Abstract
BackgroundMouse infection studies have shown that interferon-γ (IFN-γ), a T helper 1 (Th1) cytokine, is required for the development of severe pathology induced by chronic Helicobacter infection. This finding is largely based on studies performed using mice that have polarised Th1 responses i.e. C57BL/6 animals. The current work aims to investigate the role of IFN-γ in Helicobacter-induced inflammation in BALB/c mice which have Th2-polarised immune responses.ResultsAt 7 months post-infection with Helicobacter felis, IFN-γ deficiency in BALB/c mice had no significant effect on H. felis colonisation levels in the gastric mucosa, nor on humoral responses, or gastritis severity. Ifng −/− animals with chronic H. felis infection did, however, develop significantly fewer lymphoid follicle lesions, as well as increased IL-4 splenocyte responses, when compared with infected Ifng +/+ mice (P = 0.015 and P = 0.0004, respectively).ConclusionsThe work shows that in mice on a BALB/c background, IFN-γ is not required for bacterial clearance, antibody responses, nor gastric inflammation. Conversely, IFN-γ appears to play a role in the development of gastric lymphoid follicles, which are precursor lesions to mucosa-associated lymphoid tissue (MALT) lymphoma. This study highlights the importance of mouse host background on the susceptibility to Helicobacter-induced pathologies.
Highlights
Mouse infection studies have shown that interferon-γ (IFN-γ), a T helper 1 (Th1) cytokine, is required for the development of severe pathology induced by chronic Helicobacter infection
IFN‐γ is not required to control H. felis colonisation in BALB/c mice To determine whether the absence of IFN-γ in BALB/c mice may have an effect on Helicobacter bacterial burden, we infected Ifng+/+ and Ifng−/− mice on a BALB/c background with H. felis
No differences were observed in either Helicobacter-specific IgA and IgG levels in the gastric compartment, nor in serum IgG1 and IgG2a levels, which are indicative of Th2- and Th1-responses, respectively (Fig. 3)
Summary
Mouse infection studies have shown that interferon-γ (IFN-γ), a T helper 1 (Th1) cytokine, is required for the development of severe pathology induced by chronic Helicobacter infection. This finding is largely based on studies performed using mice that have polarised Th1 responses i.e. C57BL/6 animals. The prolonged immune responses generated during Helicobacter pylori infection in humans drive the development of diseases that vary in severity, ranging from peptic ulcers to gastric adenocarcinomas and lymphomas [1]. One of the key soluble mediators induced during Helicobacter infection is interferon-γ (IFN-γ), a pro-inflammatory cytokine that contributes to gastric inflammation and is a hallmark of T helper (Th) type 1 responses [2,3,4]. We proposed that the default Th phenotypes of mice may be one factor contributing to the different types of pathology seen in animals [21]
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