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Brief report
Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): Indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased
gut-intestinal permeability.
Journal: J Affect Disord. 2006 Sep 26; [Epub ahead of print]
doi:10.1016/j.jad.2006.08.021
Authors: Michael Maes [a, b, *], Ivana Mihaylova [a] and Jean-Claude Leunis
[c]
Affiliations:
[a] MCare4U Outpatient Clinics, Belgium
[b] Department of Psychiatry, Vanderbilt University Nashville, TN, USA
[c] Laboratory Ategis, Waver, Belgium
Received 18 December 2005;
revised 14 August 2006;
accepted 16 August 2006.
Available online 27 September 2006.
NLM Citation: PMID: 17007934
Abstract
There is now evidence that chronic fatigue syndrome (CFS) is accompanied by immune disorders and by increased oxidative stress.
The present study has been designed in order to examine the serum concentrations of IgA and IgM to LPS of gram-negative enterobacteria, i.e. Hafnia alvei; Pseudomonas aeruginosa, Morganella morganii, Proteus mirabilis, Pseudomonas putida, Citrobacter koseri, and Klebsiella pneumoniae in CFS patients, patients with partial CFS and normal controls.
We found that the prevalences and median values for serum IgA against the LPS of enterobacteria are significantly greater in patients with CFS than in normal volunteers and patients with partial CFS. Serum IgA levels were significantly correlated to the severity of illness, as measured by the FibroFatigue scale and to symptoms, such as irritable bowel, muscular tension, fatigue, concentration difficulties, and failing memory.
The results show that enterobacteria are involved in the etiology of CFS and that an increased gutintestinal permeability has caused an immune response to the LPS of gram-negative enterobacteria. It is suggested that all patients with CFS should be checked by means of the IgA panel used in the present study and accordingly should be treated for increased gut permeability.
Keywords: Chronic fatigue syndrome; Inflammation; Immunity; Autoimmune;
IgA; Enterobacteria; Gut permeability; Oxidative stress; Leaky |
El aumento en suero de los IgA e IgM de los LPS de las enterobacteria en el Sindrome de Fatiga Crónica: Indica la participación de las enterobacterias gram-negativas en la etiología del SFC y la presencia de un incremento en la permeabilidad de la pared intestinal.
Authors: Michael Maes [a, b, *], Ivana Mihaylova [a] and Jean-Claude Leunis
[c]
Affiliations:
[a] MCare4U Outpatient Clinics, Belgium
[b] Department of Psychiatry, Vanderbilt University Nashville, TN, USA
[c] Laboratory Ategis, Waver, Belgium
Received 18 December 2005;
revised 14 August 2006;
accepted 16 August 2006.
Available online 27 September 2006.
NLM Citation: PMID: 17007934
Abstract:
Hay ahora evidencias de que el sindrome de fatiga crónica (SFC) está acompañado por desórdenes inmunológicos y por un incremento del estress oxidativo.
El presente estudio ha sido diseñado en orden a examinar las concentraciones en suero de IgA e IgM de LPS de enterobacterias gram-negativas, p.e, Hafnia alvei, Pseudomonas putida, Citrobacter Hoseri, and Klebsiella pneumoniae en pacientes con SFC, con parcial SFC y pacientes control.
Encontramos que la prevalencia y los valores medios de IgA en suero conta los de LPS son mucho más significativos en pacientes con SFC, que en los controles normales, y los pacientes con SFC parcial.los niveles de IgA se correlacionan con la severidad del SFC, y por la medida de la escala de Fibrofatiga y por los sintomas, como intestino irritable, tensión muscular, dificultades de concentración y falta de memoria.
Los resultados muestran que las enterobacterias estan complicadas en la etiologia del SFC, y que un incremento en la permeabilidad de la pared intestinal ha causado una respuesta inmune a la LPS de de las enterobacterias gram.negativas. Esto sugiere que todos los enfermos de SFC deberían ser revisados según los resultados del IgA según presente estudio, y deberían ser tratados en caso por un aumento de su permeabilidad intestinal. |