Artículo

Alvarez, M.E.; Bass, J.I.F.; Geffner, J.R.; Calotti, P.X.F.; Costas, M.; Coso, O.A.; Gamberale, R.; Vermeulen, M.E.; Salamone, G.; Martinez, D.; Tanos, T.; Trevani, A.S. "Neutrophil signaling pathways activated by bacterial DNA stimulation" (2006) Journal of Immunology. 177(6):4037-4046
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Abstract:

We have previously shown that bacterial DNA activates human neutrophils in a CpG-independent manner. In this study, we have characterized the signaling pathways involved in the activation mechanism. We found that p38 MAPK, ERK1/2, and JNK pathways, as well as the PI3K/Akt pathway, are activated by bacterial DNA. We also determined that bacterial DNA induces NF-κB and AP-1 activation. When analyzing the role of these pathways on neutrophil functions, we observed that up-regulation of CD11b triggered by bacterial DNA was decreased by pharmacological inhibitors of the p38 MAPK, ERK1/2, and JNK, whereas stimulation of IL-8 release was dependent on p38, ERK1/2, and NF-κB. Moreover, we found that IL-8 production was markedly enhanced by inhibition of JNK, suggesting that this pathway negatively modulates NF-κB-dependent transcription. We also observed that bacterial DNA stimulated IL-1R-associated kinase-1 kinase activity and its partial degradation. Finally, we determined that bacterial DNA stimulated CD11b up-regulation in TLR9 -/- but not in MyD88 -/- mouse neutrophils, supporting that bacterial DNA induces neutrophil activation through a TLR9-independent and MyD88-dependent pathway. Copyright © 2006 by The American Association of Immunologists, Inc.

Registro:

Documento: Artículo
Título:Neutrophil signaling pathways activated by bacterial DNA stimulation
Autor:Alvarez, M.E.; Bass, J.I.F.; Geffner, J.R.; Calotti, P.X.F.; Costas, M.; Coso, O.A.; Gamberale, R.; Vermeulen, M.E.; Salamone, G.; Martinez, D.; Tanos, T.; Trevani, A.S.
Filiación:Departamento de Inmunología, Instituto de Estudios Oncológicos Fundación Maissa, Academia Nacional de Medicina, Buenos Aires, Argentina
Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina
Laboratorio de Fisiología y Biología Molecular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Instituto de Investigaciones Médicas Alfredo Lanari, Buenos Aires, Argentina
Instituto de Investigaciones Hematológicas-Academia Nacional de Medicina, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina
Palabras clave:bacterial DNA; CD11b antigen; immunoglobulin enhancer binding protein; interleukin 1 receptor associated kinase 1; interleukin 8; mitogen activated protein kinase 1; mitogen activated protein kinase 3; mitogen activated protein kinase inhibitor; mitogen activated protein kinase p38; mitogen activated protein kinase p38 inhibitor; myeloid differentiation factor 88; phosphatidylinositol 3 kinase; protein kinase B; stress activated protein kinase; stress activated protein kinase inhibitor; toll like receptor 9; transcription factor AP 1; animal cell; animal experiment; article; controlled study; cytokine production; cytokine release; enzyme activation; enzyme activity; enzyme degradation; enzyme inhibition; gene; human; human cell; immunomodulation; leukocyte activation; male; mouse; myd88 gene; neutrophil; nonhuman; normal human; priority journal; signal transduction; tlr9 gene
Año:2006
Volumen:177
Número:6
Página de inicio:4037
Página de fin:4046
DOI: http://dx.doi.org/10.4049/jimmunol.177.6.4037
Título revista:Journal of Immunology
Título revista abreviado:J. Immunol.
ISSN:00221767
CODEN:JOIMA
CAS:interleukin 8, 114308-91-7; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; phosphatidylinositol 3 kinase, 115926-52-8; protein kinase B, 148640-14-6; stress activated protein kinase, 155215-87-5; toll like receptor 9, 352486-49-8, 390883-32-6
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00221767_v177_n6_p4037_Alvarez

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Citas:

---------- APA ----------
Alvarez, M.E., Bass, J.I.F., Geffner, J.R., Calotti, P.X.F., Costas, M., Coso, O.A., Gamberale, R.,..., Trevani, A.S. (2006) . Neutrophil signaling pathways activated by bacterial DNA stimulation. Journal of Immunology, 177(6), 4037-4046.
http://dx.doi.org/10.4049/jimmunol.177.6.4037
---------- CHICAGO ----------
Alvarez, M.E., Bass, J.I.F., Geffner, J.R., Calotti, P.X.F., Costas, M., Coso, O.A., et al. "Neutrophil signaling pathways activated by bacterial DNA stimulation" . Journal of Immunology 177, no. 6 (2006) : 4037-4046.
http://dx.doi.org/10.4049/jimmunol.177.6.4037
---------- MLA ----------
Alvarez, M.E., Bass, J.I.F., Geffner, J.R., Calotti, P.X.F., Costas, M., Coso, O.A., et al. "Neutrophil signaling pathways activated by bacterial DNA stimulation" . Journal of Immunology, vol. 177, no. 6, 2006, pp. 4037-4046.
http://dx.doi.org/10.4049/jimmunol.177.6.4037
---------- VANCOUVER ----------
Alvarez, M.E., Bass, J.I.F., Geffner, J.R., Calotti, P.X.F., Costas, M., Coso, O.A., et al. Neutrophil signaling pathways activated by bacterial DNA stimulation. J. Immunol. 2006;177(6):4037-4046.
http://dx.doi.org/10.4049/jimmunol.177.6.4037