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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Immunol
2018 ; 9
(ä): 272
Nephropedia Template TP
gab.com Text
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Extracellular Vesicles Released from Mycobacterium tuberculosis-Infected
Neutrophils Promote Macrophage Autophagy and Decrease Intracellular Mycobacterial
Survival
#MMPMID29520273
Alvarez-Jiménez VD
; Leyva-Paredes K
; García-Martínez M
; Vázquez-Flores L
; García-Paredes VG
; Campillo-Navarro M
; Romo-Cruz I
; Rosales-García VH
; Castañeda-Casimiro J
; González-Pozos S
; Hernández JM
; Wong-Baeza C
; García-Pérez BE
; Ortiz-Navarrete V
; Estrada-Parra S
; Serafín-López J
; Wong-Baeza I
; Chacón-Salinas R
; Estrada-García I
Front Immunol
2018[]; 9
(ä): 272
PMID29520273
show ga
Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis (Mtb).
In the lungs, macrophages and neutrophils are the first immune cells that have
contact with the infecting mycobacteria. Neutrophils are phagocytic cells that
kill microorganisms through several mechanisms, which include the lytic enzymes
and antimicrobial peptides that are found in their lysosomes, and the production
of reactive oxygen species. Neutrophils also release extracellular vesicles (EVs)
(100-1,000?nm in diameter) to the extracellular milieu; these EVs consist of a
lipid bilayer surrounding a hydrophilic core and participate in intercellular
communication. We previously demonstrated that human neutrophils infected in
vitro with Mtb H37Rv release EVs (EV-TB), but the effect of these EVs on other
cells relevant for the control of Mtb infection, such as macrophages, has not
been completely analyzed. In this study, we characterized the EVs produced by
non-stimulated human neutrophils (EV-NS), and the EVs produced by neutrophils
stimulated with an activator (PMA), a peptide derived from bacterial proteins
(fMLF) or Mtb, and observed that the four EVs differed in their size. Ligands for
toll-like receptor (TLR) 2/6 were detected in EV-TB, and these EVs favored a
modest increase in the expression of the co-stimulatory molecules CD80, a higher
expression of CD86, and the production of higher amounts of TNF-? and IL-6, and
of lower amounts of TGF-?, in autologous human macrophages, compared with the
other EVs. EV-TB reduced the amount of intracellular Mtb in macrophages, and
increased superoxide anion production in these cells. TLR2/6 ligation and
superoxide anion production are known inducers of autophagy; accordingly, we
found that EV-TB induced higher expression of the autophagy-related marker LC3-II
in macrophages, and the co-localization of LC3-II with Mtb inside infected
macrophages. The intracellular mycobacterial load increased when autophagy was
inhibited with wortmannin in these cells. In conclusion, our results demonstrate
that neutrophils produce different EVs in response to diverse activators, and
that EV-TB activate macrophages and promote the clearance of intracellular Mtb
through early superoxide anion production and autophagy induction, which is a
novel role for neutrophil-derived EVs in the immune response to Mtb.
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