Skip to main content
Article thumbnail
Location of Repository

P2x7 purinergic receptors and extracellular ATP mediate apoptosis of human monocyte/macrophages infected with Mycobacterium tuberculosis reducing the intracellular bacterial viability

By PLACIDO R, AURICCHIO G, FALZINI F, BATTISTINI L, COLIZZI V, BRUNETTI E, F. DI VIRGILIO and MANCINO G

Abstract

Mycobacterium tuberculosis (MTB) is a monocyte/macrophage (M/M) parasite, which has developed several mechanisms to survive and multiply intracellularly. On the other hand, infected cells are engaged in the effort to reduce mycobacterial viability. On this ground, we report that MTB infection predisposes M/M to a pro-apoptotic ATP-based signalling, which is aimed at decreasing MTB replication. In fact, we show that mycobacterial infection leads to an increased expression of P2X(7) purinergic receptors, which is paralleled by intracellular accumulation and subsequent extracellular release of ATP by infected macrophages. Activation of this signal is conceived to induce apoptosis in MTB-infected cells, since blocking P2X(7) receptor by means of oxidized ATP (oATP) prevents MTB induced cell death. Finally, we show that an ATP stimulation of MTB-infected M/M, besides increasing cellular apoptosis, strongly enhances intracellular MTB killing, as evaluated through Colony Forming Unit assay, and such effect is subverted through oATP pulsing of infected cells. Taken together, our data indicate a role of P2X(7) purinergic receptors in MTB-induced M/M apoptosis, suggesting the existence of an autocrine/paracrine loop leading to apoptosis of infected M/M and the feasible protective role of ATP-triggered cell death in tuberculosis

Publisher: Academic Press Incorporated:6277 Sea Harbor Drive:Orlando, FL 32887:(800)543-9534, (407)345-4100, EMAIL: ap@acad.com, INTERNET: http://www.idealibrary.com, Fax: (407)352-3445
Year: 2006
OAI identifier: oai:iris.unife.it:11392/470428
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.idealibrary.com, (external link)
  • http://hdl.handle.net/11392/47... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.