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a Department of
Anatomy, Christian Albrecht University of Kiel, D-24098 Kiel, Germany, b Anatomical Centre, Hanover Medical School,
Germany, c Department of Forensic Medicine, Hanover Medical
School, Germany
Correspondence to: Dr med F Paulsen fpaulsen{at}anat.uni-kiel.de
Received 19 June 2000; Returned to authors 8 September 2000; Revised version received 16 October 2000; Accepted for publication 10 December 2000
BACKGROUND
It has been
speculated that non-specific defence mechanisms of the epithelium and
subepithelial seromucous glands play a role in the larynx and lungs in
cases of sudden infant death.
METHODS
The larynx and
trachea from five children who had died of sudden infant death (SID)
syndrome and five control cases of comparable age were compared for the
presence of lectin binding sites (12 different lectins tested).
RESULTS
The secretory
product of mucin producing cells contained carbohydrates including
galactose and sialic acids. Binding sites for fucose and
N-acetyl-galactosamine were only present in some of the specimens and
distribution revealed no correlation between cases of SID and controls.
Epithelial cells and serous cells of seromucous glands contained
binding sites for sialic acid in cases of SID and controls. Moreover,
binding sites for mannose were detected in these cells but were only
present in SID cases. The difference between the SID and control groups
as to the presence/expression of concanavalin A was highly significant.
CONCLUSIONS
It is
suggested that mucus hypersecretion in SID occurs in response to
bacterial toxins or viral infection and is not specific. The different
binding sites for mannose in cases of SID and controls could indicate
differences in the production of antimicrobial peptides. A
disturbed expression pattern of antimicrobial peptides in children
who later succumb to SID could be responsible for an imbalance of the
local microflora with a higher density of microorganisms on the mucosa.
Further studies are required to elucidate the pattern of expression of
antimicrobial peptides in subsequent SID victims.
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