16 March 2008
Possible role for early-life immune insult including developmental immunotoxicity in chronic fatigue syndrome (CFS) or myalgic
encephalomyelitis (ME).
Journal: Toxicology. 2008 Feb 8
Authors: Dietert RR, Dietert JM.
Affiliation: Department
of Microbiology and Immunology, C5-135 VMC, College of Veterinary Medicine,
North Tower Road, Cornell University, Ithaca, NY 14853, USA.
NLM
Citation: PMID: 18336982
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.