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J. Clin. Med. 2017, 6(2), 15; doi:10.3390/jcm6020015

Effector Mechanisms of Neutrophils within the Innate Immune System in Response to Mycobacterium tuberculosis Infection

1
Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, 309 East Second Street, Pomona, CA 91766-1854, USA
2
Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766-1854, USA
*
Author to whom correspondence should be addressed.
Academic Editors: Christophe Dubois and Laurence Panicot-Dubois
Received: 5 August 2016 / Revised: 24 January 2017 / Accepted: 3 February 2017 / Published: 7 February 2017
(This article belongs to the Special Issue Neutrophil Functions: From Immunity to Disease)
View Full-Text   |   Download PDF [496 KB, uploaded 7 February 2017]   |  

Abstract

Neutrophils have a significant yet controversial role in the innate immune response to Mycobacterium tuberculosis (M. tb) infection, which is not yet fully understood. In addition to neutrophils’ well-known effector mechanisms, they may also help control infection of M. tb through the formation of neutrophil extracellular traps (NETs), which are thought to further promote the killing of M. tb by resident alveolar macrophages. Cytokines such as IFN-γ have now been shown to serve an immunomodulatory role in neutrophil functioning in conjunction to its pro-inflammatory function. Additionally, the unique transcriptional changes of neutrophils may be used to differentiate between infection with M. tb and other bacterial and chronic rheumatological diseases such as Systemic Lupus Erythematosus. Adversely, during the innate immune response to M. tb, inappropriate phagocytosis of spent neutrophils can result in nonspecific damage to host cells due to necrotic lysis. Furthermore, some individuals have been shown to be more genetically susceptible to tuberculosis (TB) due to a “Trojan Horse” phenomenon whereby neutrophils block the ability of resident macrophages to kill M. tb. Despite these aforementioned negative consequences, through the scope of this review we will provide evidence to support the idea that neutrophils, while sometimes damaging, can also be an important component in warding off M. tb infection. This is exemplified in immunocompromised individuals, such as those with human immunodeficiency virus (HIV) infection or Type 2 diabetes mellitus. These individuals are at an increased risk of developing tuberculosis (TB) due to a diminished innate immune response associated with decreased levels of glutathione. Consequently, there has been a worldwide effort to limit and contain M. tb infection through the use of antibiotics and vaccinations. However, due to several significant limitations, the current bacille Calmette-Guerin vaccine (BCG, vaccine against TB) does not meet the criteria for universal utilization for all ages and populations across the globe. New research involving neutrophils has yielded a new vaccine called M. smegmatis-Ag85C-MPT51-HspX (mc2-CMX) that has been shown to elicit a humoral and cellular response against M. tb in mice that is superior to the BCG vaccine. View Full-Text
Keywords: Tuberculosis; TB; Mycobacterium tuberculosis; M. tb; polymorphonuclear leukocytes; PMN; Neutrophils; Innate immunity; NETs; Cytokines; Phagocytosis-induced cell death Tuberculosis; TB; Mycobacterium tuberculosis; M. tb; polymorphonuclear leukocytes; PMN; Neutrophils; Innate immunity; NETs; Cytokines; Phagocytosis-induced cell death
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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. (CC BY 4.0).

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Warren, E.; Teskey, G.; Venketaraman, V. Effector Mechanisms of Neutrophils within the Innate Immune System in Response to Mycobacterium tuberculosis Infection. J. Clin. Med. 2017, 6, 15.

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