Sudden Infant Death Syndrome Victims Show Local Immunoglobulin M Response in Tracheal Wall and Immunoglobulin A Response in Duodenal Mucosa

Abstract

ABSTRACT. Twenty-two sudden infant death syndrome (SIDS) cases and 22 controls were examined immunohistochemically with regard to IgA, IgM, and IgG plasma cells in tracheal wall and duodenal mucosa. Furthermore, the presence of secretory component in tracheal surface and gland epithelium as well as in duodenal crypt and villus epithelium were evaluated. The examined specimens were obtained at autopsies. The control groups consisted of 11 infants who died of noninfectious causes and 11 who died of infections. In the tracheal wall, the SIDS group had higher IgM cell numbers than the control group that died of noninfectious causes ( p < 0.01), whereas the SIDS Among the Scandinavian countries, Norway has the highest incidence of SIDS, and the incidence seems to be increasing (1). Both the etiology and the pathogenesis of SIDS are at present unclear. We have, however, recently published data that indicate that hypoxia precedes death in approximately 80% of the SIDS cases (2, 3). There are several factors that might initiate respiratory inhibition and hypoxia. Because SIDS is more common in colder climates and an increased incidence correlates with the season of respiratory tract infections (4), an immune response in the respiratory tract might be one possible "trigger mechanism." Adaptive immunity at mucosal surfaces of children and adults is mainly exerted by secretory IgA and IgM antibodies, which represent the quantitatively most important humoral immune system of the body (5-8). SC, the poly-Ig receptor, is imperative for the secretion of secretory IgA and secretory IgM (9). Increased concentrations of IgM, IgG, and to a lesser extent IgA in lung lavage fluid from SIDS victims (10) and raised numbers of IgA, IgM, and IgG producing cells in salivary glands (1 1) indicate a stimulation of the secretory immune system in the upper airways and lungs. Furthermore, lack of SC in the tracheal epithelium preventing the transport of dimeric IgA and pentameric IgM has been suggested as an etiologic factor in SIDS (12).The purpose of this study was to investigate the humoral immune response and the expression of epithelial SC in the wall of the upper respiratory tract and the duodenal mucosa in SIDS. MATERIALS AND METHODSTissue specimens. Tracheal wall and duodenal mucosa specimens were obtained from 22 infants who died from SIDS (15 males and seven females; median age 4 mo, range 1-7 mo). Tracheal wall samples were taken from the canna; one sample was rejected because of bacterial growth.The control group consisted of 22 specimens from tracheal wall and from duodenal mucosa. The median age of the control group was 4 mo (range 1-12 mo). Eleven infants died of the following causes: congenital heart disease (n = 4), head injury (n = 2), infanticide (n = I), CO intoxication (n = I), drowning (n = I), battered child syndrome (n = l), and accidental suffocation (n = 1). None of these infants had clinical evidence of an infection. Eleven infants died of a specific infection: sepsis (n = 4), pneumonia (n = 6), or meningitis (n = 1...

Helicobacter pylori Antigen in Stool Is Associated With SIDS and Sudden Infant Deaths due to Infectious Disease

“…The mucosal immunity is developing rapidly during the first months of life (32)(33)(34) and an activation of mucosal immunity in the aerodigestive tract has been demonstrated in SIDS victims (13,35). In the present study detection of H. pylori stool antigen also varied significantly with age; cases below 5 mo of age being accountable for the difference between SIDS and live controls.…”

“…Increased concentrations of IL-6 in cerebrospinal fluid (CSF) have been found in SIDS victims (11), and elevated IL-6 levels is found to be associated with immunoreactivity in the larynx and with symptoms of cold before death (12). Mucosal immune activation in the duodenum has also been shown in SIDS (13). Epidemiologic studies have disclosed that SIDS is associated with symptoms of cold before death, winter season, and occurrence of respiratory epidemic infections (14,15).…”

Adverse Effects of Nicotine and Interleukin-1β on Autoresuscitation After Apnea in Piglets: Implications for Sudden Infant Death Syndrome

“…Nonetheless, our findings should be linked to SIDS as many characteristics of typical SIDS infants seem to point in the direction of a vicious circle that includes the presence of apneas: periodic breathing and apneas, sleep, vomiting, low gestational age, overheating, hypoxia, infection, and release of interleukines. [12][13][14][15][16] These characteristics are separately known to enhance, produce, and prolong apneas, and interfere with normal autoresuscitation after apnea. 9,11,[17][18][19] Early in life, the infant is more susceptible to apnea by laryngeal stimulation 11 and hypoxia during apnea, 20 and probably responds inadequately to mild hypoxia by increased periodic breathing.…”

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.…”