Increase of pulmonary density of macrophages in sudden infant death syndrome

Citation
Gl. De La Grandmaison et al., Increase of pulmonary density of macrophages in sudden infant death syndrome, FOREN SCI I, 104(2-3), 1999, pp. 179-187
Citations number
27
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology
Journal title
FORENSIC SCIENCE INTERNATIONAL
ISSN journal
03790738 → ACNP
Volume
104
Issue
2-3
Year of publication
1999
Pages
179 - 187
Database
ISI
SICI code
0379-0738(19991011)104:2-3<179:IOPDOM>2.0.ZU;2-J
Abstract
A 1996 cytodensitometric study found increased cellular density in the pulm onary parenchyma of infants who died of sudden infant death syndrome (SIDS) . The present study clarifies these results in quantifying the density of i mmunohistochemical subtyped inflammatory cells. Histomorphometry was used t o compare the density of macrophages, granulocytes and T and B lymphocytes in the lungs of two groups of infants. From the post-mortem records of infa nt deaths between 1983 and 1995, 29 (mean age = 5 months) were randomly sel ected including 16 cases of SIDS and 13 who died of other non-pulmonary cau ses. Densities of immunoreactive cells were measured under blind conditions in the parenchyma. The mean density of macrophages was significantly highe r in cases of SIDS compared with the controls (P = 0.0318), but there were no differences for the lymphocytes and the granulocytes. These morphometric al results must be interpreted within the methodological limits of this stu dy, especially the non-uniform level of lung inflation between selected sub jects. However, the differences in level of inflation are not sufficient to explain the observed increase of macrophage density. Indeed, the mean valu es of alveolar surface area, which represent an indirect measure of lung in flation, are not significantly different between the two groups. Increase o f pulmonary macrophage density in SIDS agrees with three non-exclusive hypo theses: (1) an abnormal inflammatory reaction by expression of Th1 helper c ell phenotype activation; (2) consequence of passive smoking; and (3) post- agonal mechanisms. Bacterial superantigens produced by toxigenic bacteria i n the respiratory tract could play a role as a trigger factor that initiate s a fatal cascade with overproduction of cytokines leading to death. The si gnificant increase of pulmonary macrophage density would be the morphologic al expression of this potential mechanism of death. (C) 1999 Elsevier Scien ce Ireland Ltd. All rights reserved.