From Anna Kurdowska and colleagues: Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response

Mediators Inflamm. 2015;2015:124762. doi: 10.1155/2015/124762. Epub 2015 Aug 2.

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

Krupa A1, Fol M2, Dziadek BR3, Kepka E2, Wojciechowska D2, Brzostek A4, Torzewska A5, Dziadek J4, Baughman RP6, Griffith D7, Kurdowska AK8.

Author information

• 1Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA ; Institute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland.
• 2Department of Immunology and Infectious Biology, University of Lodz, 90-237 Lodz, Poland.
• 3Department of Immunoparasitology, University of Lodz, 90-237 Lodz, Poland.
• 4Institute of Medical Biology, Polish Academy of Sciences, 93-232 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.
• 8Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.

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.