HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by ENGELICH, G. Articles by HARTSHORN, K. L. Search for Related Content PubMed PubMed Citation Articles by ENGELICH, G. Articles by HARTSHORN, K. L. Agricola Articles by ENGELICH, G. Articles by HARTSHORN, K. L.

Role of the respiratory burst in co-operative reduction in neutrophil survival by influenza A virus and Escherichia coli

Section of Hematology/Oncology, Department of Medicine and Pathology, Boston University School of Medicine, 650 Albany Street, Boston, MA 02218, USA

Corresponding author: Dr K. Hartshorn (e-mail: khartsho{at}bu.edu).

Received 26 June 2001; revised version received 17 Oct. 2001; accepted 6 Dec. 2001.

Abstract

Influenza A virus (IAV)-induced impairment of neutrophil function or survival may be a cause of bacterial superinfection of IAV-infected subjects. This study was performed to determine the mechanism through which the combination of IAV and Escherichia coli co-operatively reduces neutrophil survival. Neutrophil binding of annexin-V and caspase-3 activation was significantly increased by either IAV or E. coli, supporting the concept that the micro-organisms accelerate neutrophil apoptosis. The anti-apoptotic agent granulocyte-macrophage colony stimulating factor (GM-CSF) did not improve, but further reduced, survival of neutrophils treated with IAV and E. coli. As addition of E. coli resulted in greater neutrophil uptake of IAV and greater neutrophil respiratory burst responses to IAV, this study tested whether respiratory burst activation by IAV and E. coli contributes to reducing neutrophil survival. The cell-permeant NADPH oxidase inhibitor, diphenylene iodonium, significantly increased survival of neutrophils treated with either E. coli alone or the combination of IAV and E. coli. In contrast, catalase, which is not cell permeant, did not alter survival of E. coli- and IAV-treated neutrophils. Azide enhanced neutrophil hydrogen peroxide responses to IAV and E. coli, and reduced survival of these cells. These results indicate that co-operative induction of intracellular respiratory burst responses by IAV and E. coli mediates the reduced neutrophil survival caused by these pathogens in vitro.

This article has been cited by other articles:

				C. R. Baskin, A. Garcia-Sastre, T. M. Tumpey, H. Bielefeldt-Ohmann, V. S. Carter, E. Nistal-Villan, and M. G. Katze Integration of Clinical Data, Pathology, and cDNA Microarrays in Influenza Virus-Infected Pigtailed Macaques (Macaca nemestrina) J. Virol., October 1, 2004; 78(19): 10420 - 10432. [Abstract] [Full Text] [PDF]

				H. Scaife, Z. Woldehiwet, C. A. Hart, and S. W. Edwards Anaplasma phagocytophilum Reduces Neutrophil Apoptosis In Vivo Infect. Immun., April 1, 2003; 71(4): 1995 - 2001. [Abstract] [Full Text]