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Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies.

Dietert RR - Adv Med (2014)

Bottom Line: As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations.The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals).Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, North Tower Road, Ithaca, NY 14853, USA.

ABSTRACT
Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations. This review of DIT considers: (1) the history and context of DIT research, (2) the fundamental features of DIT, (3) the emerging role of DIT in risk of noncommunicable diseases (NCDs) and (4) the range of risk factors that have been investigated through human research. The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals). Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

No MeSH data available.


Related in: MedlinePlus

This figure depicts a model following the “Completed Self” paradigm [91] in which the immune system and infant microbiome need to comature without interference or disruption to reduce later-life health risks. The categories of environmental risk factors reported to cause prenatal and/or postnatal disruption are illustrated.
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fig1: This figure depicts a model following the “Completed Self” paradigm [91] in which the immune system and infant microbiome need to comature without interference or disruption to reduce later-life health risks. The categories of environmental risk factors reported to cause prenatal and/or postnatal disruption are illustrated.

Mentions: Extensive antibiotic use is of particular concern when viewed in the context of the hygiene hypothesis or the recently-described “Completed Self” model (i.e., where unimpeded comaturation of the development immune system and infant microbiome is critical) [91] (see Figure 1). Under the “Completed Self” paradigm, successful development of a balanced, well-regulated immune system needs co-maturation with a complete microbiome in the infant. The developing immune system receives important signals from the commensal microbes and eventually matures to perceive self as a combination of the mammalian cells and commensal microbes. The successful merger of the infant's mammalian and microbial components into the fully formed human-microbial superorganism may well represent the single most important step distinguishing later-life health from disease. As a result, any prenatal or postnatal environmental exposure that interferes with timely and effective self-completion is a significant health risk [91]. This new immunological view of what constitutes a fully completed infant could impact risk-benefit considerations for antibiotic administration in early life.


Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies.

Dietert RR - Adv Med (2014)

This figure depicts a model following the “Completed Self” paradigm [91] in which the immune system and infant microbiome need to comature without interference or disruption to reduce later-life health risks. The categories of environmental risk factors reported to cause prenatal and/or postnatal disruption are illustrated.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4590951&req=5

fig1: This figure depicts a model following the “Completed Self” paradigm [91] in which the immune system and infant microbiome need to comature without interference or disruption to reduce later-life health risks. The categories of environmental risk factors reported to cause prenatal and/or postnatal disruption are illustrated.
Mentions: Extensive antibiotic use is of particular concern when viewed in the context of the hygiene hypothesis or the recently-described “Completed Self” model (i.e., where unimpeded comaturation of the development immune system and infant microbiome is critical) [91] (see Figure 1). Under the “Completed Self” paradigm, successful development of a balanced, well-regulated immune system needs co-maturation with a complete microbiome in the infant. The developing immune system receives important signals from the commensal microbes and eventually matures to perceive self as a combination of the mammalian cells and commensal microbes. The successful merger of the infant's mammalian and microbial components into the fully formed human-microbial superorganism may well represent the single most important step distinguishing later-life health from disease. As a result, any prenatal or postnatal environmental exposure that interferes with timely and effective self-completion is a significant health risk [91]. This new immunological view of what constitutes a fully completed infant could impact risk-benefit considerations for antibiotic administration in early life.

Bottom Line: As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations.The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals).Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, North Tower Road, Ithaca, NY 14853, USA.

ABSTRACT
Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations. This review of DIT considers: (1) the history and context of DIT research, (2) the fundamental features of DIT, (3) the emerging role of DIT in risk of noncommunicable diseases (NCDs) and (4) the range of risk factors that have been investigated through human research. The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals). Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

No MeSH data available.


Related in: MedlinePlus