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 Cockeran, R.
Right arrow Articles by Anderson, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cockeran, R.
Right arrow Articles by Anderson, R.

 Previous Article  |  Next Article 

Infection and Immunity, May 2001, p. 3494-3496, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3494-3496.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Pneumolysin Potentiates Production of Prostaglandin E2 and Leukotriene B4 by Human Neutrophils

Riana Cockeran,1 Helen C. Steel,1 Timothy J. Mitchell,2 Charles Feldman,3 and Ronald Anderson1,*

Medical Research Council Unit for Inflammation and Immunity, Department of Immunology, Institute for Pathology, University of Pretoria, Pretoria,1 and Division of Pulmonology, Johannesburg Hospital and University of the Witwatersrand, Johannesburg,3 South Africa, and Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, Scotland2

Received 16 January 2001/Returned for modification 5 February 2001/Accepted 22 February 2001

Exposure to pneumolysin (8.37 and 41.75 ng/ml) caused a calcium-dependent increase in the generation of prostaglandin E2 and leukotriene B4 by both resting and chemoattractant-activated human neutrophils in vitro. These interactions of pneumolysin with neutrophils may result in dysregulation of inflammatory responses during pneumococcal infection.


* Corresponding author. Mailing address: Institute for Pathology, P.O. Box 2034, Pretoria 0001, South Africa. Phone: 27-12-319 2425. Fax: 27-12-323 0732. E-mail: randerso{at}postillion.up.ac.za or rcockera{at}postillion.up.ac.za.


Infection and Immunity, May 2001, p. 3494-3496, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3494-3496.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Ratner, A. J., Hippe, K. R., Aguilar, J. L., Bender, M. H., Nelson, A. L., Weiser, J. N. (2006). Epithelial Cells Are Sensitive Detectors of Bacterial Pore-forming Toxins. J. Biol. Chem. 281: 12994-12998 [Abstract] [Full Text]  
  • Thornton, J., McDaniel, L. S. (2005). THP-1 Monocytes Up-Regulate Intercellular Adhesion Molecule 1 in Response to Pneumolysin from Streptococcus pneumoniae. Infect. Immun. 73: 6493-6498 [Abstract] [Full Text]  
  • Cockeran, R., Theron, A. J., Feldman, C., Mitchell, T. J., Anderson, R. (2004). Docosahexaenoic Acid and Eicosapentaenoic Acid Antagonize the Proinflammatory Interactions of Pneumolysin with Human Neutrophils. Infect. Immun. 72: 4327-4329 [Abstract] [Full Text]  
  • Spreer, A., Kerstan, H., Bottcher, T., Gerber, J., Siemer, A., Zysk, G., Mitchell, T. J., Eiffert, H., Nau, R. (2003). Reduced Release of Pneumolysin by Streptococcus pneumoniae In Vitro and In Vivo after Treatment with Nonbacteriolytic Antibiotics in Comparison to Ceftriaxone. Antimicrob. Agents Chemother. 47: 2649-2654 [Abstract] [Full Text]  
  • Baba, H., Kawamura, I., Kohda, C., Nomura, T., Ito, Y., Kimoto, T., Watanabe, I., Ichiyama, S., Mitsuyama, M. (2002). Induction of Gamma Interferon and Nitric Oxide by Truncated Pneumolysin That Lacks Pore-Forming Activity. Infect. Immun. 70: 107-113 [Abstract] [Full Text]