccine in stool samples (OR = 0.31, 95% CI = 0.102–0.962), <italic>p</italic> = 0.043. Our observations suggest that the abundance of SFB at the time of vaccination may impede the vaccine virus infection and therefore its performance in the study population.