Complement activation in a model of chronic fatigue syndrome

Sorensen, Bristol; Streib, Joanne E.; Strand, Matthew; Make, Barry J.; Giclas, Patricia C.; Fleshner, Monika; Jones, James F.

doi:10.1067/mai.2003.1615

Cited by 71 publications

(88 citation statements)

References 31 publications

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“…Previous reports of serum or plasma levels of complement activation products suggest that C activation takes place immediately with exhaustive exercise (36), but more slowly in the subjects in this study undergoing submaximal exercise (9). The trend of downregulation of expression with return to baseline levels in control subjects that precedes by several hours the activated proteins is in keeping with built-in regulatory processes inherent in the complement system.…”

Section: Discussionsupporting

confidence: 59%

“…Except for one Asian subject in the control group, all study subjects were white. Although age and sex of the CFS and control subjects were matched in the previous C4a split product study (9), this matching was not retained in the present study. Furthermore, no attempt was made to stratify the data on the basis of age and sex because of the small sample size and a previous report of no difference in the activation of complement pathways associated with age or sex in healthy individuals (20).…”

Section: Subjects and Blood Collectionmentioning

confidence: 77%

“…This study used a subset of subjects (eight CFS patients and seven controls) from a previous case-control study that identified a significant increase of C4a split product at 6 h postexercise in CFS subjects (9). All subjects were recruited from the National Jewish Medical and Research Center (NJMRC), Denver, CO, USA.…”

Section: Subjects and Blood Collectionmentioning

confidence: 99%

“…Therefore we previously used an exercise paradigm to determine alterations in complement split products and found that exercise induced a significant increase of C4a, a putative anaphylatoxin, at 6 hours after exercise only in CFS subjects (9). Mean symptom scores and mean scores for reduced activity and mental fatigue categories of the Multidimensional Fatigue Inventory were also significantly increased in these CFS subjects following exercise.…”

Section: Introductionmentioning

confidence: 99%

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Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Sorensen

Jones

Vernon

et al. 2009

Mol Med

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Complement activation resulting in significant increases of C4a split product may be a marker of postexertional malaise in individuals with chronic fatigue syndrome (CFS). This study focused on identification of the transcriptional control that may contribute to the increased C4a in CFS subjects after exercise. We used quantitative reverse-transcription polymerase chain reaction to evaluate differential expression of genes in the classical and lectin pathways in peripheral blood mononuclear cells (PBMCs). Calibrated expression values were normalized to the internal reference gene peptidylpropyl isomerase B (PPIB), the external reference gene ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit (rbcL), or the geometric mean (GM) of the genes ribosomal protein, large, P0 (RPLP0) and phosphoglycerate kinase 1 (PGK1). All nine genes tested, except mannose-binding lectin 2 (MBL2), were expressed in PBMCs. At 1 hour postexercise, C4, mannan-binding lectin serine protease 2 (MASP2) and ficolin 1 (FCN1) transcripts were detected at higher levels (≥2-fold) in at least 50% (4 of 8) of CFS subjects and were detected in 88% (7 of 8) CFS subjects when subjects with overexpression of either C4 or MASP2 were combined. Only an increase in the MASP2 transcript was statistically significant (PPIB, P = 0.001; GM, P = 0.047; rbcL, P = 0.045). This result may be due to the significant but transient downregulation of MASP2 in control subjects (PPIB, P = 0.023; rbcL, P = 0.027). By 6 hours postexercise, MASP2 expression was similar in both groups. In conclusion, lectin pathway responded to exercise differentially in CFS than in control subjects. MASP2 downregulation may act as an antiinflammatory acute-phase response in healthy subjects, whereas its elevated level may account for increased C4a and inflammation-mediated postexertional malaise in CFS subjects.

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Section: Discussionsupporting

confidence: 59%

Section: Subjects and Blood Collectionmentioning

confidence: 77%

Section: Subjects and Blood Collectionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Sorensen

Jones

Vernon

et al. 2009

Mol Med

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“…9 The severe exacerbation of symptoms following exercise, as seen in CFS patients, is not present in other disorders where fatigue is a predominant symptom such as depression, rheumatoid arthritis, systemic lupus erythematosus, or multiple sclerosis. 10,11 Indeed a recent study has shown that post-exertional malaise was one of the best predictors of the differential diagnosis of CFS and major depressive disorder. 12 Success of exercise therapy in CFS most likely relates initially to its ability to demonstrate to sufferers that exercise can be safely undertaken without the consequence of post-exertional malaise, therefore assisting CFS sufferers to abandon any avoidance behaviors to which they may have previously adhered.…”

Section: Introductionmentioning

confidence: 99%

Can exercise limits prevent post-exertional malaise in chronic fatigue syndrome? An uncontrolled clinical trial

et al. 2008

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Objective: It was hypothesized that the use of exercise limits prevents symptom increases and worsening of their health status following a walking exercise in people with chronic fatigue syndrome. Design: An uncontrolled clinical trial (semi-experimental design). Setting: Outpatient clinic of a university department. Subjects: Twenty-four patients with chronic fatigue syndrome. Interventions: Subjects undertook a walking test with the two concurrent exercise limits. Each subject walked at an intensity where the maximum heart rate was determined by heart rate corresponding to the respiratory exchange ratio = 1.0 derived from a previous submaximal exercise test and for a duration calculated from how long each patient felt they were able to walk. Main outcome measures: The Short Form 36 Health Survey or SF-36, the Chronic Fatigue Syndrome Symptom List, and the Chronic Fatigue Syndrome — Activities and Participation Questionnaire were filled in prior to, immediately after and 24 hours after exercise. Results: The fatigue increase observed immediately post-exercise (P= 0.006) returned to pre-exercise levels 24 hours post-exercise. The increase in pain observed immediately post-exercise was retained at 24 hours post-exercise (P=0.03). Fourteen of the 24 subjects experienced a clinically meaningful change in bodily pain (change of SF-36 bodily pain score ≥10); 6 indicated that the exercise bout had slightly worsened their health status, and 2 had a clinically meaningful decrease in vitality (change of SF-36 vitality score ≥20). There was no change in activity limitations/participation restrictions. Conclusion: It was shown that the use of exercise limits (limiting both the intensity and duration of exercise) prevents important health status changes following a walking exercise in people with chronic fatigue syndrome, but was unable to prevent short-term symptom increases.

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Chronische pijn bij patiënten met het chronisch vermoeidheidssyndroom: een indicatie voor fysiotherapie?

Nijs

Meeus²

2004

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Complement activation in a model of chronic fatigue syndrome

Cited by 71 publications

References 31 publications

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Can exercise limits prevent post-exertional malaise in chronic fatigue syndrome? An uncontrolled clinical trial

Chronische pijn bij patiënten met het chronisch vermoeidheidssyndroom: een indicatie voor fysiotherapie?

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