Journal of Leukocyte Biology eBioscience full spectrum cell analysis
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on December 1, 2005

Published online before print October 4, 2005
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0505253v1
78/6/1242    most recent
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Blackwell, C. C.
Right arrow Articles by Busuttil, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Blackwell, C. C.
Right arrow Articles by Busuttil, A.
© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0505253

Received for publication May 9, 2005.
Revised June 1, 2005.
Accepted for publication June 6, 2005.

Article

Cytokine responses and sudden infant death syndrome: genetic, developmental, and environmental risk factors

C. Caroline Blackwell *@, Sophia M. Moscovis *, Ann E. Gordon {dagger}, Osama M. Al Madani {dagger}, Sharron T. Hall *{ddagger}, Maree Gleeson *, Rodney J. Scott *{sect}, June Roberts-Thomson *{sect}, Donald M. Weir {dagger}, and Anthony Busuttil

*Faculty of Health, School of Biomedical Sciences, University of Newcastle, and Hunter Medical Research Institute, New South Wales, Australia; {ddagger}Immunology and {sect}Genetics, Hunter Area Pathology Service, John Hunter Hospital, New Lambton, New South Wales, Australia; and {dagger}Medical Microbiology and Forensic Medicine Unit, University of Edinburgh, United Kingdom

@ To whom correspondence should be addressed. E-mail: Caroline.Blackwell{at}newcastle.edu.au.


  Abstract

Despite the success of the campaigns to reduce the risk of sudden infant death syndrome (SIDS), it still remains the major cause of postneonatal mortality. The incidence of SIDS is higher among ethnic groups, in which there are also high incidences of serious infectious diseases. The risk factors for SIDS parallel those for susceptibility to infection, and recent data have provided evidence to support the mathematical model of the common bacterial toxin hypothesis. One current hypothesis for the etiology of SIDS is that the deaths are a result of overwhelming proinflammatory responses to bacterial toxins; as in inflammatory responses to sepsis, cytokines, induced by bacterial toxins, cause physiological changes leading to death. The genetic, developmental, and environmental risk factors for SIDS are reviewed in relation to colonization by potentially harmful bacteria and the inflammatory responses induced in the nonimmune infant to microorganisms or their products.

Key Words: cot deaths • bacterial toxins • ethnicity • cigarette smoke • gene polymorphisms




This article has been cited by other articles:


Home page
 Innate ImmunityHome page
J. Blood-Siegfried, C. Rambaud, A. Nyska, and D. R. Germolec
Evidence for infection, inflammation and shock in sudden infant death: parallels between a neonatal rat model of sudden death and infants who died of sudden infant death syndrome
Innate Immunity, June 1, 2008; 14(3): 145 - 152.
[Abstract] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
J. Zhao, K. D. Kim, X. Yang, S. Auh, Y.-X. Fu, and H. Tang
From the Cover: Hyper innate responses in neonates lead to increased morbidity and mortality after infection
PNAS, May 27, 2008; 105(21): 7528 - 7533.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2005 by the Society for Leukocyte Biology.