Lactobacillus Shielding Against E. coli O157:H7 in Mouse Enterocytes: A Prophylactic Approach

Abstract

Background: Escherichia coli (E. coli O157:H7), a Shiga-like toxin-producing Escherichia coli (STEC) serotype, is harmful, especially for children, elderly people, and immunocompromised persons. This strain can induce serious enterocyte problems, requiring careful mitigation. We intend to study Lactobacillus prophylactic ability against E. coli O157:H7-induced cellular damage in mouse enterocytes. Methods: The binding affinity of bacterial intimin and its human target, integrin, was assessed using a docking study. Next, Lactobacillus supplementation was tested in E. coli O157:H7-infected mice enterocytes using transmission electron microscopy (TEM) and light microscope (LM). The rats, weighing between 100 and 200 g, were randomly categorized into three groups (n = 6): uninfected (control), STEC-infected, and probiotics + STEC-infected. The randomization process was conducted using a computer-generated method that considered factors such as age, sex, and initial body weight. This approach was employed to minimize potential biases during the grouping process. Subsequently, specimens from the ileum were meticulously examined utilizing both transmission electron microscopy (TEM) and light microscopy (LM). Results: ClusPro showed Lactobacillus bound more efficiently than E. coli (–632.5). In STEC-infected mice, LM revealed intestinal epithelial cells (IECs) compromises that probiotic improved. Moreover, TEM showcased structural disruptions in infected mice, rectified by probiotics. Statistical scrutiny, using parameters such as the number of intact microvilli per enterocyte and the extent of membrane damage, underscored significant improvements in STEC-infected mice treated with probiotics, emphasizing their pivotal role in preserving cellular integrity. Conclusions: Certain probiotics may protect enterocytes from pathogens. These results imply that probiotics may reduce pathogenicity, offering new avenues for enteric infection research.