Helicobacter pyloriAntigens Inducing Early Immune Response in Infants

Abstract

To identify the Helicobacter pylori antigens operating during early infection in sera from infected infants using proteomics and immunoblot analysis. Two-dimensional (2D) large and small gel electrophoresis was performed using H. pylori strain 51. We performed 2D immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin M (IgM) antibody immunoblotting using small gels on sera collected at the Gyeongsang National University Hospital from 4–11-month-old infants confirmed with H. pylori infection by pre-embedding immunoelectron microscopy. Immunoblot spots appearing to represent early infection markers in infant sera were compared to those of the large 2D gel for H. pylori strain 51. Corresponding spots were analyzed by matrix-assisted laser desorption/ionization time of flight-mass spectrometry (MALDI-TOF-MS). The peptide fingerprints obtained were searched in the National Center for Biotechnology Information (NCBI) database. Eight infant patients were confirmed with H. pylori infection based on urease tests, histopathologic examinations, and pre-embedding immunoelectron microscopy. One infant showed a 2D IgM immunoblot pattern that seemed to represent early infection. Immunoblot spots were compared with those from whole-cell extracts of H. pylori strain 51 and 18 spots were excised, digested in gel, and analyzed by MALDI-TOF-MS. Of the 10 peptide fingerprints obtained, the H. pylori proteins flagellin A (FlaA), urease β subunit (UreB), pyruvate ferredoxin oxidoreductase (POR), and translation elongation factor Ts (EF-Ts) were identified and appeared to be active during the early infection periods. These results might aid identification of serological markers for the serodiagnosis of early H. pylori infection in infants.

Changing prevalence of Helicobacter pylori infection in children and adolescents

“…15,29) Thirty-three H. pylori isolates obtained from 11 members of three families showed familial clustering of identical random amplified polymorphic DNA fingerprinting types, which might be supportive evidence of person-to-person transmission among closely related individuals such as family members. 6,33) Many epidemiologic studies involving children showed that H. pylori infection occurred in early childhood and that the infection rate increased at around 5-7 years of age. 2,28) During these ages, children usually start to experience group life, for example, kindergarten or elementary school, which may support the possibility of person-to-person transmission.…”

“…3) H. pylori infection may occur in infancy or early childhood and generally persists for life if left untreated. 2,[4][5][6] Chronic H. pylori infection plays a pivotal role in the development of peptic ulcer, atrophic gastritis, and gastric cancer. 7) The H. pylori infection status in children versus adults is not fully known since most infected children remain asymptomatic and studies are limited.…”

Changes in Seroprevalence ofHelicobacter pyloriInfection Over 20 Years in Jinju, Korea, from Newborns to the Elderly

“… 24 H. pylori strain 51 was isolated from a patient with duodenal ulcer at GNUH in 1988 and has been studied extensively since then. 14 15 18 22 24 25 26 27 Briefly, H. pylori strain 51 was cultured for 18 hours under the environment of 37°C, 5%–10% CO 2 and 100% humidity on Mueller-Hinton agar supplemented with 10% bovine serum. Bacterial cells from each plate were harvested and pelleted by centrifugation at 4,000 × g for 15 minutes.…”

“… 11 12 13 14 15 H. pylori infection can take hold during infancy or early childhood and colonization generally persists for life if left untreated. 16 17 18 …”

The study on the stimulation of the immune system in the infused BALB/C mice by pCDNA3.1(-)-flaA recombinant vector against Helicobacter pylori infection using molecular techniques

“…H. pylori flagellin is an important virulent factor in the pathogenesis of gastric mucosal and is considered as one of the most important stimulators of the immune system and acts as a ligand for toll-like receptor 5 (TLR5) of the host cells (YAN et al, 2003;SADEGHI and DOOSTI, 2017). FlaA protein is the predominant subtype and reduces TLR5 internal activity in this pathogen so it might help the bacterium to escape from the host immune response and causes continuous bacterial colonization (SADEGHI and DOOSTI, 2017;SEO et al, 2017).…”