This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bonner, S.
Right arrow Articles by Bortolussi, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bonner, S.
Right arrow Articles by Bortolussi, R.

 Previous Article  |  Next Article 

Infection and Immunity, May 2001, p. 3143-3149, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3143-3149.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Activation of Extracellular Signal-Related Protein Kinases 1 and 2 of the Mitogen-Activated Protein Kinase Family by Lipopolysaccharide Requires Plasma in Neutrophils from Adults and Newborns

S. Bonner,1 S. R. Yan,1 D. M. Byers,1,2 and R. Bortolussi1,3,*

Departments of Pediatrics,1 Microbiology and Immunology,3 and Biochemisty and Molecular Biology,2 Dalhousie University and IWK Grace Health Centre, Halifax, Nova Scotia, Canada

Received 5 October 2000/Returned for modification 20 December 2000/Accepted 21 February 2001

Neutrophils exposed to low concentrations of gram-negative lipopolysaccharide (LPS) become primed and have an increased oxidative response to a second stimulus (e.g., formyl-methionyl-leucyl-phenylalanine [fMLP]). In studies aimed at understanding newborn sepsis, we have shown that neutrophils of newborns are not primed in response to LPS. To further understand the processes involved in LPS-mediated priming of neutrophils, we explored the role of extracellular signal-related protein kinases (ERK 1 and 2) of the mitogen-activated protein kinase family. We found that LPS activated ERK 1 and 2 in cells of both adults and newborns and that activation was plasma dependent (maximal at >= 5%) through LPS-binding protein. Although fibronectin in plasma is required for LPS-mediated priming of neutrophils of adults assessed by fMLP-triggered oxidative burst, it was not required for LPS-mediated activation of ERK 1 and 2. LPS-mediated activation was dose and time dependent; maximal activation occurred with approximately 5 ng of LPS per ml and at 10 to 40 min. We used the inhibitor PD 98059 to study the role of ERK 1 and 2 in the LPS-primed fMLP-triggered oxidative burst. While Western blotting showed that 100 µM PD 98059 completely inhibited LPS-mediated ERK activation, oxidative response to fMLP by a chemiluminescence assay revealed that the same concentration inhibited the LPS-primed oxidative burst by only 40%. We conclude that in neutrophils, LPS-mediated activation of ERK 1 and 2 requires plasma and that this activation is not dependent on fibronectin. In addition, we found that the ERK pathway is not responsible for the lack of LPS priming in neutrophils of newborns but may be required for 40% of the LPS-primed fMLP-triggered oxidative burst in cells of adults.

* Corresponding author. Mailing address: 8th Floor East Research Laboratories, IWK Heath Centre, 5850 University Ave., Halifax, Nova Scotia B3J 3G9, Canada. Phone: (902) 428-8498. Fax: (902) 428-3217. E-mail: Robert.Bortolussi{at}DAL.ca.

Infection and Immunity, May 2001, p. 3143-3149, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3143-3149.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Kanayama, S., Yamada, Y., Onogi, A., Shigetomi, H., Ueda, S., Tsuji, Y., Haruta, S., Kawaguchi, R., Yoshida, S., Sakata, M., Sado, T., Kitanaka, T., Oi, H., Yagyu, T., Kobayashi, H. (2007). Bikunin suppresses expression of pro-inflammatory cytokines induced by lipopolysaccharide in neutrophils. Innate Immunity 13: 369-376 [Abstract]  
  • Yan, S. R., Joseph, R. R., Wang, J., Stadnyk, A. W. (2006). Differential Pattern of Inflammatory Molecule Regulation in Intestinal Epithelial Cells Stimulated with IL-1. J. Immunol. 177: 5604-5611 [Abstract] [Full Text]  
  • Lin, K.-I, Kao, Y.-Y., Kuo, H.-K., Yang, W.-B., Chou, A., Lin, H.-H., Yu, A. L., Wong, C.-H. (2006). Reishi Polysaccharides Induce Immunoglobulin Production through the TLR4/TLR2-mediated Induction of Transcription Factor Blimp-1. J. Biol. Chem. 281: 24111-24123 [Abstract] [Full Text]  
  • Yan, S. R., Byers, D. M., Bortolussi, R. (2004). Role of Protein Tyrosine Kinase p53/56lyn in Diminished Lipopolysaccharide Priming of Formylmethionylleucyl- phenylalanine-Induced Superoxide Production in Human Newborn Neutrophils. Infect. Immun. 72: 6455-6462 [Abstract] [Full Text]  
  • Weiss, T., Shalit, I., Blau, H., Werber, S., Halperin, D., Levitov, A., Fabian, I. (2004). Anti-Inflammatory Effects of Moxifloxacin on Activated Human Monocytic Cells: Inhibition of NF-{kappa}B and Mitogen-Activated Protein Kinase Activation and of Synthesis of Proinflammatory Cytokines. Antimicrob. Agents Chemother. 48: 1974-1982 [Abstract] [Full Text]  
  • Yan, S. R., Qing, G., Byers, D. M., Stadnyk, A. W., Al-Hertani, W., Bortolussi, R. (2004). Role of MyD88 in Diminished Tumor Necrosis Factor Alpha Production by Newborn Mononuclear Cells in Response to Lipopolysaccharide. Infect. Immun. 72: 1223-1229 [Abstract] [Full Text]  
  • Asehnoune, K., Strassheim, D., Mitra, S., Kim, J. Y., Abraham, E. (2004). Involvement of Reactive Oxygen Species in Toll-Like Receptor 4-Dependent Activation of NF-{kappa}B. J. Immunol. 172: 2522-2529 [Abstract] [Full Text]  
  • Yan, S. R., Al-Hertani, W., Byers, D., Bortolussi, R. (2002). Lipopolysaccharide-Binding Protein- and CD14-Dependent Activation of Mitogen-Activated Protein Kinase p38 by Lipopolysaccharide in Human Neutrophils Is Associated with Priming of Respiratory Burst. Infect. Immun. 70: 4068-4074 [Abstract] [Full Text]  
  • Pilette, C., Ouadrhiri, Y., Van Snick, J., Renauld, J.-C., Staquet, P., Vaerman, J.-P., Sibille, Y. (2002). IL-9 Inhibits Oxidative Burst and TNF-{alpha} Release in Lipopolysaccharide-Stimulated Human Monocytes Through TGF-{beta}. J. Immunol. 168: 4103-4111 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»