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Expression of adhesion and activation molecules on circulating monocytes in children with Helicobacter pylori

Anna Helmin-Basa1, Mieczyslawa Czerwionka-Szaflarska, Grazyna Bala

  • 1Department of Immunology, Collegium Medicum Nicolaus Copernicus University, M. Sklodowskiej-Curie 9, Bydgoszcz 85-094, Poland. a.helminbasa@gmail.com

Helicobacter
|April 21, 2012
PubMed

Insights

Helicobacter pylori (H. pylori) eradication therapy in children can suppress inflammation by reducing monocyte expression of key adhesion molecules like CD11b, CD11c, and CD18 beta2 integrins.

Area of Science:

  • Immunology
  • Pediatrics
  • Gastroenterology

Background:

  • Helicobacter pylori (H. pylori) infection is a common cause of gastritis in children.
  • Monocytes play a crucial role in the inflammatory response during H. pylori infection.

Purpose of the Study:

  • To evaluate the expression of adhesion and activation molecules on monocytes in H. pylori-infected children with gastritis.
  • To compare monocyte expression profiles between infected children, those with failed eradication, and controls.

Main Methods:

  • Flow cytometry was used to analyze monocyte surface molecule expression (CD11a, CD11b, CD11c, CD18, CD54, CD58, CD14, HLA-DR, CD16).
  • Ninety-four children were studied, including H. pylori-infected, H. pylori-negative gastritis, and control groups.
  • H. pylori status was confirmed using [¹³C] urea breath test, rapid urease test, and histology.

Main Results:

  • Children with failed H. pylori eradication showed decreased expression of CD11c, CD14, CD11b, CD18, and HLA-DR on monocytes.
  • Increased CD16 expression was observed on monocytes in children with failed eradication.
  • Non-infected children with gastritis had lower CD16-positive monocytes compared to controls.

Conclusions:

  • H. pylori eradication therapy in children appears to inhibit the inflammatory response.
  • This inhibition is associated with a reduction in monocyte expression of CD11b, CD11c, and CD18 beta2 integrins.
Abstract

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