A Murine Model of Enterohemorrhagic Escherichia coli O157:H7 Infection to Assess Immunopotentiating Activity of Drugs on Mucosal Immunity: Effect of Drugs

Abstract

An enterohemorrhagic Escherichia coli (EHEC) O157 oral infection murine model was established to examine the potentiating activity of drugs on mucosal immune responses. Groups of ICR mice inoculated intragastrically with 10(11) CFU/kg EHEC O157 showed chronic intestinal infection with the pathogen that persisted over 3 weeks and resulted in the synthesis of relatively high levels of antigen specific fecal IgA antibody. Intraperitoneal administration of 80 NU/kg Neurotropin, an immunopotentiator, augmented the antigen specific mucosal immune responses to EHEC O157. On the other hand, FK506 clearly suppressed the response. To further document the augmenting effect of Neurotropin on mucosal immune responses, mice were immunized intranasally with a mixture of ovalbumin and cholera toxin. Co-administration of 80 NU/kg Neurotropin significantly potentiated the synthesis of fecal IgA and serum IgG antibodies. These results suggest that Neurotropin has potential as a mucosal adjuvant to promote secretory IgA antibody production and that the mice model of oral infection with EHEC O157 is useful for immunopharmacological studies of bacterial infection-defensive mucosal immune responses.

Effect of feeding whey peptide fractions on the immune response in healthy and Escherichia coli infected mice

“…Serum IgA levels were higher on day 7 than on day 1 in all infected groups, indicating a delayed response even though the mice were back to their pre-infection body weights and no longer showed any symptoms of the infection. Nagano et al (2003) demonstrated that fecal IgA antibody titres against EHEC O157 whole cells and O157-LPS peaked at 4-weeks after inoculation with 10 11 cfu kg À1 , which suggests that the increased secretion of IgA continues for weeks after the infection.…”

Adhesion of Enterohemorrhagic <i>Escherichia coli</i> O157:H7 to the Intestinal Epithelia Is Essential for Inducing Secretory IgA Antibody Production in the Intestine of Mice

“…ous paper. 18) On the other hand, GPU991 and GPU992 disappeared from the feces within 2 weeks and did not induce the fecal IgA antibody production. Then, GPU991 as well as heatkilled GPU96MM and IID5208 (nonpathogenic E. coli) were repeatedly inoculated 4 times into mice to increase the antigen loading.…”

“…Again, GPU991 (espA-deletion mutant), GPU992 (sepLdeletion mutant) and A6-E7 (sepL-insetion mutant) could not form the TTSS, and showed no adherence to cultured epithelial cells. 10,18) On the other hand, G1-E11 (tir-insertion mutant) and Δeae (eae-deletion mutant) adhered diffusely to Caco-2 cells through the TTSS but not establish intimate adhesion through intimin-Tir interaction. 10) Considering all together, the results strongly suggest that the adhesion of EHEC through the intimin-Tir interaction is essential for the induction of antigen-specific S-IgA antibody production in the intestine of mice.…”

“…We also reported that fecal immunoglobulin A (IgA) antibodies against EHEC O157:H7 increased not only in children infected with the pathogen 17) but also in mice inoculated orally. 18) Camara et al 19) demonstrated that colostrum IgA antibodies against intimin of enteropathogenic E. coli, which have a LEE cluster similar to that of EHEC, inhibited the adherence of the bacteria to HeLa cells. Thus, secretory IgA (S-IgA) antibodies are transported to the mucosal surface through the epithelial cells by a receptor-mediated mechanism, and may function to eliminate the pathogen from the intestine by inhibiting the adhesion and colonization as one major effector molecule for the mucosal immunity.…”

Specific Egg Yolk Immunoglobulin as a New Preventive Approach for Shiga-Toxin-Mediated Diseases

“…Stx-1 and Stx-2 concentrations were determined by ELISA [61] using mouse anti-Stx-1B subunit monoclonal antibody (STX1-13C4; Toxin Technology, Sarasota, FL, USA) or anti-Stx-2B subunit monoclonal antibody (STX2-BB12; Toxin Technology) as a capture antibody, and mouse anti Stx-1 and Stx-2 pooled antibodies conjugated to horseradish peroxidase (STXPC-1; Toxin Technology) as a developing antibody. Purified Stx-1 and Stx-2 purchased from Nacalai Tesque, Inc. (Kyoto, Japan) were used to prepare the standard curves.…”