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Helicobacter pylori lipopolysaccharide in the IL-2 milieu activates lymphocytes from dyspeptic children

Wieslawa Rudnicka1, Agnieszka Jarosinska, Leokadia Bak-Romaniszyn

  • 1Department of Immunology and Infectious Biology, Institute for Microbiology and Immunology, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland. rudw@biol.uni.lodz.pl

FEMS Immunology and Medical Microbiology
|May 10, 2003
PubMed

Insights

Helicobacter pylori lipopolysaccharide (LPS) can stimulate immune cells in children with dyspepsia. Interleukin-2 (IL-2) enhances this response, potentially reducing gastric inflammation and prolonging infection.

Area of Science:

  • Immunology
  • Gastroenterology
  • Microbiology

Background:

  • Chronic dyspepsia affects children and young adolescents.
  • Helicobacter pylori infection is a common cause of gastrointestinal issues.
  • The role of H. pylori lipopolysaccharide (LPS) in modulating the immune response in dyspeptic patients requires further investigation.

Purpose of the Study:

  • To assess the proliferative response of peripheral blood mononuclear leukocytes (PBML) to H. pylori LPS in children with chronic dyspepsia.
  • To evaluate the effect of Interleukin-2 (IL-2) on PBML proliferation in response to H. pylori LPS.
  • To correlate immune cell responsiveness with clinical and histological findings.

Main Methods:

  • PBML were isolated from 33 children/young adolescents with chronic dyspepsia.
  • Patients were classified as H. pylori rapid urease test/Helicobacter-like organisms (RUT/HLO)-positive or -negative.
  • PBML proliferation was measured in response to H. pylori LPS, with and without IL-2, and phytohemagglutinin (PHA).

Main Results:

  • H. pylori LPS alone induced PBML proliferation in a small subset of patients.
  • IL-2 significantly increased the prevalence of PBML response to LPS in both RUT/HLO-positive and -negative groups.
  • PBML from RUT/HLO-positive patients showed a diminished response to LPS and IL-2 compared to RUT/HLO-negative patients, despite similar PHA responses.
  • A negative correlation was observed between PBML responsiveness to LPS and type B gastric inflammation.

Conclusions:

  • H. pylori LPS contributes to the immune response outcome in H. pylori infections.
  • IL-2 enhances the proliferative capacity of PBML to H. pylori LPS in dyspeptic children.
  • H. pylori LPS may modulate immune cell activation, potentially reducing gastric inflammation, decreasing bacterial load, and prolonging infection.

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