SIDS pathogenesis: pathological findings indicate infection and inflammatory responses are involved

Goldwater, Paul N.

doi:10.1016/j.femsim.2004.06.013

Cited by 27 publications

(21 citation statements)

References 82 publications

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“…The investigation of sudden unexpected death in infants and mechanisms leading to SIDS have been the subject of research over the past decades [2][3][4][5] Several researchers have discussed the possible role of cytokines as a pathophysiological factor which could contribute to SIDS because cytokines are proteins which regulate immune responses in allergic reactions, virus infection and septicaemia [1][2][3][4][17][18][19][20][21][22][23]. This hypothesis was investigated as a part of the GeSID study [13].…”

Section: Discussionmentioning

confidence: 99%

Cytokines and sudden infant death

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Cytokines and sudden infant death

et al. 2011

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“…An interesting observation was made in which CsgA antisera was found in babies who died from sudden infant death syndrome (SIDS), but age-matched controls did not contain CsgA antiserum (29,30). No infectious agent has been demonstrated in SIDS, but it is interesting to speculate that curli or curliated bacteria could play some role.…”

Section: Role Of Curli In Attachment and Invasion Of Host Cellsmentioning

confidence: 99%

Curli Biogenesis and Function

Barnhart

Chapman

2006

Annu. Rev. Microbiol.

1,024

1,028

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Curli are the major proteinaceous component of a complex extra-cellular matrix produced by many Enterobacteriaceae. Curli were first discovered in the late 1980s on Escherichia coli strains that caused bovine mastitis, and have since been implicated in many physiological and pathogenic processes of E. coli and Salmonella spp. Curli fibers are involved in adhesion to surfaces, cell aggregation, and biofilm formation. Curli also mediate host cell adhesion and invasion, and they are potent inducers of the host inflammatory response. The structure and biogenesis of curli are unique among bacterial fibers that have been described to date. Structurally and biochemically, curli belong to a growing class of fibers known as amyloids. Amyloid fiber formation is responsible for several human diseases including Alzheimer's, Huntington's, and prion diseases, although the process of in vivo amyloid formation is not well understood. Curli provide a unique system to study macromolecular assembly in bacteria and in vivo amyloid fiber formation. Here, we review curli biogenesis, regulation, role in biofilm formation, and role in pathogenesis.

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“…The other class of infectionrelated genes that has been frequently studied in SIDS is cytokines due to the evidence for inflammatory responses, particularly in the respiratory tract, in SIDS [reviewed in Goldwater, 2004;Vege and Rognum, 2004]. Cytokines are a large class of molecules that play a key regulatory roles in inflammation and immune response; the risk of acquiring infection and the risk of developing severe complications are related to genetic variability in cytokine genes, particularly IL10 [see e.g., pneumonia, Gallagher et al, 2003; Epstein-Barr virus infection, Helminen et al, 2001].…”

Section: Infection/inflammation Genes In Sidsmentioning

confidence: 99%

Sudden Infant Death Syndrome: Review of implicated genetic factors

Weese‐Mayer

Ackerman

Marazita

et al. 2007

American J of Med Genetics Pt A

123

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Genetic studies in Sudden Infant Death Syndrome (SIDS) have been motivated by clinical, epidemiological, and/or neuropathological observations in SIDS victims, with subsequent pursuit of candidate genes in five categories: (1) genes for ion channel proteins based on electrocardiographic evidence of prolonged QT intervals in SIDS victims, (2) gene for serotonin transporter based on decreased serotonergic receptor binding in brainstems of SIDS victims, (3) genes pertinent to the early embryology of the autonomic nervous system (ANS) (and with a link to the 5-HT system) based on reports of ANS dysregulation in SIDS victims, (4) genes for nicotine metabolizing enzymes based on evidence of cigarette smoking as a modifiable risk factor for SIDS, and (5) genes regulating inflammation, energy production, hypoglycemia, and thermal regulation based on reports of postnatal infection, low birth weight, and/or overheating in SIDS victims. Evidence for each of these classes of candidate genes is reviewed in detail. As this review indicates, a number of genetically controlled pathways appear to be involved in at least some cases of SIDS. Given the diversity of results to date, genetic studies support the clinical impression that SIDS is heterogeneous with more than one entity and with more than one possible genetic etiology. Future studies should consider expanded phenotypic features that might help clarify the heterogeneity and improve the predictive value of the identified genetic factors. Such features should be evaluated to the extent possible in both SIDS victims and their family members. With 2,162 infants dying from SIDS in 2003 in the U.S. alone, and improved but still imperfect parent and caretaker compliance with known modifiable risk factors for SIDS, it behooves clinicians, researchers, and parents to combine efforts to reach a common goal. The message of the "Back to Sleep" campaign needs to be re-introduced/re-engineered to reach families and caretakers of all ethnic groups. Clinicians and researchers need to gently inform new SIDS parents about the opportunity to contribute tissue to the NICHD-funded University of Maryland Brain and Tissue Bank. By expanding the network of clinicians, scientists, and families working together, and by combined efforts in a collaborative multi-center study of candidate genes and/or genomics, the discovery of the genetic profile of the infant at risk for SIDS can ultimately be determined.

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SIDS pathogenesis: pathological findings indicate infection and inflammatory responses are involved

Cited by 27 publications

References 82 publications

Cytokines and sudden infant death

Cytokines and sudden infant death

Curli Biogenesis and Function

Sudden Infant Death Syndrome: Review of implicated genetic factors

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