Izabela Planeta-Malecka

Detection of specific Helicobacter pylori DNA and antigens in stool samples in dyspeptic patients and healthy subjects

In this study stool samples from dyspeptic patients and healthy subjects were used for detection of specific Helicobacter pylori antigens and DNA by immunoenzymatic test (PPHpSA) and semi‐nested PCR (ureA‐PCR), respectively. The H. pylori status was estimated by invasive endoscopy‐based rapid urease test and histology or noninvasive urea breath test (UBT), and by serology (ELISA, Western blot). The coincidence of H. pylori‐negative invasive tests or UBT and negative antigen or DNA stool tests was very high (mean 95%). The PPHpSA results were found positive for 56% and ureA‐PCR for 26% of individuals with H. pylori infection confirmed by invasive tests or UBT. The detection of specific H. pylori antigens and especially DNA in feces is not sufficient as a one‐step diagnosis of H. pylori infection.

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

In this study, we assessed the proliferative response of peripheral blood mononuclear leukocytes (PBML) from 33 children/young adolescents with chronic dyspepsia, to H. pylori LPS in the presence and absence of IL-2 as a T cell growth factor. A rapid urease test (RUT) and a presence of Helicobacter-like organisms (HLO) in the biopsy specimens allowed us to distinguish RUT/HLO-positive (17/33) and -negative (16/33) patients. H. pylori LPS alone induced a proliferation of PBML from 4 out of 33 dyspeptic patients. IL-2 increased the prevalence of the response to LPS to 59% and 74% of RUT/HLO-positive and -negative patients, respectively. PBML from RUT/HLO-positive patients responded significantly less intensively to H. pylori LPS in the presence of IL-2, to IL-2 alone and to H. pylori LPS+IL-2. However, there was no difference in PHA-driven proliferation of PBML from the patients of those two groups. A negative correlation between the responsiveness to H. pylori LPS of PBML and occurrence of type B inflammation in gastric mucosa was demonstrated. The results suggest a contribution of H. pylori LPS to an outcome of H. pylori infection. It is speculated that H. pylori LPS by an activation of immunocompetent cells may reduce gastric inflammation, decrease bacterial load and prolong H. pylori infection.