Abstract
BackgroundPersistent infections that induce prolonged inflammation might negatively affect the leukocyte telomere length (LTL); however, the role in LTL of Helicobacter pylori (H. pylori) infection, which persistently colonizes the stomach, remains unknown.The study objective was to examine associations of sero-prevalence of H. pylori immunoglobulin G (IgG) antibody and serum pepsinogens (PGs), as markers of atrophic gastritis, with LTL.A cross-sectional study was performed among 934 Arab residents of East Jerusalem, aged 27–78 years, randomly selected from Israel’s national population registry. Sera were tested for H. pylori IgG and PG levels by ELISA. LTL was measured by southern blots. Multiple linear regression models were fitted to adjust for sociodemographic and lifestyle factors.ResultsLTL decreased significantly with age (p < 0.001) and was shorter in men than women (p = 0.032). The mean LTL was longer in H. pylori sero-positive persons than negative ones: mean difference 0.13 kb (95% CI 0.02, 0.24), p = 0.016. Participants with atrophic gastritis (PGI < 30 μg/L or a PGI: PGII < 3.0) had shorter LTL than did those without: mean difference − 0.18 (95% CI − 0.32, − 0.04). The difference was of larger magnitude between persons who had past H. pylori infection (sero-negative to H. pylori IgG antibody) and atrophic gastritis, compared to those who were H. pylori sero-negative and did not have atrophic gastritis: mean difference − 0.32 kb (95% CI − 0.55, − 0.10). This association remained significant after adjustment for age, sex, and religiosity: beta coefficient − 0.21 kb (95% CI − 0.41, − 0.001), p = 0.049. The results were similar after further adjustment for lifestyle factors. In bivariate analysis, mean LTL was longer in physically active persons than non-active ones, and shorter in persons with than without obesity; however, these differences were diminished and were not significant in the multivariable model.ConclusionsH. pylori IgG sero-positivity per se was not related to reduced LTL. However, persons with past H. pylori infection (i.e., lacking H. pylori IgG serum antibody) and with serological evidence of atrophic gastritis, had a significantly shorter LTL than did those without atrophic gastritis.
Highlights
Persistent infections that induce prolonged inflammation might negatively affect the leukocyte telomere length (LTL); the role in LTL of Helicobacter pylori (H. pylori) infection, which persistently colonizes the stomach, remains unknown
Associations were reported of exposure to cytomegalovirus (CMV), herpes simplex virus type 1 (HSV-1), and human herpes virus 6 with greater LTL attrition in healthy adults [31], these associations were not affected by systemic non-specific inflammatory markers such as C-reactive protein and interleukin 6 [31]
Compared to participants who were H. pylori sero-negative without atrophic gastritis, those with past H. pylori infection and with atrophic gastritis had shorter LTL: beta coefficient − 0.21 kb, p = 0.049; the difference was not significant in H. pylori sero-positive persons either with (p = 0.10) or without atrophic gastritis (p = 0.3)
Summary
Persistent infections that induce prolonged inflammation might negatively affect the leukocyte telomere length (LTL); the role in LTL of Helicobacter pylori (H. pylori) infection, which persistently colonizes the stomach, remains unknown. The study objective was to examine associations of sero-prevalence of H. pylori immunoglobulin G (IgG) antibody and serum pepsinogens (PGs), as markers of atrophic gastritis, with LTL. While H. pylori cause chronic gastritis in almost all infected persons, some present with peptic ulcers and gastric cancer in adulthood, especially those infected with strains that express cytotoxin-associated gene A (CagA) virulence antigen (reviewed in [33, 34]). The objective of the current study was to examine associations of the sero-prevalence of H. pylori immunoglobulin G (IgG) antibody and serological evidence of atrophic gastritis with LTL in a general population sample
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