Document Detail

Mycobacterium tuberculosis-induced neutrophil ectosomes decrease macrophage activation.
MedLine Citation:
PMID:  22391089     Owner:  NLM     Status:  Publisher    
BACKGROUND: The existence of ectosome-like microvesicles released by neutrophils was proposed a few decades ago. Other studies revealed that the innate immune response during mycobacterial infection is accompanied by an intense migration of neutrophils to the site of infection, which may be important during the acute phase of tuberculosis. We found that the ectosomes derived from infected neutrophils are biologically active and can influence the survival of Mycobacterium tuberculosis within macrophages. METHODS: Mycobacteria were cultured on supplemented Middlebrook-7H9 broth. All strains were grown to the exponential phase and quantitated by serial dilution. Human neutrophils and macrophages were infected with mycobacteria. Ectosomes from neutrophils were isolated post-infection and characterized by transmission electron microscopy and flow cytometry. To determine whether these microvesicles influenced mycobactericidal activity, mycobacteria-infected macrophages were treated with isolated ectosomes. RESULTS: Ectosomes were released from neutrophils infected with mycobacteria. These ectosomes were derived from neutrophil plasma membrane and a small proportion stained with PKH26. These microvesicles, when incubated with infected macrophages, influenced antimycobacterial activity. CONCLUSIONS: This is the first study to demonstrate that ectosomes that are shed from infected neutrophils influence mycobactericidal activity in macrophages in vitro, suggesting that these microvesicles have biological significance. Nevertheless, major gaps in our knowledge of microvesicle biology remain.
Tonya Azevedo Duarte; Alberto Augusto Noronha-Dutra; Joilda Silva Nery; Samantha Brum Ribeiro; Thassila Nogueira Pitanga; José R Lapa E Silva; Sérgio Arruda; Neio Boéchat
Related Documents :
22837699 - Role of microglia in oxidative toxicity associated with encephalomycarditis virus infec...
23956759 - Il-17a and th17 cells in lung inflammation: an update on the role of th17 cell differen...
23691219 - Cytomegalovirus impairs the induction of indoleamine 2,3-dioxygenase mediated antimicro...
23942009 - Deep sequencing-based identification of pathogen-specific micrornas in the plasma of ra...
22440399 - Black yeast-like fungi associated with lethargic crab disease (lcd) in the mangrove-lan...
22875029 - Case study: treating an infected wound of unknown aetiology.
23185469 - Multiple-clone activation of hypnozoites is the leading cause of relapse in plasmodium ...
3134769 - Suitability of in-vitro xenodiagnosis: development of trypanosoma cruzi in triatoma inf...
2200549 - Interaction of penetrating missiles with tissues: some common misapprehensions and impl...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-3-3
Journal Detail:
Title:  Tuberculosis (Edinburgh, Scotland)     Volume:  -     ISSN:  1873-281X     ISO Abbreviation:  -     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-3-6     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100971555     Medline TA:  Tuberculosis (Edinb)     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
Health Science Institute, Federal University of Bahia, Salvador, BA, Brazil; Multidisciplinary Research Laboratory, Clementino Fraga Filho University Hospital, Department of Internal Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Global and disease-specific health-related quality of life after complete endoscopic resection of an...
Next Document:  Macrophage immunomodulatory activity of extracellular polysaccharide (PEP) of Antarctic bacterium Ps...