AUTHOR=Zeng Qing , He Xiaolong , Puthiyakunnon Santhosh , Xiao Hansen , Gong Zelong , Boddu Swapna , Chen Lecheng , Tian Huiwen , Huang Sheng-He , Cao Hong 

TITLE=Probiotic Mixture Golden Bifido Prevents Neonatal Escherichia coli K1 Translocation via Enhancing Intestinal Defense

JOURNAL=Frontiers in Microbiology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2017.01798

DOI=10.3389/fmicb.2017.01798

ISSN=1664-302X

ABSTRACT=<p><italic>Escherichia coli</italic> (<italic>E. coli</italic>) K1 sepsis and meningitis is a severe infection characterized by high mortality in neonates. Successful colonization and translocation across the intestinal mucosa have been regarded as the critical steps for <italic>E. coli</italic> K1 sepsis and meningitis. We recently reported that the probiotic mixture, Golden Bifido (containing live <italic>Lactobacillus bulgaricus, Bifidobacterium</italic>, and <italic>Streptococcus thermophilus</italic>, LBS) has a preventive role against neonatal <italic>E. coli</italic> K1 bacteremia and meningitis. However, the interaction between the neonatal gut barrier, probiotics and <italic>E. coli</italic> K1 is still not elucidated. The present study aims to investigate how LBS exerts its protective effects on neonatal gut barrier during <italic>E. coli</italic> K1 infection. The beneficial effects of LBS were explored <italic>in vitro</italic> and <italic>in vivo</italic> using human colon carcinoma cell lines HT-29 and rat model of neonatal <italic>E. coli</italic> K1 infection, respectively. Our results showed that stimulation with <italic>E. coli</italic> K1 was able to cause intestinal barrier dysfunction, which were reflected by <italic>E. coli</italic> K1-induced intestinal damage and apoptosis of intestinal epithelial cells, reduction of mucin, immunoglobulin A (IgA) and tight junction proteins expression, as well as increase in intestinal permeability, all these changes facilitate <italic>E. coli</italic> K1 intestinal translocation. However, these changes were alleviated when HT-29 cells were treated with LBS before <italic>E. coli</italic> K1 infection. Furthermore, we found that LBS-treated neonatal rats (without <italic>E. coli</italic> K1 infection) have showed higher production of mucin, ZO-1, IgA, Ki67 in intestinal mucosa as well as lower intestinal permeability than that of non-treated rats, indicating that LBS could accelerate the development of neonatal intestinal defense. Taken together, our results suggest that enhancement of the neonatal intestinal defense to fight against <italic>E. coli</italic> K1 translocation could be the potential mechanism to elucidate how LBS confers a protective effect against neonatal <italic>E. coli</italic> K1 bacteremia and meningitis. This indirect mechanism makes LBS exert preventive effect on most of gut-derived pathogenic infections rather than only <italic>E. coli</italic>.</p>