Is sudden infant death syndrome (SIDS) an autoimmune disorder of endogenous vasoactive neuropeptides?

Staines, Donald

doi:10.1016/j.mehy.2004.01.004

Cited by 10 publications

(7 citation statements)

References 45 publications

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“…The finding of respiratory control defects in PACAP‐deficient neonates raises the possibility of a link between mutations in genes encoding components of the PACAP signaling pathways and sudden infant death syndrome in humans 31,74 …”

Section: Potential Involvement In Human Diseases and Future Outlookmentioning

confidence: 99%

“…71 The finding of respiratory control defects in PACAP-deficient neonates raises the possibility of a link between mutations in genes encoding components of the PACAP signaling pathways and sudden infant death syndrome in humans. 31,74 Although a detailed review of peripheral roles of PACAP are beyond the scope of this article, PACAP has potent insulinotropic action as a pancreatic islet neuropeptide and insulin-sensitizing properties, 75,76 as well as playing a significant role in carbohydrate and lipid metabolism. 5 As discussed above, PACAP deficiency is associated with higher neonatal death.…”

Section: Potential Involvement In Human Diseases and Future Outlookmentioning

confidence: 99%

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New Insights into the Central PACAPergic System from the Phenotypes in PACAP‐ and PACAP Receptor‐Knockout Mice

Hashimoto

Shintani

Baba

2006

Annals of the New York Academy of Sciences

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Pituitary adenylate cyclase-activating polypeptide (PACAP) is a structurally highly conserved neuropeptide and displays pleiotropic activity, including functioning as a neurotransmitter, neuromodulator, and neurotrophic factor. A series of recent experiments, including genetic manipulation of PACAP and its receptors, has led to better understanding of both normal and pathological processes in which PACAP has been proposed to play a role, and sheds light on previously uncharacterized functions of endogenous PACAP. The aim of this article is to briefly review the recent advances in understanding the role of PACAP in the central nervous system from PACAP- and PACAP receptor-deficient mice, particularly with respect to behavioral and neurological features, including psychomotor behavior, feeding, stress responses, memory performance, ethanol sensitivity, chronic pain, and circadian rhythms. This article also discusses their potential involvement in human diseases.

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Section: Potential Involvement In Human Diseases and Future Outlookmentioning

confidence: 99%

Section: Potential Involvement In Human Diseases and Future Outlookmentioning

confidence: 99%

New Insights into the Central PACAPergic System from the Phenotypes in PACAP‐ and PACAP Receptor‐Knockout Mice

Hashimoto

Shintani

Baba

2006

Annals of the New York Academy of Sciences

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“…[250][251][252][253][254][255][256][257][258][259][260][261][262] PACAP, and the structurally related VIP, belong to the secretin/glucagon family of peptides produced by the lymphoid cells, which exerts a wide spectrum of immunologic functions controlling the homeostasis through different receptors expressed in various immunocompetent cells. [250][251][252][253][254][255][256][257][258][259][260][261][262] PACAP, and the structurally related VIP, belong to the secretin/glucagon family of peptides produced by the lymphoid cells, which exerts a wide spectrum of immunologic functions controlling the homeostasis through different receptors expressed in various immunocompetent cells.…”

Section: Important Role Of Pituitary Adenylate Cyclase-activating Polmentioning

confidence: 99%

Possible Pathomechanisms of Sudden Infant Death Syndrome

Prandota¹

2004

American Journal of Therapeutics

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Chronic hypoxia, viral infections/bacterial toxins, inflammation states, biochemical disorders, and genetic abnormalities are the most likely trigger of sudden infant death syndrome (SIDS). Autopsy studies have shown increased pulmonary density of macrophages and markedly more eosinophils in the lungs accompanied by increased T and B lymphocytes. The elevated levels of immunoglobulins, about 20% more muscle in the pulmonary arteries, increased airway smooth muscle cells, and increased fetal hemoglobin and erythropoietin are evidence of chronic hypoxia before death. Other abnormal findings included mucosal immune stimulation of the tracheal wall, duodenal mucosa, and palatine tonsils, and circulating interferon. Low normal or higher blood levels of cortisol often with petechiae on intrathoracic organs, depleted maternal IgG antibodies to endotoxin core (EndoCAb) and early IgM EndoCAb triggered, partial deletions of the C4 gene, and frequent IL-10-592*A polymorphism in SIDS victims as well as possible hypoxia-induced decreased production of antiinflammatory, antiimmune, and antifibrotic cytokine IL-10, may be responsible for the excessive reactions to otherwise harmless infections. In SIDS infants, during chronic hypoxia and times of infection/inflammation, several proinflammatory cytokines are released in large quantities, sometimes also representing a potential source of tissue damage if their production is not sufficiently well controlled, eg, by pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP). These proinflammatory cytokines down-regulate gene expression of major cytochrome P-450 and/or other enzymes with the specific effects on mRNA levels, protein expression, and enzyme activity, thus affecting metabolism of several endogenous lipophilic substances, such as steroids, lipid-soluble vitamins, prostaglandins, leukotrienes, thromboxanes, and exogenous substances. In SIDS victims, chronic hypoxia, TNF-alpha and other inflammatory cytokines, and arachidonic acid (AA) as well as n-3 polyunsaturated fatty acids (FA), stimulated and/or augmented superoxide generation by polymorphonuclear leukocytes, which contributed to tissue damage. Chronic hypoxia, increased amounts of nonheme iron in the liver and adrenals of these infants, enhanced activity of CYP2C9 regarded as the functional source of reactive oxygen species (ROS) in some endothelial cells, and nicotine accumulation in tissues also intensified production of ROS. These increased quantities of proinflammatory cytokines, ROS, AA, and nitric oxide (NO) also resulted in suppression of many CYP450 and other enzymes, eg, phosphoenolpyruvate carboxykinase (PEPCK), an enzyme important in the metabolism of FA during gluconeogenesis and glyceroneogenesis. PEPCK deficit found in SIDS infants (caused also by vitamin A deficiency) and eventually enhanced by PACAP lipolysis of adipocyte triglycerides resulted in an increased FA level in blood because of their impaired reesterification to triacylglycerol in adipocytes. In ...

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“…This would indicate that the modulatory action of VIP on LHRH secretion 5 develops progressively in human suggesting that, during development, VIP may influence the secretion of pituitary hormones. The data reported in this study would be relevant with regard to a possible implication of VIP in some pathologies affecting neonate/infants such as sudden infant death syndrome 6 …”

Section: Discussionmentioning

confidence: 97%

“…The data reported in this study would be relevant with regard to a possible implication of VIP in some pathologies affecting neonate/infants such as sudden infant death syndrome. 6…”

Section: Discussionmentioning

confidence: 99%

Developmental Pattern of VIP Binding Sites in the Human Hypothalamus

Najimi

2006

Annals of the New York Academy of Sciences

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We have studied the developmental patterns of vasoactive intestinal polypeptide (VIP) binding sites in the human hypothalamus. VIP recognition sites were widely distributed throughout the rostrocaudal extent of the hypothalamus. VIP binding was generally low in the fetal and neonatal periods and a tendency in increasing densities was observed during postnatal development. The age comparison of binding density indicates variations in several structures. Thus, the densities were higher in older infants in the preoptic area, lamina terminalis, and infundibular (IN) nucleus. These differences suggest the implication of VIP receptors in the development of this brain structure and the maintenance of its various functions.

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Is sudden infant death syndrome (SIDS) an autoimmune disorder of endogenous vasoactive neuropeptides?

Cited by 10 publications

References 45 publications

New Insights into the Central PACAPergic System from the Phenotypes in PACAP‐ and PACAP Receptor‐Knockout Mice

New Insights into the Central PACAPergic System from the Phenotypes in PACAP‐ and PACAP Receptor‐Knockout Mice

Possible Pathomechanisms of Sudden Infant Death Syndrome

Developmental Pattern of VIP Binding Sites in the Human Hypothalamus

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