Protection of germ-free mice from infection by Helicobacter felis after active oral or passive IgA immunization

Czinn, Steven J.; Cai, Ann; Nedrud, John G.

doi:10.1016/0264-410x(93)90309-l

Cited by 252 publications

(166 citation statements)

References 31 publications

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“…In experimental models, evidence has been presented that both supports and rejects a role for Abs in protection against infection (8,9,39,42,44,55). However, not until recently have we been able to adequately address the question of whether specific Abs have a protective role or not by comparing the bacterial colonization after challenge with live bacteria in mice that are deficient in all Ig (MT mice) or in IgA only and in WT control mice (8 -10, 43, 44).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Akhiani

Schön

Franzén

et al. 2004

The Journal of Immunology

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In recent years, Abs have been considered a correlate rather than an effector of resistance against Helicobacter pylori infection. However, it is still poorly understood to what extent Ab production correlates with gastric immunopathology. Here we report that Abs not only are dispensable for protection, but they are detrimental to elimination of the bacteria and appear to impair gastric inflammatory responses. We found that the initial colonization with H. pylori bacteria was normal in the B cell-deficient (μMT) mice, whereas at later times (>8 wk) most of the bacteria were cleared, concomitant with the development of severe gastritis. In contrast, wild-type (WT) mice exhibited extensive bacterial colonization and only mild gastric inflammation, even at 16 wk after inoculation. Oral immunizations with H. pylori lysate and cholera toxin adjuvant stimulated comparable levels of protection in μMT and WT mice. The level of protection in both strains correlated well with the severity of the postimmunization gastritis. Thus, T cells were responsible for the gastritis, whereas Abs, including potentially host cell cross-reactive Abs, were not involved in causing the gastritis. The T cells in μMT and WT mice produced high and comparable levels of IFN-γ to recall Ag at 2 and after 8 wk, whereas IL-4 was detected after 8 wk only, indicating that Th1 activity dominated the early phase of protection, whereas later a mixed Th1 and Th2 activity was seen.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Akhiani

Schön

Franzén

et al. 2004

The Journal of Immunology

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“…43,44 In addition, SIgA may play a protective role against H. pylori colonization 6,7 in early childhood or after therapeutic eradication, a possibility supported by results obtained by active or passive (IgA) local vaccines in experimental animals. 45,46 However, the role of antibodies has been questioned by recent vaccination results obtained in B cell knockout mice. 47 In conclusion, reduced J chain expression in gastritis suggested a shift from local production of pIgA to monomeric IgA.…”

Section: Discussionmentioning

confidence: 99%

Increased Mucosal Production of Monomeric IgA1 but No IgA1 Protease Activity in Helicobacter pylori Gastritis

Berstad¹,

Kilian²,

Valnes³

et al. 1999

The American Journal of Pathology

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“…Whereas specific IgA mAbs administered directly into the gastric lumen of mice mediated protection against Helicobacter felis infection, passive transfer of serum from immunized protected mice to naive recipient animals failed to protect against infection (11,12). Most importantly though, B cell-deficient MT mice, as well as IgA-deficient mice, following mucosal immunization with bacterial lysate plus adjuvant, were protected to the same extent as wild-type (WT) 3 mice (12)(13)(14)(15).…”

Section: Nfection Withmentioning

confidence: 98%

IgA Antibodies Impair Resistance againstHelicobacter pyloriInfection: Studies on Immune Evasion in IL-10-Deficient Mice

Akhiani

Stensson

Schön

et al. 2005

The Journal of Immunology

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We recently reported that Helicobacter pylori-specific Abs impair the development of gastritis and down-regulate resistance against H. pylori infection. In this study, we asked whether IgA Abs specifically can have an impact on H. pylori colonization and gastric inflammation. To obtain a sensitive model for the study of inflammation we crossed IgA- and IL-10-deficient mice. We found that IL-10−/−/IgA−/− mice were significantly less colonized than IL-10−/−/IgA+/+ mice, which in turn were less colonized than wild-type (WT) mice. The IL-10−/−/IgA−/− mice exhibited a 1.2-log reduction in bacterial counts compared with that in IL-10−/−/IgA+/+ mice, suggesting that IgA Abs rather promoted than prevented infection. The reduced colonization in IL-10−/−/IgA−/− mice was associated with the most severe gastritis observed, albeit all IL-10−/− mice demonstrated more severe gastric inflammation than wild-type mice. The gastritis score and the infiltration of CD4+ T cells into the gastric mucosa were significantly higher in IL-10−/−/IgA−/− mice than in IL-10−/−/IgA+/+ mice, arguing that IgA Abs counteracted inflammation. Moreover, following oral immunization, IL-10−/−/IgA−/− mice were significantly better protected against colonization than IL-10−/−/IgA+/+ mice. However, the stronger protection was associated with more severe postimmunization gastritis and gastric infiltration of CD4+ T cells. There was also a clear increase in complement receptor-expressing cells in IL-10−/−/IgA−/− mice, though C3b-fragment deposition in the gastric mucosa was comparable between the two. Finally, specific T cell responses to recall Ag demonstrated higher levels of IFN-γ production in IL-10−/−/IgA−/− as compared with IL-10−/−/IgA+/+ mice. Thus, it appears that IgA and IL-10 help H. pylori bacteria evade host resistance against infection.

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Protection of germ-free mice from infection by Helicobacter felis after active oral or passive IgA immunization

Cited by 252 publications

References 31 publications

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection

Increased Mucosal Production of Monomeric IgA1 but No IgA1 Protease Activity in Helicobacter pylori Gastritis

IgA Antibodies Impair Resistance againstHelicobacter pyloriInfection: Studies on Immune Evasion in IL-10-Deficient Mice

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