Clues to understanding sudden infant death : a role for Helicobacter pylori and innate immunity?
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AbstractIn this thesis in pediatric forensic medicine, a series of experimental studies was performed in order to investigate Helicobacter pylori infection and innate immunity in infancy with special regard to Sudden infant death syndrome, SIDS.
By a commercial ELISA test, the prevalence of H. pylori carriage in stool of 249 healthy children between 0 and 3 years of age was investigated. A high detection rate was found in neonates related to mode of delivery, indicating that transfection from mother to child is likely. In infants older than one week of age, the H. pylori carriage rate was 8%. In a subsequent study of 160 victims of sudden death, H. pylori carriage was significantly associated with SIDS and infections: 25% of the SIDS victims and 53% of the infants who died from infectious disease were H. pylori positive. Moreover, H. pylori carriage in SIDS victims was associated with central immune response, assessed by high Interleukin-6 levels in cerebrospinal fluid.
Surfactant protein A (SP-A), surfactant protein D (SP-D) and mannose-binding lectin (MBL) are proteins of innate immunity involved in the first-line defense against microbial agents. By immunohistochemistry, a method was established to enable semi-quantitative evaluation of SP-A and SP-D expression in post-mortem tissues from fetal to adult life. In lung tissue, an unpredicted drop in SP-A expression was demonstrated in infants between 1 week and 5 months of age, corresponding with the peak period for SIDS. This drop may imply that down-regulation of SP-A occurs in normal post-natal development. Later genotyping of the SP-A, SP-D and MBL genes revealed no significant association between genetic polymorphisms and SIDS compared to explained infant deaths.
Thesis conclusion: During a vulnerable age period in post-natal life, H. pylori infection may add to the microbial load and trigger the death mechanism in SIDS. A drop in SP-A expression may contribute to this vulnerability.
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