Protection against Helicobacter pylori infection following immunization is IL-12-dependent and mediated by Th1 cells

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Protection against Helicobacter pylori infection following immunization is IL-12-dependent and mediated by Th1 cells

Akhiani, Aliasghar, 1957 (author): Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology

Pappo, J. (author)

Kabok, Z. (author)

Schon, K. (author)

Gao, W. (author)

Franzen, L. E. (author)

Lycke, Nils Y, 1954 (author): Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology

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(creator_code:org_t)

2002
2002
English.
In: J Immunol. ; 169:12, s. 6977-84

Related links:: https://gup.ub.gu.se...

Journal article (peer-reviewed)

Abstract Subject headings

The regulatory roles of Th1 and Th2 cells in immune protection against Helicobacter infection are not clearly understood. In this study, we report that a primary H. pylori infection can be established in the absence of IL-12 or IFN-gamma. However, IFN-gamma, but not IL-12, was involved in the development of gastritis because IFN-gamma(-/-) (GKO) mice exhibited significantly less inflammation as compared with IL-12(-/-) or wild-type (WT) mice. Both IL-12(-/-) and GKO mice failed to develop protection following oral immunization with H. pylori lysate and cholera toxin adjuvant. By contrast, Th2-deficient, IL-4(-/-), and WT mice were equally well protected. Mucosal immunization in the presence of coadministered rIL-12 in WT mice increased Ag-specific IFN-gamma-producing T cells by 5-fold and gave an additional 4-fold reduction in colonizing bacteria, confirming a key role of Th1 cells in protection. Importantly, only protected IL-4(-/-) and WT mice demonstrated substantial influx of CD4(+) T cells in the gastric mucosa. The extent of inflammation in challenged IL-12(-/-) and GKO mice was much reduced compared with that in WT mice, indicating that IFN-gamma/Th1 cells also play a major role in postimmunization gastritis. Of note, postimmunization gastritis in IL-4(-/-) mice was significantly milder than WT mice, despite a similar level of protection, indicating that immune protection is not directly linked to the degree of gastric inflammation. Only protected mice had T cells that produced high levels of IFN-gamma to recall Ag, whereas both protected and unprotected mice produced high levels of IL-13. We conclude that IL-12 and Th1 responses are crucial for H. pylori-specific protective immunity.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Keyword

Animal
Antibodies
Bacterial/biosynthesis/blood
Epitopes
T-Lymphocyte/immunology
Gastritis/genetics/immunology
Helicobacter Infections/genetics/*immunology/*prevention & control
Helicobacter pylori/*immunology
Immunization
Secondary
Immunoglobulin A/biosynthesis/blood
Immunoglobulin G/biosynthesis/blood
Interferon Type II/biosynthesis/deficiency/genetics
Interleukin-12/deficiency/genetics/*physiology
Lymphopenia/genetics/immunology
Mice
Mice
Inbred C57BL
Mice
Knockout
Support
Non-U.S. Gov't
Th1 Cells/*immunology/metabolism/pathology
Th2 Cells/immunology
*Vaccination

Publication and Content Type

ref (subject category)
art (subject category)

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MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Basic Medicine; and Microbiology in ...

Articles in the publication: J Immunol

By the university: University of Gothenburg

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