BioMed Research International
Volume 2015 (2015), Article ID 354519, 2 pages
http://dx.doi.org/10.1155/2015/354519

Letter to the Editor

Comment on “Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γ Signaling”

Amin Talebi Bezmin Abadi¹ and Enzo Ierardi²

¹Department of Bacteriology, Faculty of Medical Sciences, Tarbiat Modares University, P.O. Box 14115-111, Tehran, Iran
²Division of Gastroenterology, Department of Emergency and Organ Transplantation, Piazza Giulio Cesare, 70124 Bari, Italy

Received 12 November 2014; Accepted 27 November 2014

Academic Editor: Hidekazu Suzuki

Copyright © 2015 Amin Talebi Bezmin Abadi and Enzo Ierardi. 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.

We read with interest the paper by Shan et al. [1] in a recent issue. It is an interesting paper concluding that Helicobacter pylori (H. pylori) omp18 is indirectly affecting long term bacterial colonization by successfully influencing IFN-γ-mediated immune response. Nevertheless, we found that some statements could not support the final conclusion. H. pylori infects the gastric mucosal layer of half of the human population worldwide and causes various digestive disorders such as chronic gastritis, gastric ulcer, duodenal ulcer, and gastric cancer [2]. To date, it has been established that such complex mechanism of bacterial interaction with human host can shape the successful and persistent colonization of H. pylori [3, 4]. Undoubtedly, understanding the mechanisms of immune evasion could provide new options for better management of infection. To our knowledge, the host immune response to the infection is ineffective; accordingly, the bacterium persists and remains for decades. In brief, Shan et al. [1] reported the oipA as a critical factor affecting bacterial colonization. However, we know that, in chronic process of colonization adopted by H. pylori, the connection of a unique factor to the drive of the final pattern of this phenomenon could be too speculative. Despite the interesting report of Shan et al. [1], we may hypothesize more factors involved in H. pylori colonization. Surprisingly, H. pylori colonization is not comparable with that of other pathogens [5]. Indeed, different mechanisms are contributing to this mysterious and long term biologic function. Conclusively, more studies are necessary to draw a direct and final conclusion on “the mystery” of H. pylori colonization.

Disclaimer

The contents of the paper are the sole responsibility of the authors and do not necessarily represent the official views of any institute or organization.

Conflict of Interests

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interests.

References

Y. Shan, X. Lu, Y. Han et al., “Helicobacter pylori outer membrane protein 18 (Hp1125) is involved in persistent colonization by evading interferon- signaling,” BioMed Research International, vol. 2014, Article ID 571280, 12 pages, 2014.

A. Sheh and J. G. Fox, “The role of the gastrointestinal microbiome in Helicobacter pylori pathogenesis,” Gut Microbes, vol. 4, no. 6, pp. 505–531, 2013.

A. T. B. Abadi, “Helicobacter pylori: a beneficial gastric pathogen?” Gastroenterology, vol. 1, article 26, 2014.

A. T. B. Abadi, “Therapy of helicobacter pylori: present medley and future prospective,” BioMed Research International, vol. 2014, Article ID 124607, 7 pages, 2014.

R. Bücker, M. Azevedo-Vethacke, C. Groll et al., “Helicobacter pylori colonization critically depends on postprandial gastric conditions,” Scientific Reports, vol. 2, article 994, 2012.