Gastric inflammation is enhanced in children with CagA-positive Helicobacter pylori infection
K L Kolho1, R Karttunen, P Heikkilä
1Hospital for Children and Adolescents, Helsinki University Central Hospital, Finland.
Insights
Helicobacter pylori CagA-positive infections in children are linked to increased gastric antrum inflammation. Higher serum antibody titers in these children may indicate a more severe inflammatory response.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Immunology
Background:
- Helicobacter pylori infection is common in childhood.
- Factors driving active inflammation in pediatric H. pylori infections remain unclear.
Purpose of the Study:
- To investigate the association between CagA status and gastric inflammation in children.
- To analyze the relationship between H. pylori-specific antibody titers and inflammation severity.
Main Methods:
- Determined CagA status and serum IgG/IgA antibodies to H. pylori in 39 infected children.
- Assessed mononuclear and polymorphonuclear cell infiltration in gastric antrum and body.
Main Results:
- CagA-positive children showed more intense mononuclear cell infiltration in the antrum.
- Higher IgG and IgA antibody titers to H. pylori were observed in CagA-positive infections.
- IgG antibody titers correlated with antral inflammation density.
Conclusions:
- CagA-positive H. pylori infections in children are associated with more severe antral inflammation.
- Elevated serum antibody titers in CagA-positive cases may reflect enhanced gastric inflammation.
Background:
Helicobacter pylori infection is likely to be acquired at an early age. The factors leading to active inflammation in childhood, however, are largely unknown.
Subjects And Methods:
We determined the CagA status, the best characterized virulence factor of H. pylori, and serum antibodies of IgG and IgA classes to H. pylori in 39 infected children.
Results:
Mononuclear cell infiltration in the antrum but not in the gastric body was more intense in CagA-positive children than in CagA-negative children. The degree of polymorphonuclear cell infiltration on the other hand was independent of the CagA status. The antibody titers of IgG and IgA classes to H. pylori were higher in CagA-positive than in CagA-negative infections (P<0.001 and P<0.01, respectively). IgG antibody titers to H. pylori correlated directly with the density of mononuclear and polymorphonuclear cell infiltration in the gastric antrum but not in the gastric body.
Conclusion:
H. pylori-infected children with CagA antibodies seem to have a more severe inflammation in the gastric antrum than CagA-negative children as shown by an increase in the density of antral mononuclear cells. A finding of higher serum antibody titers to H. pylori in CagA-positive children may be related to this enhancement of inflammation.
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