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Possible role for early-life immune insult including developmental

immunotoxicity in chronic fatigue syndrome (CFS) or myalgic encephalomyelitis

(ME).

Dietert RR, Dietert JM.

Department of Microbiology and Immunology, C5-135 VMC, College of Veterinary

Medicine, North Tower Road, Cornell University, Ithaca, NY 14853, USA.

Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME) in

some countries, is a debilitating disease with a constellation of multi-system

dysfunctions primarily involving the neurological, endocrine and immune systems.

While substantial information is available concerning the complex

dysfunction-associated symptoms of CFS, environmental origins of the disease

have yet to be determined. Part of the dilemma in identifying the cause(s) has

been the focus on biomarkers (hormones, neurotransmitters, cytokines, infectious

agents) that are contemporary with later-life CFS episodes. Yet, recent

investigations on the origins of environmental diseases of the neurological,

endocrine, reproductive, respiratory and immune systems suggest that early life

toxicologic and other insults are pivotal in producing later-life onset of

symptoms. As with autism and childhood asthma, CFS can also occur in children

where the causes are certainly early-life events. Immune dysfunction is

recognized as part of the CFS phenotype but has received comparatively less

attention than aberrant neurological or endocrine function. However, recent

research results suggest that early life immune insults (ELII) including

developmental immunotoxicity (DIT), which is induced by xenobiotics, may offer

an important clue to the origin(s) of CFS. The developing immune system is a

sensitive and novel target for environmental insult (xenobiotic, infectious

agents, stress) with major ramifications for postnatal health risks.

Additionally, many prenatal and early postnatal neurological lesions associated

with postnatal neurobehavioral diseases are now recognized as linked to prenatal

immune insult and inflammatory dysregulation. This review considers the

potential role of ELII including DIT as an early-life component of later-life

CFS.

PMID: 18336982 [PubMed - as supplied by publisher]

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