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Mediators of Inflammation
Volume 2015, Article ID 124762, 11 pages
http://dx.doi.org/10.1155/2015/124762
Research Article

Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response

1Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA
2Institute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland
3Department of Immunology and Infectious Biology, University of Lodz, 90-237 Lodz, Poland
4Department of Immunoparasitology, University of Lodz, 90-237 Lodz, Poland
5Department of Immunobiology of Bacteria, University of Lodz, 90-237 Lodz, Poland
6Department of Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45219, USA
7Department of Medicine, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA

Received 29 September 2014; Revised 7 January 2015; Accepted 7 February 2015

Academic Editor: Kiriakos Karkoulias

Copyright © 2015 Agnieszka Krupa 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.

Abstract

Interleukin-8 (IL-8) has been implicated in the pathogenesis of several human respiratory diseases, including tuberculosis (TB). Importantly and in direct relevance to the objectives of this report quite a few findings suggest that the presence of IL-8 may be beneficial for the host. IL-8 may aid with mounting an adequate response during infection with Mycobacterium tuberculosis (M. tb); however, the underlying mechanism remains largely unknown. The major goal of our study was to investigate the contribution of IL-8 to the inflammatory processes that are typically elicited in patients with TB. We have shown for the first time that IL-8 can directly bind to tubercle bacilli. We have also demonstrated that association of IL-8 with M. tb molecules leads to the augmentation of the ability of leukocytes (neutrophils and macrophages) to phagocyte and kill these bacilli. In addition, we have shown that significant amount of IL-8 present in the blood of TB patients associates with erythrocytes. Finally, we have noted that IL-8 is the major chemokine responsible for recruiting T lymphocytes (CD3+, CD4+, and CD8+ T cells). In summary, our data suggest that the association of IL-8 with M. tb molecules may modify and possibly enhance the innate immune response in patients with TB.