Chronic fatigue syndrome (CFS) is a heterogeneous illness in which patients can have different, overlapping signs and symptoms. No single underlying cause has been established for all CFS patients. Epidemiological studies reveal that a flu-like sickness precedes the onset in the majority of cases. The major hypothesis of the pathogenesis of CFS is that infectious agents such as viruses, may trigger and lead to chronic activation of the immune system with abnormal regulation of cytokine production. Many studies have been performed to identify the possible microbial triggers and to understand the epidemiological microbial agents. We have summarized the recent progressive literature of virus, rickettsia, and mycoplasma implicated in the pathogenesis of CFS.
"Early-life immune insults (ELII) including developmental immunotoxicity (DIT) and later-life immune dysfunctions in common with CFS Immune-host resistance dysfunctions common to ELII/DIT and CFS Environmental inducers of prenatal–neonatal immune dysfunction ELII/DIT references for agent-dysfunction CFS references for immune dysfunction -Increased susceptibility to viruses TCDD Voderstrasse et al., 2004 Chapenko et al., 2006 -Reduced vaccine responses Dexamethasone, Neonatal stress PCBs Burleson et al. (2008), Avitsur et al. (2006), Heilmann et al. (2006) Komaroff (2006), Hickie et al. (2006), Sairenji and Nagata (2007), Chia and Chia (2007) -Impaired innate immune defenses Maternal alcohol use Gauthier et al. (2005) Siegel et al. (2006) Neonatal stress Avitsur et al. (2006) Iwakami et al. (2005) LPS Hodyl et al. (2007) Kennedy et al. (2004) -Increased risk of autoimmunity TCDD Mustafa et al. (2007) Maes et al. (2006a) DES Brown et al. (2006) Margutti et al. (2006) Maternal infection Hodyl et al. (2007) Staines (2006, 2004) -Suppressed delayed-type hypersensitivity (DTH) response Lead Bunn et al. (2001) Lloyd et al. (1992) TCDD Gehrs and Smialowicz (1999) -Suppressed cytotoxic T lymphocyte (CTL) activity Maternal smoking Ng et al. (2006) Maher et al. (2005) TCDD Voderstrasse et al. (2004) Mihaylova et al. (2007) Dexamethasone Burleson et al. (2008) -Th2 bias for cytokines/immune responses Lead Miller et al. (1998) Patarca-Montero et al. (2001) Mercury Silva et al. (2005) Environmental tobacco smoke Wang et al. (2007) -Reduced NK cell activity Cadmium Pillet et al. (2005) Maher et al. (2005) Alcohol Arjona et al. (2006) Mihaylova et al. (2007), Stewart et al. (2003), Suhadolnik et al. (2004) -Myelomonocytic dysfunction and inflammation (ROI, NO, PGs) Pesticides Theus et al. (1992) Kennedy et al. (2005) Lead Miller et al. (1998) Maes et al. (2005) LPS Boisse et al. (2004) Maes et al. (2007a,b) Maternal infection Pang et al. (2005) Kennedy et al. (2004) Alcohol Ping et al. (2007) Richards et al. (2000) Maternal smoking Noakes et al. (2007) Jammes et al. (2005) PCBs, polycyclic chlorinated biphenyls; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; LPS, lipopolysaccharide; DES, diethylstilbesterol; NK, natural killer; ROI, reactive oxygen intermediates; NO, nitric oxide; PGs, prostaglandins. virus7 (HHV-7) reactivation is a biomarker in CFS patients. "
[Show abstract][Hide abstract] ABSTRACT: 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.
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