Changes in the concentration and distribution of immunoglobulin‐producing cells in SIDS palatine tonsils

Abstract

Seventeen sudden infant death syndrome (SIDS) cases and 9 controls, were examined immunohistochemically with regard to the presence of IgA-, IgM-, IgD, and IgG, as well as for the subtypes IgG1-, IgG2-, IgG3-, and IgG4-immunocytes. Differences in compartmentalization were also investigated. Differences were demonstrated between SIDS and controls in total number of IgG cells per 0.1 mm2 tissue area (median: 18.3, range: 12.3-30.2 versus median: 6.3, range: 2.0-14.6) (p < 0.01), and for IgA immunocytes (median: 3.9, range: 2.4-5.0 versus median: 1.5, range: 1.1-3.7) (p < 0.05), while no differences were demonstrated for IgM cells (median: 1.8, range: 1.2-3.3 versus median: 1.8, range: 0.7-5.6) or IgD cells (median: 1.9, range: 0.8-2.9 versus median: 1.6, range: 0.7-2.4). Differences were demonstrated between SIDS and control IgG plasma cells in all the four palatine tonsillar compartments; germinal centre (p < 0.01), mantle zone (p < 0.05), interfollicular area (p < 0.01) and reticular epithelium (p < 0.01). Furthermore, the number of IgA cells was higher in SIDS vs. controls in both the germinal centre (median: 1.4, range: 0.6-2.1 versus median: 0.6, range: 0.3-1.3) (p < 0.05) and in the interfollicular area (median: 2.2, range: 1.1-3.1 versus median: 0.5, range: 0.4-2.0) (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Il-10 gene polymorphisms are associated with infectious cause of sudden infant death

“…Several studies indicate an activation of the mucosal immune system in sudden infant death syndrome (SIDS) [7][8][9]. About half of the SIDS victims had slight signs of infection prior to death, and there is an association between such infections and partial deletions of the complement component C4 gene [10].…”

Detection rate of Helicobacter pylori stool antigen in newborn infants and small children

“…During the last 20 years, extensive immunohistochemical examination of the mucosal immune system in SIDS has been performed on tissue samples form the SIDS Biobank of the Institute of Forensic Medicine at the University of Oslo. Salivary glands, tonsils, tracheal walls, and intestinal mucosa have all shown immune stimulation in SIDS, though to a somewhat lesser degree than in victims of infectious deaths [80][81][82][83] . The findings are summarized in figure 4.…”

Synergistic Effect of Influenza A Virus on Endotoxin-Induced Mortality in Rat Pups: A Potential Model for Sudden Infant Death Syndrome

“…Generalized signs of inflammation on postmortem examinations of infants dying of SIDS suggested that an infectious agent was involved (27,28). The respiratory tract was the most common site of inflammation, with 80% of infants dying of SIDS having intrathoracic, subserosal petechial hemorrhages and lung congestion with signs of immune stimulation in mucosa of trachea, duodenum, and nasopharynx (29,30) Lung congestion is often seen in humans or animals after death and may be a sign of agonal changes. These signs would not be expected in animals humanely euthanized with pentobarbital.…”