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Published online before print October 4, 2005

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(Journal of Leukocyte Biology. 2005;78:1242-1254.)
© 2005 by Society for Leukocyte Biology

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

C. Caroline Blackwell^*,1, Sophia M. Moscovis^*, Ann E. Gordon, Osama M. Al Madani, Sharron T. Hall^*,, Maree Gleeson^*, Rodney J. Scott^*,, June Roberts-Thomson^*,, Donald M. Weir and Anthony Busuttil^¶

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

¹ Correspondence: HAPS Immunology, John Hunter Hospital, Lookout Road, New Lambton, NSW 2300, Australia. E-mail: Caroline.Blackwell{at}newcastle.edu.au

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

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