De zoon heeft besloten een deel van de schuur verder uit te mesten. I love that kid! Twntig jaar rommel, wat zeg ik, 35 jaar rommel opgestapeld door hubby. Af en toe krijgt de rest van het gezin dus ook de kriebels van die stal en gaan ze opruimen.
Resultaat op einde van de dag was mijn mini-auto volgestouwd met oud ijzer, plastic, hout en afgedankte electronica.
Met de neus tegen de voorruit geplakt en de koffer met een koord aan de bumper bolden we richting containerpark om de boel te dumpen. Daar moesten we vaststellen dat het sluitingsuur voorbij was. We hebben nog net in onze broek gedaan van het lachen. Daar stonden we.
Info:
Wat is de weg naar een betere gezondheid?
Zelfredzaamheid is het sleutelwoord.
zondag 2 oktober 2011
Dag 504 Phosphor
Afspraak bij de neuraal arts. Ze geeft me spuitjes in de slapen en een shot in mijn arm. Niet in de borstkast of buik ditmaal.
We gaan door met de Phosphor 200K, 2 x per week 10 bolletjes maar op die dag mag ik geen hydrocortisone nemen omdat deze laatste homeopathie tegenwerkt.
Een dag zonder cortisone lukt me nu veel beter dan pakweg een maand geleden. Toen was het contrast tussen 2 dagen nog te extreem, dan werd ik agressief, lastig of steeg de pijn enorm.
Het lijkt of de ontstekingen in het algemeen minder zijn. Volgende keer ga ik aan de huisarts vragen om de dosis hydrocortisone te verlagen met 5mg. Ik denk dat het belangrijkste anti-ontstekings effect bereikt is en we nu kunnen minderen.
Info:
Onze biologische klok zit ook in de darmen
Interestingly, it has been found that clocks in the GIT (gastrointestinal tract) are responsible for the periodic activity of its various segments and transit along the GIT; they are localized in special interstitial cells, with unstable membrane potentials located between the longitudinal and circular muscle layers.
Additionally, melatonin, produced by neuro-endocrine cells of the GIT mucosa, plays an important role in the internal biological clock, related to food intake (hunger and satiety) and the myoelectric rhythm (produced primarily by the pineal gland during the dark period of the light-dark cycle).
Disruption of circadian physiology, due to sleep disturbance or shift work, may result in various gastrointestinal diseases, such as irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD) or peptic ulcer disease.
Het controle-systeem dat honger en verzadiging controleert zit in de suprachiasmatic nucleus (SCN) van de hypothalamus. Dit communiceert via diverse kanalen met het lichaam waaronder het verteringsstelsel. Dat blijkt een eigen biologische klok te hebben dat verstoord kan worden.
Dit kan leiden tot versnelde celdeling en dus veroudering en kans op kans in de lever en het darmkanaal alsook obesitas vanwege een verkeerde voedselopname in tijd.
Melatonine blijkt het darmslijmvlies te beschermen tegen IBS en GERD. Melatonin blijkt ook het darmslijmvlies te beschermen bij patienten met niet-alcoholische steatohepatitis (NASH).
Bron: http://www.ncbi.nlm.nih.gov/pubmed/21673361
We gaan door met de Phosphor 200K, 2 x per week 10 bolletjes maar op die dag mag ik geen hydrocortisone nemen omdat deze laatste homeopathie tegenwerkt.
Een dag zonder cortisone lukt me nu veel beter dan pakweg een maand geleden. Toen was het contrast tussen 2 dagen nog te extreem, dan werd ik agressief, lastig of steeg de pijn enorm.
Het lijkt of de ontstekingen in het algemeen minder zijn. Volgende keer ga ik aan de huisarts vragen om de dosis hydrocortisone te verlagen met 5mg. Ik denk dat het belangrijkste anti-ontstekings effect bereikt is en we nu kunnen minderen.
Info:
Onze biologische klok zit ook in de darmen
Interestingly, it has been found that clocks in the GIT (gastrointestinal tract) are responsible for the periodic activity of its various segments and transit along the GIT; they are localized in special interstitial cells, with unstable membrane potentials located between the longitudinal and circular muscle layers.
Additionally, melatonin, produced by neuro-endocrine cells of the GIT mucosa, plays an important role in the internal biological clock, related to food intake (hunger and satiety) and the myoelectric rhythm (produced primarily by the pineal gland during the dark period of the light-dark cycle).
Disruption of circadian physiology, due to sleep disturbance or shift work, may result in various gastrointestinal diseases, such as irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD) or peptic ulcer disease.
Het controle-systeem dat honger en verzadiging controleert zit in de suprachiasmatic nucleus (SCN) van de hypothalamus. Dit communiceert via diverse kanalen met het lichaam waaronder het verteringsstelsel. Dat blijkt een eigen biologische klok te hebben dat verstoord kan worden.
Dit kan leiden tot versnelde celdeling en dus veroudering en kans op kans in de lever en het darmkanaal alsook obesitas vanwege een verkeerde voedselopname in tijd.
Melatonine blijkt het darmslijmvlies te beschermen tegen IBS en GERD. Melatonin blijkt ook het darmslijmvlies te beschermen bij patienten met niet-alcoholische steatohepatitis (NASH).
Bron: http://www.ncbi.nlm.nih.gov/pubmed/21673361
Dag 503 Winning combination
Ik slaap al een week zonder LDN en het wordt met de dag erger. Mijn huisarts is op vakantie, de neuraal arts kent het (nog) niet en ik zit zonder voorschrift.
Enige tijd geleden had ik al eens een poging ondernomen om zonder slaapmiddel door te slapen maar dat was een ramp. Zonder LDN dus ook. De twee medicijnen samen blijkt dus een winnende combinatie.
Enige tijd geleden had ik al eens een poging ondernomen om zonder slaapmiddel door te slapen maar dat was een ramp. Zonder LDN dus ook. De twee medicijnen samen blijkt dus een winnende combinatie.
Dag 502 Blind
Al enige dagen van een slecht zicht met name mijn linkeroog. Dat wordt zogoed als stekeblind, het komt en het gaat. Ik zie alleen nog maar troebel grijs dan. Dikke klieren, rugpijn, pijn in de borstkast, ... het klassieke plaatje. Slapen is even nodig tegen de middag maar dan gaat het weer beter.
Dag 501 Niks nieuws
We slapen een gat in de dag. Erg productief ben ik niet vandaag, zeker niet op cognitief vlak. De fysieke vermoeidheid laat zich voelen tegen het einde van de namiddag.
Dag 500 Linkerarm
Het ene moment denk je dat de spierpijn eindelijk opgelost is. De volgende dag scheuren brandende striemen door de spieren van je armen en benen om je eraan te herinneren dat het nog niet voorbij is. Mijn linker bovenarm doet zo’n pijn. Als dat maar goed zit met die dagelijkse pijn in de borstkast.
Info:
In 1908 was er al een arts, Carnegie Brown, die opmerkte dat neuropathie (zenuwziekte) en coeliakie minder werd als er gestopt werd met het eten van tarwe. Nu in 2010, ruim honderd jaar later lijkt het eindelijk te zijn doorgedrongen in de medische wetenschap en zo waar verscheen in maart een artikel in The Lancet Neurology, met de titel: Gluten sensitivity: from gut to brain (glutenintolerantie van darmen naar hersenen).
Gluten sensitivity is a systemic autoimmune disease with diverse manifestations. This disorder is characterised by abnormal immunological responsiveness to ingested gluten in genetically susceptible individuals.
Coeliac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. Although neurological manifestations in patients with established coeliac disease have been reported since 1966, it was not until 30 years later that, in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction.
Furthermore, the concept of extraintestinal presentations without enteropathy has only recently become accepted.
In this personal view, we review the range of neurological manifestations of gluten sensitivity and discuss recent advances in the diagnosis and understanding of the pathophysiological mechanisms underlying neurological dysfunction related to gluten sensitivity.
M.a.w. men accepteert sinds zeer kort in de medische wereld dat glutenintolerantie zich kan manifesteren ZONDER darmafwijking en dus enkel met zenuwafwijkingen.
Eindelijk een deftige verklaring voor 36 jaar dagelijkse hoofdpijn/migraine (en neurolupus)?
Bron: ://www.thelancet.com/journals/laneur/article/PIIS1474-4422(09)70290-X/abstract
Info:
In 1908 was er al een arts, Carnegie Brown, die opmerkte dat neuropathie (zenuwziekte) en coeliakie minder werd als er gestopt werd met het eten van tarwe. Nu in 2010, ruim honderd jaar later lijkt het eindelijk te zijn doorgedrongen in de medische wetenschap en zo waar verscheen in maart een artikel in The Lancet Neurology, met de titel: Gluten sensitivity: from gut to brain (glutenintolerantie van darmen naar hersenen).
Gluten sensitivity is a systemic autoimmune disease with diverse manifestations. This disorder is characterised by abnormal immunological responsiveness to ingested gluten in genetically susceptible individuals.
Coeliac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. Although neurological manifestations in patients with established coeliac disease have been reported since 1966, it was not until 30 years later that, in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction.
Furthermore, the concept of extraintestinal presentations without enteropathy has only recently become accepted.
In this personal view, we review the range of neurological manifestations of gluten sensitivity and discuss recent advances in the diagnosis and understanding of the pathophysiological mechanisms underlying neurological dysfunction related to gluten sensitivity.
M.a.w. men accepteert sinds zeer kort in de medische wereld dat glutenintolerantie zich kan manifesteren ZONDER darmafwijking en dus enkel met zenuwafwijkingen.
Eindelijk een deftige verklaring voor 36 jaar dagelijkse hoofdpijn/migraine (en neurolupus)?
Bron: ://www.thelancet.com/journals/laneur/article/PIIS1474-4422(09)70290-X/abstract
Dag 499 You look great
De kapper heeft me mega-veel geld gekost maar het resultaat mag er wezen. Een toevallig passerende vriendin vindt me er geweldig uitzien. Als de controle-arts me zo ziet, mag ik direct weer aan het werk. Schijn bedriegt.
Info:
Welke ziekten kan je krijgen door gluten?
• gewichtsverlies / overgewicht
• botontkalking
• bloedarmoede / ijzer tekort / vitamine B12 tekort /koper tekort / vitamine D3 tekort
• vermoeidheid
• haaruitval
• onvruchtbaarheid /miskramen
• groei achterstand bij kinderen
• Lymfomen / (dunne)darmkanker
• leerstoornissen / adhd /autisme
• migraine, neurologische afwijkingen als epilepsie, neuropathie en ataxie
• schildklierstoornissen
• auto-immuunstoornissen als Diabetes type I, reuma, SLE, ALS
depressiviteit / overspannenheid / angstklachten
Bron: http://www.natuurarts.nl/artikelen/johans-columns-voor-het-maandblad-gezondnu/ziek-van-gluten/index.html
Info:
Welke ziekten kan je krijgen door gluten?
• gewichtsverlies / overgewicht
• botontkalking
• bloedarmoede / ijzer tekort / vitamine B12 tekort /koper tekort / vitamine D3 tekort
• vermoeidheid
• haaruitval
• onvruchtbaarheid /miskramen
• groei achterstand bij kinderen
• Lymfomen / (dunne)darmkanker
• leerstoornissen / adhd /autisme
• migraine, neurologische afwijkingen als epilepsie, neuropathie en ataxie
• schildklierstoornissen
• auto-immuunstoornissen als Diabetes type I, reuma, SLE, ALS
depressiviteit / overspannenheid / angstklachten
Bron: http://www.natuurarts.nl/artikelen/johans-columns-voor-het-maandblad-gezondnu/ziek-van-gluten/index.html
vrijdag 30 september 2011
Genes changes after moderate exercise in CFS patients
Authors: Light AR, Bateman L, Jo D, Hughen RW, Vanhaitsma TA, White AT, Light KC.
Source. Department of Anesthesiology, University of Utah, Salt Lake City, UT The Brain Institute, University of Utah, Salt Lake City, UT Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT Department of Exercise and Sprt Science, University of Utah, Salt Lake City, UT.
Publication: J Intern Med.
Publication date: 26 May 2011
Abstract
Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AT, Light KC (University of Utah Dept. Anesthesiology, Dept. Neurobiology and Anatomy, Dept. Exercise and Sport Science) Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.
Objectives: To determine mRNA expression differences in genes involved in signaling and modulating sensory fatigue, and muscle pain in patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia Syndrome (FM) at baseline, and following moderate exercise.
Design: Forty eight Patients with CFS-only, or CFS with comorbid FM, 18 Patients with FM that did not meet criteria for CFS, and 49 healthy Controls underwent moderate exercise (25 minutes at 70% maximum age predicted heart-rate). Visual-analogue measures of fatigue and pain were taken before, during, and after exercise. Blood samples were taken before, and 0.5, 8, 24, and 48 hours after exercise. Leukocytes were immediately isolated from blood, number coded for blind processing and analyses, and flash frozen. Using real-time, quantitative PCR, the amount of mRNA for 13 genes (relative to control genes) involved in sensory, adrenergic, and immune functions was compared between groups at baseline, and following exercise. Changes in amounts of mRNA were correlated with behavioral measures, and functional clinical assessments.
Results: No gene expression changes occurred following exercise in Controls. In 71% of CFS patients, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48 hours. These post-exercise increases correlated with behavioral measures of fatigue and pain. In contrast, for the other 29% of CFS patients, adrenergic α-2A receptor's transcription was decreased at all time points after exercise; other genes were not altered. History of orthostatic intolerance was significantly more common in the α-2A decrease subgroup. FM only patients showed no post-exercise alterations in gene expression, but their pre-exercise baseline mRNA for two sensory ion channels and one cytokine were significantly higher than Controls.
Conclusions: At least two subgroups of CFS patients can be identified by gene expression changes following exercise. The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine. The smaller subgroup contained most of the CFS patients with orthostatic intolerance, showed no post-exercise increases in any gene, and was defined by decreases in mRNA for α-2A. FM only patients can be identified by baseline increases in 3 genes. Post-exercise increases for 4 genes meet published criteria as an objective biomarker for CFS, and could be useful in guiding treatment selection for different subgroups.
Copyright © 2011 The Association for the Publication of the Journal of Internal Medicine.
PMID:21615807[PubMed - as supplied by publisher]
Source:
http://www.actionforme.org.uk/get-informed/news/archived-news/research-news/2011/gene-expression-alterations-following-moderate-exercise
More info:
http://www.research1st.com/2011/06/02/exercise-challenge-reveals-potential-cfs-biomarkers/
http://www.ncbi.nlm.nih.gov/pubmed/21615807
Source. Department of Anesthesiology, University of Utah, Salt Lake City, UT The Brain Institute, University of Utah, Salt Lake City, UT Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT Department of Exercise and Sprt Science, University of Utah, Salt Lake City, UT.
Publication: J Intern Med.
Publication date: 26 May 2011
Abstract
Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AT, Light KC (University of Utah Dept. Anesthesiology, Dept. Neurobiology and Anatomy, Dept. Exercise and Sport Science) Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.
Objectives: To determine mRNA expression differences in genes involved in signaling and modulating sensory fatigue, and muscle pain in patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia Syndrome (FM) at baseline, and following moderate exercise.
Design: Forty eight Patients with CFS-only, or CFS with comorbid FM, 18 Patients with FM that did not meet criteria for CFS, and 49 healthy Controls underwent moderate exercise (25 minutes at 70% maximum age predicted heart-rate). Visual-analogue measures of fatigue and pain were taken before, during, and after exercise. Blood samples were taken before, and 0.5, 8, 24, and 48 hours after exercise. Leukocytes were immediately isolated from blood, number coded for blind processing and analyses, and flash frozen. Using real-time, quantitative PCR, the amount of mRNA for 13 genes (relative to control genes) involved in sensory, adrenergic, and immune functions was compared between groups at baseline, and following exercise. Changes in amounts of mRNA were correlated with behavioral measures, and functional clinical assessments.
Results: No gene expression changes occurred following exercise in Controls. In 71% of CFS patients, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48 hours. These post-exercise increases correlated with behavioral measures of fatigue and pain. In contrast, for the other 29% of CFS patients, adrenergic α-2A receptor's transcription was decreased at all time points after exercise; other genes were not altered. History of orthostatic intolerance was significantly more common in the α-2A decrease subgroup. FM only patients showed no post-exercise alterations in gene expression, but their pre-exercise baseline mRNA for two sensory ion channels and one cytokine were significantly higher than Controls.
Conclusions: At least two subgroups of CFS patients can be identified by gene expression changes following exercise. The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine. The smaller subgroup contained most of the CFS patients with orthostatic intolerance, showed no post-exercise increases in any gene, and was defined by decreases in mRNA for α-2A. FM only patients can be identified by baseline increases in 3 genes. Post-exercise increases for 4 genes meet published criteria as an objective biomarker for CFS, and could be useful in guiding treatment selection for different subgroups.
Copyright © 2011 The Association for the Publication of the Journal of Internal Medicine.
PMID:21615807[PubMed - as supplied by publisher]
Source:
http://www.actionforme.org.uk/get-informed/news/archived-news/research-news/2011/gene-expression-alterations-following-moderate-exercise
More info:
http://www.research1st.com/2011/06/02/exercise-challenge-reveals-potential-cfs-biomarkers/
http://www.ncbi.nlm.nih.gov/pubmed/21615807
donderdag 29 september 2011
Alcohol intolerance - a question of immunity
http://www.adelaide.edu.au/news/news48561.html
Drunk behaviour - a question of immunity
Thursday, 29 September 2011
University of Adelaide researchers have found that immune cells in your brain may contribute to how you respond to alcohol.
Lead researcher Dr Mark Hutchinson, ARC Research Fellow with the University's School of Medical Sciences, said his team's research provided new evidence that an immune response in the brain was involved in behavioural responses to alcohol.
This immune response lies behind some of the well-known alcohol-related behavioural changes, such as difficulty controlling the muscles involved in walking and talking.
"It's amazing to think that despite 10,000 years of using alcohol, and several decades of investigation into the way that alcohol affects the nerve cells in our brain, we are still trying to figure out exactly how it works," says lead researcher Dr Mark Hutchinson from the University's School of Medical Sciences.
"Alcohol is consumed annually by two billion people world-wide with its abuse posing a significant health and social problem," said Dr Hutchinson. "Over 76 million people are diagnosed with an alcohol abuse disorder.
"This work has significant implications for our understanding of the way alcohol affects us, as it is both an immunological and neuronal response. Such a shift in mindset has significant implications for identifying individuals who may have bad outcomes after consuming alcohol, and it could lead to a way of detecting people who are at greater risk of developing brain damage after long-term drinking."
The research is published in the latest edition of the British Journal of Pharmacology by PhD student Yue Wu, supervisor Dr Hutchinson, and others. Laboratory mice were given a single shot of alcohol and the researchers studied the effect of blocking toll-like receptors, a particular element of the immune system, on the behavioural changes induced by alcohol.
The researchers studied the effects of blocking the receptors by drugs, and also the effects of giving alcohol to mice that had been genetically altered so that they were lacking the functions of the selected receptors.
"The results showed that blocking this part of the immune system, either with the drug or genetically, reduced the effects of alcohol," Dr Hutchinson said. He believes similar treatment could work in humans.
"Medications targeting this specific receptor - toll-like receptor 4 - may prove beneficial in treating alcohol dependence and acute overdoses," Dr Hutchinson said.
Finally an explanation for the alcohol intolerance of ME-patients? Brain inflammation responsible for alcohol intolerance? We're on the right track!
Drunk behaviour - a question of immunity
Thursday, 29 September 2011
University of Adelaide researchers have found that immune cells in your brain may contribute to how you respond to alcohol.
Lead researcher Dr Mark Hutchinson, ARC Research Fellow with the University's School of Medical Sciences, said his team's research provided new evidence that an immune response in the brain was involved in behavioural responses to alcohol.
This immune response lies behind some of the well-known alcohol-related behavioural changes, such as difficulty controlling the muscles involved in walking and talking.
"It's amazing to think that despite 10,000 years of using alcohol, and several decades of investigation into the way that alcohol affects the nerve cells in our brain, we are still trying to figure out exactly how it works," says lead researcher Dr Mark Hutchinson from the University's School of Medical Sciences.
"Alcohol is consumed annually by two billion people world-wide with its abuse posing a significant health and social problem," said Dr Hutchinson. "Over 76 million people are diagnosed with an alcohol abuse disorder.
"This work has significant implications for our understanding of the way alcohol affects us, as it is both an immunological and neuronal response. Such a shift in mindset has significant implications for identifying individuals who may have bad outcomes after consuming alcohol, and it could lead to a way of detecting people who are at greater risk of developing brain damage after long-term drinking."
The research is published in the latest edition of the British Journal of Pharmacology by PhD student Yue Wu, supervisor Dr Hutchinson, and others. Laboratory mice were given a single shot of alcohol and the researchers studied the effect of blocking toll-like receptors, a particular element of the immune system, on the behavioural changes induced by alcohol.
The researchers studied the effects of blocking the receptors by drugs, and also the effects of giving alcohol to mice that had been genetically altered so that they were lacking the functions of the selected receptors.
"The results showed that blocking this part of the immune system, either with the drug or genetically, reduced the effects of alcohol," Dr Hutchinson said. He believes similar treatment could work in humans.
"Medications targeting this specific receptor - toll-like receptor 4 - may prove beneficial in treating alcohol dependence and acute overdoses," Dr Hutchinson said.
Finally an explanation for the alcohol intolerance of ME-patients? Brain inflammation responsible for alcohol intolerance? We're on the right track!
maandag 26 september 2011
Immunological abnormalities as potential biomarkers
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3120691/?tool=pubmed
Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis.
Brenu EW, van Driel ML, Staines DR, Ashton KJ, Ramos SB, Keane J, Klimas NG, Marshall-Gradisnik SM.
Source
Population Health and Neuroimmunology Unit, Faculty of Health Science and Medicine, Bond University, Robina, Queensland, Australia.
Abstract
BACKGROUND:
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is characterised by severe prolonged fatigue, and decreases in cognition and other physiological functions, resulting in severe loss of quality of life, difficult clinical management and high costs to the health care system. To date there is no proven pathomechanism to satisfactorily explain this disorder. Studies have identified abnormalities in immune function but these data are inconsistent. We investigated the profile of markers of immune function (including novel markers) in CFS/ME patients.
METHODS:
We included 95 CFS/ME patients and 50 healthy controls. All participants were assessed on natural killer (NK) and CD8(+) T cell cytotoxic activities, Th1 and Th2 cytokine profile of CD4(+) T cells, expression of vasoactive intestinal peptide receptor 2 (VPACR2), levels of NK phenotypes (CD56(bright) and CD56(dim)) and regulatory T cells expressing FoxP3 transcription factor.
RESULTS:
Compared to healthy individuals, CFS/ME patients displayed significant increases in IL-10, IFN-γ, TNF-α, CD4(+)CD25(+) T cells, FoxP3 and VPACR2 expression. Cytotoxic activity of NK and CD8(+) T cells and NK phenotypes, in particular the CD56(bright) NK cells were significantly decreased in CFS/ME patients. Additionally granzyme A and granzyme K expression were reduced while expression levels of perforin were significantly increased in the CFS/ME population relative to the control population. These data suggest significant dysregulation of the immune system in CFS/ME patients.
CONCLUSIONS:
Our study found immunological abnormalities which may serve as biomarkers in CFS/ME patients with potential for an application as a diagnostic tool.
Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis.
Brenu EW, van Driel ML, Staines DR, Ashton KJ, Ramos SB, Keane J, Klimas NG, Marshall-Gradisnik SM.
Source
Population Health and Neuroimmunology Unit, Faculty of Health Science and Medicine, Bond University, Robina, Queensland, Australia.
Abstract
BACKGROUND:
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is characterised by severe prolonged fatigue, and decreases in cognition and other physiological functions, resulting in severe loss of quality of life, difficult clinical management and high costs to the health care system. To date there is no proven pathomechanism to satisfactorily explain this disorder. Studies have identified abnormalities in immune function but these data are inconsistent. We investigated the profile of markers of immune function (including novel markers) in CFS/ME patients.
METHODS:
We included 95 CFS/ME patients and 50 healthy controls. All participants were assessed on natural killer (NK) and CD8(+) T cell cytotoxic activities, Th1 and Th2 cytokine profile of CD4(+) T cells, expression of vasoactive intestinal peptide receptor 2 (VPACR2), levels of NK phenotypes (CD56(bright) and CD56(dim)) and regulatory T cells expressing FoxP3 transcription factor.
RESULTS:
Compared to healthy individuals, CFS/ME patients displayed significant increases in IL-10, IFN-γ, TNF-α, CD4(+)CD25(+) T cells, FoxP3 and VPACR2 expression. Cytotoxic activity of NK and CD8(+) T cells and NK phenotypes, in particular the CD56(bright) NK cells were significantly decreased in CFS/ME patients. Additionally granzyme A and granzyme K expression were reduced while expression levels of perforin were significantly increased in the CFS/ME population relative to the control population. These data suggest significant dysregulation of the immune system in CFS/ME patients.
CONCLUSIONS:
Our study found immunological abnormalities which may serve as biomarkers in CFS/ME patients with potential for an application as a diagnostic tool.
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