Serum Cytokine Signature That Discriminates Helicobacter pylori Positive and Negative Juvenile Gastroduodenitis.

Svetlana F Khaiboullina,Rezeda Faizullina,Albert A Rizvanov,Dilyara Safina,Ekaterina V Martynova,Georgi V Cherepnev,Felix Khuzin,Alsu Khalikova,Yuriy Davidyuk,Vincent C Lombardi,Sayar Abdulkhakov

doi:10.3389/fmicb.2016.01916

Abstract

Gastroduodenitis caused by H. pylori, often acquired in early childhood, is found in about 50% of the adult population. Although H. pylori infections can remain asymptomatic, its virulence factors usually trigger epithelial vacuolization and degeneration, loss of microvilli, disintegration of cytoplasm, and leukocyte accumulation. It is believed that leukocyte infiltration is driven by cytokines produced locally in infected tissue. However, so far little is known about changes in serum cytokines in juvenile patients infected with H. pylori. Serum cytokine profiles were analyzed in 62 juvenile patients diagnosed with gastroduodenitis using the Bio-Plex multiplex assay. H. pylori infection was confirmed in 32 patients, while 30 patients were H. pylori-free. Cytokines CXCL5 and CXCL6, potent neutrophil chemoattractants, were upregulated in all patients diagnosed with gastroduodenitis. Serum levels of IL8, a prototype neutrophil attractant, remained unchanged in subjects with gastroduodenitis relative to controls. Therefore, our data suggest that CXCL5 and CXCL6 play a role in directing neutrophil trafficking into inflamed gastroduodenal tissue. In addition, the CCL25/GM-CSF ratio differed significantly between H. pylori-positive and -negative juveniles. Further, study is needed to evaluate the role of CCL25 and GM-CSF in the pathogenesis of the different etiologies of gastroduodenitis.

Highlights

Helicobacter pylori (H. pylori) was identified in 1982 and suggested to be a causative agent for gastritis and stomach ulcers (Marshall and Warren, 1984)
There is limited knowledge of serum cytokine expression in children infected with H. pylori, since the majority of data is from adult populations (Bayraktaroglu et al, 2004; Mehmet et al, 2004; Abdollahi et al, 2011; Eskandari-Nasab et al, 2013)
Little is known about systemic activation of cytokines in children infected with H. pylori

Summary

Introduction

Helicobacter pylori (H. pylori) was identified in 1982 and suggested to be a causative agent for gastritis and stomach ulcers (Marshall and Warren, 1984). This helix-shaped gram-negative bacterium colonizes gastric mucosa and persists as a chronic infection (Marshall et al, 1985a; Morris and Nicholson, 1987). H. pylori is one of the most common gastrointestinal infections, being found in about 50% of the adult population (Sipponen et al, 1996; Kosunen et al, 1997). The majority of H. pylori infections remain asymptomatic, with only 15% of carriers developing symptoms (Atherton, 1998; Ernst and Gold, 2000). It is believed that H. pylori is transmitted via fecal-oral or oral-oral routes (Goh et al, 2011)

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