Repression of rac2 mRNA Expression by Anaplasma phagocytophila Is Essential to the Inhibition of Superoxide Production and Bacterial Proliferation
In: The Journal of Immunology, Jg. 169 (2002-12-15), S. 7009-7018
Online
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Zugriff:
Anaplasma phagocytophila, the etiologic agent of human granulocytic ehrlichiosis, is an emerging bacterial pathogen that invades neutrophils and can be cultivated in HL-60 cells. Infected neutrophils and HL-60 cells fail to produce superoxide anion (O2−), which is partially attributable to the fact that A. phagocytophila inhibits transcription of gp91phox, an integral component of NADPH oxidase. cDNA microarray and RT-PCR analyses demonstrated that transcription of the gene encoding Rac2, a key component in NADPH oxidase activation, was down-regulated in infected HL-60 cells. Quantitative RT-PCR demonstrated that rac2 mRNA expression was reduced 7-fold in retinoic acid-differentiated HL-60 cells and 50-fold in neutrophils following A. phagocytophila infection. Rac2 protein expression was absent in infected HL-60 cells. Rac1 and Rac2 are interchangeable in their abilities to activate NADPH oxidase. HL-60 cells transfected to express myc-tagged rac1 and gp91phox from the CMV immediate early promoter maintained the ability to generate O2− 120 h postinfection. A. phagocytophila proliferation was severely inhibited in these cells. These results directly attribute the inhibition of rac2 and gp91phox transcription to the loss of NADPH oxidase activity in A. phagocytophila-infected cells and demonstrate its importance to bacterial intracellular survival.
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Repression of rac2 mRNA Expression by Anaplasma phagocytophila Is Essential to the Inhibition of Superoxide Production and Bacterial Proliferation
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Autor/in / Beteiligte Person: | Chan, Wai-Tsing ; Galán, Jorge E. ; Carlyon, Jason A. ; Fikrig, Erol ; Roos, Dirk ; Laboratory, Landsteiner |
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Zeitschrift: | The Journal of Immunology, Jg. 169 (2002-12-15), S. 7009-7018 |
Veröffentlichung: | The American Association of Immunologists, 2002 |
Medientyp: | unknown |
ISSN: | 1550-6606 (print) ; 0022-1767 (print) |
DOI: | 10.4049/jimmunol.169.12.7009 |
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