http://cdli.asm.org/search.dtl
Selected Abstracts
Returned: 6 citations and abstracts. Click on down arrow or scroll to see abstracts.
Kiet Phong Tiev, Edith Demettre, Philippe Ercolano, Lionel Bastide,
Bernard Lebleu, and Jean Cabane
RNase L
Levels in Peripheral Blood Mononuclear Cells: 37-Kilodalton/83-Kilodalton
Isoform Ratio Is a Potential Test for Chronic Fatigue Syndrome
Clin. Diagn. Lab. Immunol. 10: 315-316.
Benjamin H. Natelson, Shelley A. Weaver, Chin-Lin Tseng, and John E.
Ottenweller
Spinal
Fluid Abnormalities in Patients with Chronic Fatigue Syndrome
Clin. Diagn. Lab. Immunol. 12: 52-55.
PK Peterson, SA Sirr, FC Grammith, CH Schenck, AM Pheley, S Hu, and CC Chao
Effects
of mild exercise on cytokines and cerebral blood flow in chronic fatigue
syndrome patients
Clin. Diagn. Lab. Immunol. 1: 222-226.
María A. Puertollano, Lidia Cruz-Chamorro, Elena Puertollano, María
T. Pérez-Toscano, Gerardo Álvarez de Cienfuegos, and Manuel A. de Pablo
Assessment
of Interleukin-12, Gamma Interferon, and Tumor Necrosis Factor Alpha Secretion
in Sera from Mice Fed with Dietary Lipids during Different Stages of Listeria
monocytogenes Infection
Clin. Diagn. Lab. Immunol. 12: 1098-1103.
Quanwu Zhang, Xia-Di Zhou, Thomas Denny, John E. Ottenweller, Gudrun
Lange, John J. LaManca, Marc H. Lavietes, Claudia Pollet, William C. Gause, and
Benjamin H. Natelson
Changes
in Immune Parameters Seen in Gulf War Veterans but Not in Civilians with
Chronic Fatigue Syndrome
Clin. Diagn. Lab. Immunol. 6: 6-13.
HE Prince, J Golding, and J York
Characterization
of circulating CD4+ CD8+ lymphocytes in healthy individuals prompted by
identification of a blood donor with a markedly elevated level of CD4+ CD8+
lymphocytes
Clin. Diagn. Lab. Immunol. 1: 597-605.
Abstract 1 of 6 
Clinical and Diagnostic Laboratory
Immunology, March 2003, p. 315-316, Vol. 10, No. 2
1071-412X/03/$08.00+0 DOI: 10.1128/CDLI.10.2.315-316.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
RNase L Levels in Peripheral Blood Mononuclear Cells: 37-Kilodalton/83-Kilodalton Isoform Ratio Is a Potential Test for Chronic Fatigue Syndrome
Kiet Phong Tiev,1* Edith Demettre,2 Philippe Ercolano,1 Lionel Bastide,2 Bernard Lebleu,2 and Jean Cabane1
Service de Médecine Interne, Hôpital Saint Antoine, 75571 Paris Cedex 12,1 UMR 5124 CNRS, Université Montpellier 2, 34293 Montpellier Cedex 5, France2
Received 17 May 2002/ Returned for modification 26 September 2002/ Accepted 30 December 2002
Chronic fatigue syndrome (CFS) is a disorder characterized by debilitating fatigue associated with immunological abnormalities. The etiology remains unclear. A low-molecular-mass (37 kDa) isoform of RNase L has been described in peripheral blood mononuclear cell (PBMC) extracts, and the ratio of two isoforms of RNase L (37 kDa/83 kDa) has been proposed as a potential biochemical marker of CFS. In a prospective case-control study, we tested whether the RNase L 37-kDa/83-kDa ratio could discriminate a SFC population. We compared the ratio of RNase L isoforms in PBMCs from 11 patients with CFS (6 women and 5 men; mean age ± standard deviation, 43.2 ± 13.8 years) and PBMCs from 14 healthy well-matched volunteers (10 women and 4 men; age, 39.1 ± 11.6 years). A ratio of RNase L of 0.4 used as a threshold allowed diagnosis of CFS with high sensitivity (91%; 95% confidence interval [CI], 57 to 99%) and specificity (71%; 95% CI, 41 to 90%). The positive and negative prognostic values were 71% (95% CI, 41 to 90%) and 91% (95% CI, 57 to 99%), respectively. In the absence of acute infection or chronic inflammation, a high RNase L ratio could distinguish CFS patients from healthy volunteers. Additional large studies and follow-up studies are required to confirm the stability of this high ratio of RNase L isoforms in a CFS group.
* Corresponding author. Mailing address: Service de Médecine Interne, Hôpital Saint Antoine, 184 Rue du Faubourg Saint Antoine, 75571 Paris Cedex 12, France. Phone: 33 (1) 49 28 30 54. Fax: 33 (1) 1 49 29 28 85. E-mail: kiet.tiev@sat.ap-hop-paris.fr .
Clinical and
Diagnostic Laboratory Immunology, March 2003, p. 315-316, Vol. 10, No. 2
1071-412X/03/$08.00+0 DOI: 10.1128/CDLI.10.2.315-316.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
[ Full Text of Tiev et al.] [Reprint (PDF) Version of Tiev et al.]
Abstract 2 of 6 Clinical and Diagnostic Laboratory
Immunology, January 2005, p. 52-55, Vol. 12, No. 1
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.1.52-55.2005
Spinal Fluid Abnormalities in Patients with Chronic Fatigue Syndrome
Benjamin H. Natelson,1* Shelley A. Weaver,1 Chin-Lin Tseng,2 and John E. Ottenweller1
CFS Cooperative Research Center,1 Department of Neurosciences and Department of Preventive Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, New Jersey2
Received 2 May 2004/ Returned for modification 3 September 2004/ Accepted 6 October 2004
Arguments exist as to the cause of chronic fatigue syndrome (CFS). Some think that it is an example of symptom amplification indicative of functional or psychogenic illness, while our group thinks that some CFS patients may have brain dysfunction. To further pursue our encephalopathy hypothesis, we did spinal taps on 31 women and 13 men fulfilling the 1994 case definition for CFS and on 8 women and 5 men serving as healthy controls. Our outcome measures were white blood cell count, protein concentration in spinal fluid, and cytokines detectable in spinal fluid. We found that significantly more CFS patients had elevations in either protein levels or number of cells than healthy controls (30 versus 0%), and 13 CFS patients had protein levels and cell numbers that were higher than laboratory norms; patients with abnormal fluid had a lower rate of having comorbid depression than those with normal fluid. In addition, of the 11 cytokines detectable in spinal fluid, (i) levels of granulocyte-macrophage colony-stimulating factor were lower in patients than controls, (ii) levels of interleukin-8 (IL-8) were higher in patients with sudden, influenza-like onset than in patients with gradual onset or in controls, and (iii) IL-10 levels were higher in the patients with abnormal spinal fluids than in those with normal fluid or controls. The results support two hypotheses: that some CFS patients have a neurological abnormality that may contribute to the clinical picture of the illness and that immune dysregulation within the central nervous system may be involved in this process.
* Corresponding author. Mailing address: Fatigue Research Center (129), VA Medical Center, 385 Tremont Ave., East Orange, NJ 07018. Phone: (973) 395-7737. Fax: (973) 395-7114. E-mail: bhn@njneuromed.org .
Clinical and Diagnostic Laboratory Immunology, January
2005, p. 52-55, Vol. 12, No. 1
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.1.52-55.2005
[ Full Text of Natelson et al.] [Reprint (PDF) Version of Natelson et al.]
Clinical and Diagnostic Laboratory Immunology, Mar 1994,
222-226, Vol 1, No. 2
Copyright © 1994 by the American Society
for Microbiology. All rights reserved.
Effects of mild exercise on cytokines and cerebral blood flow in chronic fatigue syndrome patients
PK Peterson, SA Sirr,
FC Grammith, CH Schenck, AM Pheley, S Hu and CC Chao
Department of Medicine, Hennepin County Medical Center, Minneapolis, MN 54415, USA.
Chronic fatigue syndrome (CFS) is an idiopathic disorder characterized by fatigue that is markedly exacerbated by physical exertion. In the present study, we tested the hypothesis that mild exercise (walking 1 mph [1 mile = 1.609 km] for 30 min) would provoke serum cytokine and cerebral blood flow abnormalities of potential pathogenic importance in CFS. Interleukin-1 beta, interleukin-6, and tumor necrosis factor alpha were nondetectable in sera of CFS patients (n = 10) and healthy control subjects (n = 10) pre- and postexercise. At rest, serum transforming growth factor beta (TGF-beta) levels were elevated in the CFS group compared with the control group (287 +/- 18 versus 115 +/- 5 pg/ml, respectively; P < 0.01). Serum TGF-beta and cerebral blood flow abnormalities, detected by single-photon emission-computed tomographic scanning, were accentuated postexercise in the CFS group. Although these findings were not significantly different from those in the control group, the effect of exercise on serum TGF-beta and cerebral blood flow appeared magnified in the CFS patients. Results of this study encourage future research on the interaction of physical exertion, serum cytokines, and cerebral blood flow in CFS that will adopt a more rigorous exercise program than the one used in this study.
Abstract 4 of 6 Clinical and Diagnostic Laboratory
Immunology, September 2005, p. 1098-1103, Vol. 12, No. 9
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.9.1098-1103.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Assessment of Interleukin-12, Gamma Interferon, and Tumor Necrosis Factor Alpha Secretion in Sera from Mice Fed with Dietary Lipids during Different Stages of Listeria monocytogenes Infection
María A. Puertollano, Lidia Cruz-Chamorro, Elena Puertollano, María T. Pérez-Toscano, Gerardo Álvarez de Cienfuegos, and Manuel A. de Pablo*
Unit of Microbiology, Department of Health Sciences, Faculty of Experimental Sciences, University of Jaén, E-23071 Jaén, Spain
Received 22 December 2004/ Returned for modification 3 February 2005/ Accepted 22 June 2005
Recent experimental observations have determined that
long-chain n-3 polyunsaturated fatty acids suppress immune
functions and are involved in the reduction of infectious disease
resistance. BALB/c mice were fed for 4 weeks with one of four diets
containing either olive oil (OO), fish oil (FO), hydrogenated
coconut oil, or a low fat level. Interleukin-12p70 (IL-12p70), gamma
interferon (IFN-
), and tumor necrosis factor alpha (TNF-
) production in the sera of mice fed
these diets and challenged with Listeria monocytogenes were
determined by enzyme-linked immunosorbent assay. In addition,
bacterial counts from spleens of mice were carried out at 24, 72, or
96 h of infection. Here, we quantified an initial diminution of
production of both IL-12p70 and IFN-, which appear to play an important role in the reduction
of host resistance to L. monocytogenes infection. In
addition, an efficient elimination of L. monocytogenes was
observed in spleens of mice fed a diet containing OO at 96 h of
infection, despite reductions in IL-12p70 and TNF- production, suggesting an improvement of immune
resistance. Overall, our results indicate that the initial reduction
of both IL-12 and IFN- production before L. monocytogenes infection
represents the most relevant event that corroborates the impairment
of immune resistance by n-3 polyunsaturated fatty acids
during the different stages of infection. However, we speculate that
the modulation of other cytokines must be also involved in this
response, because the alteration of cytokine production in mice fed
an FO diet in a late phase of L. monocytogenes infection was
similar to that in mice fed OO, whereas the ability to eliminate
this bacterium from the spleen was improved in the latter group.
* Corresponding author. Mailing address: Universidad de Jaén, Facultad de Ciencias Experimentales, Departamento de Ciencias de la Salud, Área de Microbiología, E-23071 Jaén, Spain. Phone: 34 953 212 003. Fax: 34 953 212 943. E-mail: mapablo@ujaen.es .
Clinical and
Diagnostic Laboratory Immunology, September 2005, p. 1098-1103, Vol. 12, No. 9
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.9.1098-1103.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
[ Full Text of Puertollano et al.] [Reprint (PDF) Version of Puertollano et al.]
Clinical and Diagnostic Laboratory Immunology, January
1999, p. 6-13, Vol. 6, No. 1
1071-412X/99/$00.00+0
Changes in Immune Parameters Seen in Gulf War Veterans but Not in Civilians with Chronic Fatigue Syndrome
Quanwu Zhang,1,2 Xia-Di Zhou,3 Thomas Denny,1,4 John E. Ottenweller,1,2 Gudrun Lange,1,5 John J. LaManca,1,2 Marc H. Lavietes,6 Claudia Pollet,1,6 William C. Gause,1,3 and Benjamin H. Natelson1,2,*
Center for Environmental Hazards Research, DVA Medical
Center, E. Orange,1 and Departments of Neurosciences,2
Pediatrics,4 Psychiatry,5 and Medicine,6
University of Medicine and Dentistry
New Jersey Medical School, Newark, New Jersey,
and Department of Microbiology, Uniformed Services University of the Health
Sciences, Bethesda, Maryland3
Received 28 May 1998/Returned for modification 14 August 1998/Accepted 2 October 1998
The purpose of this study was to evaluate immune function
through the assessment of lymphocyte subpopulations (total T cells, major
histocompatibility complex [MHC] I- and II-restricted T cells, B
cells, NK cells, MHC II-restricted T-cell-derived naive and memory
cells, and several MHC I-restricted T-cell activation markers) and
the measurement of cytokine gene expression (interleukin 2 [IL-2],
IL-4, IL-6, IL-10, IL-12, gamma interferon [IFN-
], and tumor necrosis
factor alpha [TNF-
]) from peripheral blood lymphocytes.
Subjects included two groups of patients meeting published case
definitions for chronic fatigue syndrome (CFS)a group of veterans who developed
their illness following their return home from participating in the
Gulf War and a group of nonveterans who developed the illness
sporadically. Case control comparison groups were comprised of
healthy Gulf War veterans and nonveterans, respectively. We found no
significant difference for any of the immune variables in the
nonveteran population. In contrast, veterans with CFS had
significantly more total T cells and MHC II+ T cells and
a significantly higher percentage of these lymphocyte subpopulations,
as well as a significantly lower percentage of NK cells, than the
respective controls. In addition, veterans with CFS had
significantly higher levels of IL-2, IL-10, IFN-, and TNF- than the controls. These data do not support
the hypothesis of immune dysfunction in the genesis of CFS for
sporadic cases of CFS but do suggest that service in the Persian Gulf is associated with an altered immune status in veterans who
returned with severe fatiguing illness.
* Corresponding author. Present address: Fatigue Research Center (127A), VA Medical Center, E. Orange, NJ 07018. Phone: (973) 676-1000. Fax: (973) 676-4661. E-mail: bhn@nbunj.jvnc.net .
Clinical and
Diagnostic Laboratory Immunology, January 1999, p. 6-13, Vol. 6, No. 1
1071-412X/99/$00.00+0
[ Full Text of Zhang et al.] [Reprint (PDF) Version of Zhang et al.]
Clinical and Diagnostic Laboratory Immunology, 09 1994,
597-605, Vol 1, No. 5
Copyright © 1994 by the American Society
for Microbiology. All rights reserved.
Characterization of circulating CD4+ CD8+ lymphocytes in healthy individuals prompted by identification of a blood donor with a markedly elevated level of CD4+ CD8+ lymphocytes
HE Prince, J Golding
and J York
Cellular Immunology Laboratory, American Red Cross Blood and Tissue Services,
Southern California Region, Los Angeles, USA.
During flow cytometric analysis of lymphocytes from healthy donors, we identified a donor (donor A) with 22% CD4+ CD8+ cells (versus values of < 4% for 65 other controls). To determine if CD4+ CD8+ cells from donor A and other controls were similar, we first defined the phenotypic profile of control CD4+ CD8+ cells. Enriched CD4+ CD8+ cell populations for 10 controls were prepared by a two-step positive selection scheme with anti-CD4-coated magnetic beads and anti-CD8-coated culture flasks; the selected population averaged 69% CD4+ CD8+ cells and 31% CD4+ CD8- cells. For all 10 controls, two subsets of CD4+ CD8+ cells, CD4dim CD8bright and CD4bright CD8dim, were observed. Phenotypic profiles of these two CD4+ CD8+ subsets were defined by pairing anti-CD8 with other monoclonal antibodies, and the profiles were compared with each other and with those of CD4+ CD8-, CD4- CD8bright, and CD4- CD8dim cells. CD8bright and CD4bright CD8dim cells differed in their proportions of CD62-L+ cells and in their levels of CD11a and CD2 expression. Both CD4+ CD8+ subsets resembled CD4+ CD8- cells in CD45RA, CD45RO, and CD25 expression; the comparable CD- CD8+ cells in CD62-L expression; and CD4- CD8bright cells in CD11b, CD11b, CD16/56, and CD28 expression. CD38 expression in both CD4+ CD8+ subsets was decreased compared with those of other cell subsets. Whereas control CD4+ CD8+ cells averaged 33% CD4dim CD8bright, CD4+ CD8+ cells from donor A were > 90% CD4dim CD8bright. Donor A CD4dim CD8bright cells exhibited proportional decreases in CD25 and CD62-L expression and increases in CD11b and CD54 expression compared with those of control CD4dim CD8bright cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Variability of the RNase L Isoform Ratio (37 Kilodaltons/83 Kilodaltons) in Diagnosis of Chronic Fatigue Syndrome
|
|
LETTER |
|
|
Chronic fatigue syndrome (CFS)
is a disorder characterized by debilitating fatigue whose etiology and pathophysiology remain unclear. Previous studies
showed abnormalities
of the RNase
L
pathway in
peripheral
blood
mononuclear
cells
(PBMC) from patients with CFS (1, 2). The ratio of RNase L isoforms (37 kDa/83
kDa ratio [37/83 R]) has therefore been proposed as a potential biochemical marker of CFS, with a sensitivity
of 91% and a specificity of 71% when the cutoff ratio was 0.4 (3).
In order to evaluate the variability and reproducibility of the 37/83 R in the diagnosis of CFS, we assayed it in duplicate as described by Demettre et al. (2) once a month for 3 months with nine patients fulfilling CFS criteria (mean age ± standard deviation = 43.1 ± 10.4 years). The accuracy of this ratio in the diagnosis of CFS was also tested and correlated with a clinical tool, the Multidimensional Fatigue Inventory (MFI) score, in a case-control study involving 28 CFS patients (mean age, 43.1 ± 10.4 years; MFI, 60.9 ± 14.6) and 24 healthy volunteers (mean age, 40.5 ± 9.9 years; MFI, 27.1 ± 7.7).
The results of these two assays were correlated by the Spearman test for each sample; the means of the results of the assays were calculated, and the results from 3 consecutive months were correlated. Sensitivities, specificities, and positive and negative prognostic values were calculated with different threshold ratios of RNase L isoforms (0.4, 0.45, and 0.5). Ninety-five percent confidence intervals (95% CIs) were estimated. The ages of subjects in the two groups were comparable, and the MFI scores of the CFS group were higher than those of the control group (Mann-Whitney U test; P < 0.05).
The correlation between two 37/83 R assays from the PBMC sample was lower for the CFS group than for the control group. Moreover, the correlation decreased with time (r = 0.69, 0.69, and 0.33 at the first, second, and third months, respectively) for the CFS group while staying unchanged for the control group (r = 0.95). The correlations between two average results of 37/83 R at two different months were low. The correlations between the two first two months, the second and third months, and the first and third months were 0.16, 0.14, and –0.03, respectively. The 37/83 R cutoff of 0.4 yielded the best discrimination of CFS patients from controls, with 78.6% sensitivity (95% CI, 20.5 to 46.1%) and 33.3% specificity (95% CI, 46.2 to 72.8%). The positive and negative prognostic values were 59.5% (95% CI, 67.5 to 89.7%) and 53.3% (95% CI, 39.7 to 66.9%), respectively. Finally, the correlations between the MFI and 37/83 R were very weak: 0.14 at the first month, 0.51 at the second month, and -0.3 at the last month.
Our data suggest a high variability and poor reproducibility of the 37/83 R for CFS patients and variations of the 37 kDa/83kDa R results while fatigue remains stable. This variability might be due to the increased proteolytic activity reported for PMBC of patients with CFS (2). Thus, we draw attention to the use of this test. The small sample size of this study could have lowered some correlations, but could not have lowered the variability results.
|
|
REFERENCES |
- De Meirleir, K., C. Bisbal, I. Campine, P. De Becker, T. Salehzada, E. Demettre, and B. Lebleu. 2000. A 37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome. Am. J. Med. 108:99-105.[CrossRef][Medline]
- Demettre, E., L. Bastide, A. D'Haese, K. De Smet, K. De Meirleir, K. P. Tiev, P. Englebienne, and B. Lebleu. 2002. Ribonuclease L proteolysis in peripheral blood mononuclear cells of chronic fatigue syndrome patients. J. Biol. Chem. 277:35746-35751.[Abstract/Free Full Text]
- Tiev, K. P., E. Demettre, P. Ercolano, L. Bastide, B. Lebleu, and J. Cabane. 2003. RNase L levels in peripheral blood mononuclear cells: 37-kilodalton/83-kilodalton isoform ratio is a potential test for chronic fatigue syndrome. Clin. Diagn. Lab. Immunol. 10:315-316.[Abstract/Free Full Text]
|
Kiet Phong Tiev1* |