A. Vege et al., IL-6 cerebrospinal fluid levels are related to laryngeal IgA and epithelial HLA-DR response in sudden infant death syndrome, PEDIAT RES, 45(6), 1999, pp. 803-809
The objective was to investigate whether there is any correlation between s
igns of central and peripheral immune stimulation in victims of sudden infa
nt death syndrome (SIDS), the former expressed by IL-6 in cerebrospinal flu
id (CSF), the latter by IgA, IgG, and I,IgM immunocytes, T lymphocytes, and
HLA-DR expression in laryngeal mucosa. Seventeen SIDS cases with low CSF I
L-6 levels (less than or equal to 5 pg/mL) and 20 cases with high CSF IL-6
levels (greater than or equal to 30 pg/mL) were subjected to immunohistoche
mical quantitation of IgA, IgG, and IglvI immunocytes; semiquantitative sco
ring of T lymphocytes in the mucosa of epiglottis and larynx: and semiquant
itative evaluation of HLA-DR expression. SIDS cases with IL-6 levels greate
r than or equal to 30 pg/mL had a significantly higher number of IgA immuno
cytes in laryngeal mucosa (p = 0.007) and in epiglottis (p = 0.03) than cas
es with IL-6 levels less than or equal to 5 pg/mL. Furthermore, laryngeal H
LA-DR expression was significantly more extensive in SIDS cases with IL-6 l
evels greater than or equal to 30 pg/mL than in those with levels less than
or equal to 5 pg/mL (p = 0.05). No differences were found for IgG and IgM
immunocytes or for T cells. In addition, babies found prone more often had
symptoms of slight infection before death and had a higher number of IgA im
munocytes in the larynx (p = 0.02) than babies sleeping on their side or ba
ck. Because IL-6 levels greater than or equal to 30 pg/mL correspond to the
levels found in infants who die from infectious diseases such as meningiti
s/septicemia and pneumonia, the findings favor the hypothesis that many SID
S cases may be caused by an "overreaction" of the immune system to an other
wise harmless infection.