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.