Efficacy of Passive Immunization with IgY Antibodies to a 58-kDaH. pyloriAntigen on Severe Gastritis in BALB/c Mouse Model

Abstract Consecutive triple doses of 1 × 108 CFU/mL of a pathogenic H. pylori strain isolated from stomach of Egyptian patients with severe gastritis were used to establish infection in BALB/c mice model. White Leghorn hens were immunized with H. pylori whole cell lysate (HpLysate) antigen and with a highly reactive 58-kDa H. pylori (Hp58) antigen. Two months later, IgY antibodies (IgY-HpLysate & IgY-Hp58) were purified from egg yolk and its efficacy was evaluated in the adopted model. Microbiological culture and immunohistochemical staining revealed that H. pylori infection was inhibited 1 week after oral passive immunization in 70% of infected BALB/c mice with a significant decrease (p < 0.05) in the degrees of gastritis. In conclusion, we have adapted BALB/c mice model for human H. pylori pathogenic strain and oral passive immunization with specific IgY antibodies to the 58-kDa antigen inhibited active H. pylori infection and decreased gastritis. Keywords: 58-kDa antigenBALB/c mice H. pylori IgY antibodiesPassive immunization ACKNOWLEDGMENTS The authors would like to thank Dr. Hoda M. El-Emshaty at Gastroenterology and Surgery Center, Mansoura University, Mansoura and Dr. Tamer E. Mosa at National Research Center, Dokki, Giza for their kind help. Notes ∗Mice (10 per group) received either single, double or triple oral doses each of 1 × 108 CFU/mL mouse-adopted H. pylori strain and killed 2 or 4 or 8 weeks after oral infection. Control were non-infected mice. ∗∗All mice showing positive results for microbiological culture were positive for H. pylori antigen detection in stomach tissues using immunohistochemical staining. ∗∗∗Immunohistochemical staining using specific antibodies to HpLysate. ∗Mice (10 per group) received either single, double or triple oral doses each of 1 × 108 CFU/mL mouse-adopted H. pylori strain as described in details under experimental section and killed 8 weeks after oral infection. Controls were non-infected mice. ∗∗0 (no gastritis); + (mild gastritis); ++ (moderate gastritis) and +++ (severe gastritis). ∗Control: mice passively immunized with IgY-N at 1 day, 1 week, 4 weeks and 12 weeks after infection with 3 × 108 CFU/mL; Treated: mice passively immunized with IgY-Hp58 1 day, 1 week, 4 weeks and 12 weeks after infection with 3 × 108 CFU/mL. All were killed 8 weeks after passive immunization. ∗∗Immunohistochemical staining using specific antibodies to the 58-kDa antigen. ∗∗∗Significantly different from the control mice (p < 0.05). ∗Treated: mice passively immunized with IgY-Hp58 1 day, 1 week, 4 weeks and 12 weeks after infection with 3 × 108 CFU/mL; Control: mice passively immunized with IgY-N at 1 day, 1 week, 4 weeks and 12 weeks after infection with 3 × 108 CFU/mL. All mice were killed 8 weeks after passive immunization. ∗∗Significantly different from the control mice (p < 0.001).