Survival of Staphylococcus aureus Inside Neutrophils Contributes to Infection1 (original) (raw)

Journal Article

Hattie D Gresham ,

Research Service, Albuquerque Veterans Affairs Medical Center

,

Albuquerque, NM, 87108

Department of Molecular Genetics and Microbiology, University of New Mexico

,

Albuquerque, NM 87131

Address correspondence and reprint requests to Dr. Hattie D. Gresham, Department of Molecular Genetics and Microbiology, Room 379, Basic Biomedical Science Building, 915 Camino de Salud, University of New Mexico, Albuquerque, NM 87131-5276. E-mail address: [email protected]

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Jon H Lowrance ,

Research Service, Albuquerque Veterans Affairs Medical Center

,

Albuquerque, NM, 87108

Department of Molecular Genetics and Microbiology, University of New Mexico

,

Albuquerque, NM 87131

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Tony E Caver ,

Research Service, Albuquerque Veterans Affairs Medical Center

,

Albuquerque, NM, 87108

Department of Molecular Genetics and Microbiology, University of New Mexico

,

Albuquerque, NM 87131

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Bridget S Wilson ,

Department of Pathology, University of New Mexico

,

Albuquerque, NM 87131

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Ambrose L Cheung ,

Department of Microbiology, Dartmouth Medical School

,

Hanover, NH 03755

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Frederik P Lindberg

Departments of Infectious Diseases and Molecular Microbiology, Washington University School of Medicine

,

St. Louis, MO 63110

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Received:

25 October 1999

Accepted:

21 January 2000

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Hattie D Gresham, Jon H Lowrance, Tony E Caver, Bridget S Wilson, Ambrose L Cheung, Frederik P Lindberg, Survival of Staphylococcus aureus Inside Neutrophils Contributes to Infection, The Journal of Immunology, Volume 164, Issue 7, April 2000, Pages 3713–3722, https://doi.org/10.4049/jimmunol.164.7.3713
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Abstract

Neutrophils have long been regarded as essential for host defense against Staphylococcus aureus infection. However, survival of the pathogen inside various cells, including phagocytes, has been proposed as a mechanism for persistence of this microorganism in certain infections. Therefore, we investigated whether survival of the pathogen inside polymorphonuclear neutrophils (PMN) contributes to the pathogenesis of S. aureus infection. Our data demonstrate that PMN isolated from the site of infection contain viable intracellular organisms and that these infected PMN are sufficient to establish infection in a naive animal. In addition, we show that limiting, but not ablating, PMN migration into the site of infection enhances host defense and that repletion of PMN, as well as promoting PMN influx by CXC chemokine administration, leads to decreased survival of the mice and an increased bacterial burden. Moreover, a global regulator mutant of S. aureus (_sar_−) that lacks the expression of several virulence factors is less able to survive and/or avoid clearance in the presence of PMN. These data suggest that the ability of S. aureus to exploit the inflammatory response of the host by surviving inside PMN is a virulence mechanism for this pathogen and that modulation of the inflammatory response is sufficient to significantly alter morbidity and mortality induced by S. aureus infection.

Copyright © 2000 by The American Association of Immunologists

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