Influence of age and duration of infection on bacterial load and immune responses to Helicobacter pylori infection in a murine model

Abstract

SummaryUsing a murine model, we previously showed that Helicobacter pylori infects and colonizes offspring via maternal transmission during the nursing period. The aim of this study was to investigate the influence of age and duration of infection on inflammatory and immune responses to H. pylori in infant and adult mice. During the breast-feeding period, the number of bacteria was significantly suppressed in 1-week-old mice infected with H. pylori at an early stage of nursing, compared with adult mice, suggesting that breast-milk induces such low colonization. In addition, these mice had weaker gastric inflammation, especially Th1 cytokine and humoral responses than in mice infected with H. pylori after weaning in spite of elevated levels of Th1 cytokines. Although infant mice showed low inflammatory responses against H. pylori , they produced H. pylori -specific antibodies following vaccination with oral or parenteral adjuvant. Our results suggest the importance of age at the time of primary infection on bacterial load, gastric inflammation and humoral responses in a murine model of H. pylori infection.

Tolerance Rather Than Immunity Protects From Helicobacter pylori–Induced Gastric Preneoplasia

“…H. pylori -specific Treg are long-lived and independent of continuous antigenic stimulation, and require TGF-β signalling. Vaccination of neonatal mice with an adjuvanted vaccine overrides the suppressive capacity of Treg; this observation is clinically important as all vaccine development efforts targeting H. pylori envisage early childhood vaccination; it also confirms earlier data validating childhood vaccination with other, less immunogenic strains 31, 32. Indeed, neonatal tolerance to H. pylori is particularly evident with strains that are strongly immunogenic in adults, such as PMSS1 and H. felis .…”

Helicobacter pylori infection in mother and infant pairs in Anatolia

“…Chronic H. pylori infection has been shown together with chronic active gastritis, peptic ulceration and moreover with gastric malignancies. Infection with this microorganism is acquired mainly in the first and second years of life (11). As shown in Table 2, breastfeeding rates are quite high in our study group, and there is a parallelism with the seropositivity rates of anti-Hp IgG in infants' sera and breastmilk samples by age.…”

“…These maternal IgG antibodies may last until the postpartum period and may help to protect the child for the first months of life while its own immune system matures (7). Though it is still under debate in the literature, human milk is shown to have protective effects against H. pylori infection by a variety of mechanisms with different studies (8,(10)(11)(12). These include antibody effects targeted at protection against pathogens in the infant's environment (through milk IgA, IgG, and IgM) and nonspecific inhibition of bacterial adherence to gastric mucosal cells (8,10).…”

Gastric Helicobacter pylori Infection Affects Local and Distant Microbial Populations and Host Responses

“…Low-level gastric H. pylori load in neonatal mice may reflect antimicrobial functions of mother’s milk (Minoura et al, 2005), but in any event, appears to yield tolerogenic rather than immunogenic responses (Arnold et al, 2012). We excluded possible effects of nursing by challenging post-weaned (4-week old) mice and sexually mature 6-week old mice with H. pylori .…”