Acid-tolerant ZDY2013 shows a colonization niche preference and interacts with enterotoxigenic in specific-pathogen-free mice.

Probiotics have long been utilized as functional food and modulate gut microbial homeostasis, but their colonization niche is mostly unclear and transient, which restrains the development of microbiome-targeted strategies. () ZDY2013 is an allochthonous species of the human gastrointestinal tract with acid-tolerant properties. It serves as an antagonistic agent against the food-borne pathogen () and a potent regulator of the gut microbiota. However, there is a knowledge gap regarding the colonization dynamics of ZDY2013 in the host intestine and the colonization niche of its interaction with pathogens. Here, we designed a pair of specific primers targeting ZDY2013 based on its whole genome sequence. We evaluated their accuracy and sensitivity with other host-derived strains and confirmed their availability with artificially spiked fecal samples from different mouse models. Additionally, the content of ZDY2013 was quantified by qPCR in fecal samples from BALB/c mice, followed by the analysis of its colonization niche preference. Moreover, the interactions between ZDY2013 and enterotoxigenic HN001 were also elucidated. The results revealed that the newly designed primers could identify ZDY2013 with high specificity and were resistant to the influence of the complex fecal matrix and gut microbes from different hosts. Interestingly, the content of mixed ZDY2013 and HN001 when orally administered remained higher when compared with the single strain group in BALB/c mice upon discontinuation of intragastric administration. In addition, ZDY2013 was mainly enriched in the large intestine during the ingestion period and maintained the highest content in the stomach after discontinuing supplementation on day 7. Moreover, ZDY2013 colonization neither damaged the intestine nor ameliorated the damage triggered by in BALB/c mice. Overall, our study constructed two efficient specific primers targeting ZDY2013 and provided the potential to explore the underlying mechanism of competition between ZDY2013 and pathogens in host species.