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Disease Markers
Volume 35 (2013), Issue 4, Pages 229–234
Research Article

CagA-Positive Helicobacter pylori Infection and Reduced Sperm Motility, Vitality, and Normal Morphology

1Department of Molecular and Developmental Medicine, University of Siena, Policlinico S. Maria alle Scotte, V. le Bracci, 53100 Siena, Italy
2Department of Medical and Surgical Sciences and Neurosciences, University of Siena, Policlinico S. Maria alle Scotte, V. le Bracci, 53100 Siena, Italy

Received 25 June 2013; Revised 20 August 2013; Accepted 26 August 2013

Academic Editor: Olav Lapaire

Copyright © 2013 E. Moretti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Helicobacter pylori (HP) infection, particularly when caused by strains expressing CagA, may be considered a concomitant cause of male and female reduced fertility. This study explored, in 87 HP-infected males, the relationship between infection by CagA-positive HP strains and sperm parameters. HP infection and CagA status were determined by ELISA and Western blotting; semen analysis was performed following WHO guidelines. The amino acid sequence of human enzymes involved in glycolysis and oxidative metabolism were “blasted” with peptides expressed by HP J99. Thirty-seven patients (42.5%) were seropositive for CagA. Sperm motility (18% versus 32%; ), sperm vitality (35% versus 48%; ) and the percentage of sperm with normal forms (18% versus 22%; ) in the CagA-positive group were significantly reduced versus those in the CagA-negative group. All the considered enzymes showed partial linear homology with HP peptides, but four enzymes aligned with four different segments of the same cag island protein. We hypothesize a relationship between infection by strains expressing CagA and decreased sperm quality. Potentially increased systemic levels of inflammatory cytokines that occur in infection by CagA-positive strains and autoimmune phenomena that involve molecular mimicry could explain the pathogenetic mechanism of alterations observed.