Transmaternal Helicobacter pylori exposure reduces allergic airway inflammation in offspring through regulatory T cells

Abstract

We conclude that exposure to H pylori has consequences not only for the carrier but also for subsequent generations that can be exploited for interventional purposes.

Review: Helicobacter: Inflammation, immunology, and vaccines

“…15 Indeed, the same group showed that transmaternal exposure to H pylori extract in utero and/or during lactation induced strong protective effects against allergic airway inflammation in both the first-and, intriguingly, second-generation offspring. 28 Treatment with H pylori VacA mediated a similar protective effect which correlated with the skewing of T-cell responses toward regulatory rather than effector functions, as characterized by the expansion of Treg cell subsets expressing CXC chemokine receptor 3 (Cxcr3) or RORγt, as well as demethylation of the Foxp3 locus. 28 These findings raise interesting questions about the potential of H pylori to protect against allergic asthma and other atopic conditions, warranting investigations in human subjects under controlled laboratory conditions.…”

“…26 Thus, NOD1-driven IL-33 production during chronic H pylori infection may protect against excessive inflammatory responses and favor bacterial persistence. 15,28 Altobelli et al 15 15 The induction of immune tolerance was mediated, at least in part, by VacA. 27 In addition to dampening host inflammatory responses, there is increasing evidence that H pylori induces a form of immune tolerance and, moreover, that this condition may develop very early in life.…”

“…15,28 Altobelli et al 15 15 The induction of immune tolerance was mediated, at least in part, by VacA. 28 Treatment with H pylori VacA mediated a similar protective effect which correlated with the skewing of T-cell responses toward regulatory rather than effector functions, as characterized by the expansion of Treg cell subsets expressing CXC chemokine receptor 3 (Cxcr3) or RORγt, as well as demethylation of the Foxp3 locus. 15 Indeed, the same group showed that transmaternal exposure to H pylori extract in utero and/or during lactation induced strong protective effects against allergic airway inflammation in both the first-and, intriguingly, second-generation offspring.…”

“…15 In addition to being a strategy by which H pylori can evade host immunity and colonize its host for life, pulmonary Treg accumulation may have an impact on immune responses to allergens. 28 These findings raise interesting questions about the potential of H pylori to protect against allergic asthma and other atopic conditions, warranting investigations in human subjects under controlled laboratory conditions. 28 Treatment with H pylori VacA mediated a similar protective effect which correlated with the skewing of T-cell responses toward regulatory rather than effector functions, as characterized by the expansion of Treg cell subsets expressing CXC chemokine receptor 3 (Cxcr3) or RORγt, as well as demethylation of the Foxp3 locus.…”

“…27 In addition to dampening host inflammatory responses, there is increasing evidence that H pylori induces a form of immune tolerance and, moreover, that this condition may develop very early in life. 15,28 Altobelli et al 15 15 The induction of immune tolerance was mediated, at least in part, by VacA. 15 In addition to being a strategy by which H pylori can evade host immunity and colonize its host for life, pulmonary Treg accumulation may have an impact on immune responses to allergens.…”