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Denise Kviatcovsky [1] and Leonardo Rivadeneyra [1] and Luciana Balboa [1] and Noemí Yokobori [1] and Beatriz López [2] and Viviana Ritacco [2] and Mirta Schattner [1] and María del Carmen Sasiain [1] and Silvia de la Barrera [1]

Academic Editor: Yona Keisari

1, Instituto de Medicina Experimental-CONICET-Academia Nacional de Medicina, Buenos Aires, Argentina, acamedbai.org.ar

2, Instituto Nacional de Enfermedades Infecciosas, ANLIS Carlos G. Malbrán, Buenos Aires, Argentina, anlis.gov.ar

Received Feb 23, 2017; Revised Jun 22, 2017; Accepted Jul 2, 2017

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.

1. Introduction

Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB) is transmitted via inhalation of aerosolized particles. Once inhaled, Mtb mainly infects alveolar macrophages as well as nonphagocytic cells lining the alveolar barrier such as M cells, endothelial cells, type II alveolar epithelial cells, and small airway epithelial cells as demonstrated in in vitro infection experiments [1, 2]. Besides, Mtb DNA has been isolated from bronchial epithelium of Mtb latently infected humans and mice suggesting that mycobacteria can persist intracellularly in nonphagocytic cells from lung tissue even in the absence of histological evidence of immune response [3].

Airway epithelium responds to pathogens by producing antimicrobial molecules, proinflammatory cytokines such as interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), and chemokines (IL-8, eotaxin, and macrophage chemoattractant protein-1) which recruit cells belonging to the innate immunity such as macrophages, dendritic cells, and neutrophils (PMN) in order to mount an inflammatory response and control early stages of infection [4, 5].

PMN are the first inflammatory cells that arrive to the site of infection and control microbial infections [6]. Their killing systems are highly efficient and multilayered, including secretion of hydrolytic enzymes contained in granules and antimicrobial peptides, release of neutrophil extracellular traps (NETs), and reactive oxygen species (ROS) production [7]. After phagocytosis, the major neutrophil intracellular killing mechanism is the phagosome-lysosome fusion. In humans, PMN represent the most abundant cell population harboring Mtb in bronchoalveolar lavage and sputum samples from patients with active TB [8, 9]. However, the impact of the lung environment on PMN-innate responses during mycobacterial...

         

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