Interferon-γ promotes gastric lymphoid follicle formation but not gastritis in Helicobacter-infected BALB/c mice

Michelle Chonwerawong; Patrick Avé; Michel Huerre; Richard L Ferrero

doi:10.1186/s13099-016-0142-0

Interferon-γ promotes gastric lymphoid follicle formation but not gastritis in Helicobacter-infected BALB/c mice

Gut Pathog. 2016 Nov 21:8:61. doi: 10.1186/s13099-016-0142-0. eCollection 2016.

Authors

Michelle Chonwerawong¹, Patrick Avé², Michel Huerre³, Richard L Ferrero⁴

Affiliations

¹ Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Monash University, 27-31 Wright Street, Clayton, VIC 3123 Australia.
² Unité de Recherche et d'Expertise Histotechnologie et Pathologie, Institut Pasteur, 25-28 Rue du Dr Roux, 75724 Paris, France ; Unité de Histopathologie Humaine et Modèles Animaux, Institut Pasteur, 25-28 Rue du Dr Roux, 75724 Paris, France.
³ Unité de Recherche et d'Expertise Histotechnologie et Pathologie, Institut Pasteur, 25-28 Rue du Dr Roux, 75724 Paris, France ; Département de Pathologie, Institut Curie, 26 Rue d'Ulm, 75248 Paris, France.
⁴ Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Monash University, 27-31 Wright Street, Clayton, VIC 3123 Australia ; Department of Microbiology, Monash University, Clayton, VIC Australia.

Abstract

Background: 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 current work aims to investigate the role of IFN-γ in Helicobacter-induced inflammation in BALB/c mice which have Th2-polarised immune responses.

Results: At 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).

Conclusions: The 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.

Keywords: BALB/c; Gastric inflammation; Helicobacter; Interferon-gamma; Lymphoid follicle; MALT lymphoma; Mucosa-associated lymphoid tissue; T helper response.