From: Putative roles of purinergic signaling in human immunodeficiency virus-1 infection
Microorganism | Receptor | Cell type | Involvement | Reference |
---|---|---|---|---|
Bacteria | ||||
M. tuberculosis | ND | monocyte | ATP induced apoptosis of infected monocyte and reduced viability of intracellular bacilli | [97] |
BCG | P2X7 | Human macrophage | Treatment with exogenous ATP caused cell death and killing of intracellular mycobacteria within BCG infected macrophages | [98] |
M. tuberculosis | P2X7 | Human macrophage | Treatment with ATP reduced viability of three virulent strains of mycobacteria within human macrophages, what was associated with stimulation of phospholipase D activity | [99] |
BCG | P2X7 and P2Y | Human macrophage | Apoptosis of infected cells and killing of intracellular bacilli | [100] |
M.bovis | P2X7 | Bovine macrophage | ATP induced killing Mycobacterium bovis in bovine macrophages in a mechanism P2X7R-dependent | [101] |
BCG | P2X7 | Murine bone-marrow derived macrophages and murine macrophage cell line | P2X7R stimulation with ATP induced rapid fusion of BCG-containing phagosomes with lysosomes, resulting in formation of multibacillary vacuoles. Also, P2X7R resulted in progressive acidification of BCG-containing phagosomes in infected macrophages | [102] |
BCG | P2X7 | Human macrophage | Loss-of-function polymorphism 1513A → C abolished apoptosis of infected macrophages and mycobacterial killing | [103] |
BCG | P2X7 | Human macrophage | The 1513C allele was associated to increased susceptibility to extracellular TB and ATP-mediated killing of mycobacteria in macrophages was absent in homozygous subjects and impaired in heterozygous subjects | [104] |
BCG | P2X7 | Human macrophage | Loss-of-function polymorphism 1096C → G (change Thr(357) to Ser (T357S)) associated to reduced or near to absent ATP-induced killing of intracellular mycobacteria | [105] |
M. tuberculosis | P2X7 | Human PBMC | PBMC from TB patients presented different pattern of gene expression in response to ATP when compared to healthy contacts | [106] |
M. tuberculosis | P2X7 | Human monocyte/macrophages | Mycobacterial infection induced an increase of P2X7 expression, higher release of ATP and an increment of intracellular ATP accumulation | [107] |
BCG | P2X7 | THP-1 and monocyte-derived macrophage | ATP treatment activated autophagy pathway via a Ca2 + -dependent process. This effect was associated with a phago-lysosomal fusion and of mycobacteria-containing phagosomes, resulting in reduction in intracellular BCG viability | [108] |
C. psittaci | P2X7 | Murine macrophage cell line | ATP but no other nucleotides was able to induce reduction in viability of intracellular bacteria and chlamydial infection prevented ATP-mediated apoptosis | [109] |
C. trachomatis | P2X7 | Murine peritoneal macrophage cells and macrophage cell line | Chlamydial killing upon ATP treatment of infected cells required phospholipase D activation, which is mediated by P2X7R stimulation that leads to lysosome fusion with mature Chlamydia vacuoles | [110] |
C. muridarum, | P2X7 | Human cervical adenocarcinoma cell line | Extracellular ATP or other P2X7R agonists induced a decrease in chlamydial viability in epithelial cells, which was dependent on phospholipase D activity and blocked by treatment with P2X7R antagonists and butan-1-ol (PLD inhibitor). Also, vaginal infection was more efficient in P2X7R-deficient mice, what was correlated to higher level of acute inflammation | [111] |
Protozoan | ||||
L. amazonensis | P2X7 | Murine macrophage cell line | Native and recombinant Leishmania nucleoside diphosphate kinase (NdK) prevented ATP-induced cell death | [112] |
L. amazonensis | P2X7 | Murine peritoneal macrophage | Leishmania infection leads to increased expression of P2X7R and higher responsiveness to ATP treatment. Also, incubation with ATP reduced the parasite load, which was reverted by pre-treatment with oxidized ATP and was not not dependent of cell lysis or NO production | [113] |
L. amazonensis | P2X7 | Murine peritoneal macrophage | Macrophages infected with L. amazonensis exhibit higher apoptosis rate and parasite degradation upon ATP treatment and presented differential modulation of the uptake of cationic and anionic dyes | [114] |
L. amazonensis | P2Y | Murine peritoneal macrophage | Uridine nucleotides reduced parasite load and induced morphological damage of intracellular parasites and infected cells. They also induced significant levels of apoptosis, ROI and RNI in infected cells. | [115] |
T. gondii | P2X7 | Murine peritoneal cell and macrophage cell line | ATP or BzATP treatment reduced parasite load. Parasite load was not reduced in P2X7R-deficient mouse. Furthermore, ATP treatment caused ultrastructural changes in tachyzoite inside macrophages, increased lysosome fusion with parasitophorous vacuole and ROS production | [116] |
T. gondii | P2X7 | Human macrophage and murine bone marrow-derived macrophage and macrophage-like cell line | Infected macrophages obtained from homozygous individuals for loss-of-function polymorphism 1513A → C had no significant alteration in parasite load after ATP treatment. Similarly, macrophages from P2X7R knockout mice were not able to kill T. gondii upon ATP treatment | [117] |
T. gondii | P2X7 | Human Peripheral blood cells | SNP 1068T→C was found positively associated with resistance to both congenital and ocular toxoplasmosis | [118] |
T. gondii | P2X7 | Murine peritoneal cell | In vivo infection of P2X7-deficient mouse resulted in a more severe acute infection, higher parasite burdens and pronounced liver pathology | [119] |