Abstract
Purpose To investigate the frequency and activation status of peripheral plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) as well as gastric mucosa DC subset distribution in Helicobacter pylori- (H. pylori-) infected and noninfected children. Materials and Methods Thirty-six children were studied; twenty-one had H. pylori. The frequencies of circulating pDCs (lineage−HLA-DR+CD123+) and mDCs (lineage−HLA-DR+CD11c+) and their activation status (CD83, CD86, and HLA-DR expression) were assessed by flow cytometry. Additionally, the densities of CD11c+, CD123+, CD83+, CD86+, and LAMP3+ cells in the gastric mucosa were determined by immunohistochemistry. Results The frequency of circulating CD83+ mDCs was higher in H. pylori-infected children than in the noninfected controls. The pDCs demonstrated upregulated HLA-DR surface expression, but no change in CD86 expression. Additionally, the densities of gastric lamina propria CD11c+ cells and epithelial pDCs were increased. There was a significant association between frequency of circulating CD83+ mDCs and gastric lamina propria mDC infiltration. Conclusion This study shows that although H. pylori-infected children had an increased population of mature mDCs bearing CD83 in the peripheral blood, they lack mature CD83+ mDCs in the gastric mucosa, which may promote tolerance to local antigens rather than immunity. In addition, this may reduce excessive inflammatory activity as reported for children compared to adults.
Highlights
Helicobacter pylori (H. pylori) colonizes the human stomach
The intensity and activity of antral gastritis were greater in the H. pylori-infected children
We described here peripheral Dendritic cells (DCs) subset distribution and their maturation status in the H. pylori-infected and noninfected children
Summary
Helicobacter pylori (H. pylori) colonizes the human stomach. Infection usually starts in early childhood and can persist for decades, sometimes even for the lifetime [1]. Dendritic cells (DCs) are professional antigen-presenting cells (APCs) that induce T cell response against a presented antigen. Their migration from the site of an antigen uptake. Mediators of Inflammation to the regional lymph nodes and their subsequent maturation profile decide about the type of the subsequent adaptive immune response profiles against infection (protective or nonprotective responses). The DC maturation process is associated with the expression of several membrane molecules engaged in the DC migration (CCR7), antigen presentation abilities (MHC class II), and their costimulatory activities (CD80, CD83, and CD86) [5, 6]
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