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  • Open Access

An in silico study on molecular level interactions of host Siderocalin with siderophores from Mycobacterium tuberculosis and other bacterial species

BMC Infectious Diseases201414(Suppl 3):O15

https://doi.org/10.1186/1471-2334-14-S3-O15

Published: 27 May 2014

Keywords

  • Mycobacterium Tuberculosis
  • Burkholderia Cepacia
  • Iron Acquisition
  • Host Macrophage
  • Docking Tool

Background

Tuberculosis (TB) drug research and development has witnessed resurgence in recent times primarily due to the high mortality rates despite the availability of front line drugs and a prominent BCG vaccine. Synergy of TB with HIV is another factor which has warranted a search for newer therapeutic interventions. Treatment of latent TB infection is also the need of the hour. Iron acquisition is an important virulence mechanism of Mycobacterium tuberculosis (MTB). To scavenge iron, bacterial species have developed high affinity, low molecular weight iron chelators termed as siderophores. To counteract the detrimental effect of microbial iron acquisition systems, the host secretes a 21kDa lipocalin protein (Siderocalin) that binds with these iron laden siderophores in an attempt to restrict the growth of MTB within host macrophages.

Methods

In the current study, using molecular docking tools, we assessed the interactions of host Siderocalin with Mycobactin, Parabactin and Cepabactin structurally non similar siderophores from three different bacterial species-MTB, Paracoccus and Burkholderia cepacia. A comparison of molecular level interactions of Siderocalin with these siderophores was performed.

Results

Siderocalin forms energetically favourable and stable complexes with parabactin and cepabactin. However the unfavourable positive binding energies for mycobactin- a salicylate derived MTB siderophore indicated that siderocalin does not dock well with mycobactin.

Conclusion

Siderocalin probably fails to disrupt the role of mycobactin in acquiring iron for mycobacteria thereby helping the pathogen to survive leading to progression of disease.

Authors’ Affiliations

(1)
Centre for Biotechnology, Anna University, Chennai, India

Copyright

© Goyal and Anishetty; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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