Is there any correlation between HLA-DR expression in laryngeal mucosa and interleukin gene variation in sudden infant death syndrome?
Article first published online: 27 DEC 2012
©2012 The Author(s)/Acta Pædiatrica ©2012 Foundation Acta Pædiatrica
Volume 102, Issue 3, pages 308–313, March 2013
How to Cite
Ferrante, L., Opdal, S. H., Vege, Å. and Rognum, T. O. (2013), Is there any correlation between HLA-DR expression in laryngeal mucosa and interleukin gene variation in sudden infant death syndrome?. Acta Paediatrica, 102: 308–313. doi: 10.1111/apa.12107
- Issue published online: 5 FEB 2013
- Article first published online: 27 DEC 2012
- Accepted manuscript online: 27 NOV 2012 05:23PM EST
- Manuscript Accepted: 23 NOV 2012
- Manuscript Revised: 26 OCT 2012
- Manuscript Received: 14 SEP 2012
- Norwegian Foundation for Health and Rehabilitation
- Norwegian SIDS and Stillbirth Society
- HLA ;
The mucosal immune system and cytokines are activated in a large proportion of cases of sudden infant death syndrome (SIDS). Our aim was to search for a possible association between cytokine polymorphisms and immune stimulation of the laryngeal mucosal in SIDS.
HLA-DR expression in laryngeal mucosal glands and surface epithelium in 97 SIDS victims was evaluated applying a semi-quantitative scoring system. The findings were related to cytokine gene polymorphisms as well as to the level of various cytokines in the cerebrospinal fluid (CSF). A risk score was established: a score of 0 prepresenting negative HLA-DR, supine position and no fever prior to death.
The IL-6 -176CG/CC genotype was found in 92.3% of the SIDS cases with positive score for all risk factors (p = 0.01). Infants with high HLA-DR score had high levels of IL-6 in the cerebrospinal fluid (>30 μg/L) (p = 0.005). Furthermore, the IL-8 SNPs -781 CT/TT genotypes and −251 AA/AT genotypes were observed in 93% of the SIDS cases with one or more of the risk factors present compared with SIDS cases no risk factors reported (p = 0.003 and p = 0.016, respectively).
This study adds further evidence to the hypothesis that there are genetically associated disturbances of immunological homoeostasis in SIDS.