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RESEARCH PRODUCT
Microsporidia and Its Relation to Crohn's Disease. A Retrospective Study
Rafael Gil-borrásIgnacio Catalán-serraVictoria AmigoA. MagnetCarmen Del AguilaJuan Carlos Andreu-ballesterSoledad FenoyJose Ferrando-marcoFerran BallesterCarlos Garcia-ballesterosCarmen Cuéllarsubject
Anatomy and PhysiologyNon-Clinical MedicineLymphocytePopulationlcsh:MedicineDiseaseGastroenterology and HepatologyBiologyReal-Time Polymerase Chain ReactionBiochemistryAntibodiesCrohn DiseaseT-Lymphocyte SubsetsImmune PhysiologyMicrosporidiosismedicineParasitic DiseasesCytotoxic T cellHumanslcsh:ScienceeducationBiologyRetrospective Studieseducation.field_of_studyCrohn's diseaseMultidisciplinaryHealth Care Policylcsh:RInflammatory Bowel DiseaseCase-control studyFungal DiseasesHealth Risk AnalysisEncephalitozoonImmunoglobulin Emedicine.diseaseVirologyPathophysiologymedicine.anatomical_structureInfectious DiseasesCase-Control StudiesImmunologyBlood ChemistryMicrosporidiaMedicinelcsh:QCD8Research Articledescription
Background: The cause of Crohn's Disease (CD) remains unknown. Recently a decrease in the global lymphocyte population in the peripheral blood of CD patients has been reported. This decrease was more evident in gamma delta T lymphocytes, especially gamma delta CD8+T subsets. Furthermore, a decrease of IL-7 was also observed in these patients. We propose the hypothesis that microsporidia, an obligate intracellular opportunistic parasite recently related to fungi, in CD patients can take advantage of the lymphocytes and IL-7 deficits to proliferate and to contribute to the pathophysiology of this disease. Methods and Findings: In this case-control study, serum samples were collected from 36 CD patients and from 36 healthy individuals (controls), IgE and IgG anti-Encephalitozoon antibodies were determined by ELISA; and forty-four intestinal tissue samples were analyzed through real time Polymerase Chain Reaction (PCR), twenty CD patients, nine with others diseases and 15 healthy subjects. We observed that IgE anti-Encephalitozoon levels were significantly higher in patients with CD: 0.386(+/- 0.256) vs control group, 0.201(+/- 0.147), P<0.001. However, IgG anti-Encephalitozoon values were significantly lower in CD patients: 0.361(+/- 0.256) vs control group, 0.876(+/- 0.380), P<0.001. In the group of CD patients, 6/20 (30%) were positive by real time PCR for microsporidia and, all the patients of the control group were negative by real time PCR. Conclusions: These results suggest that CD patients are a group at risk for microsporidiasis and, moreover that microsporidia may be involved as a possible etiologic factor of CD.
year | journal | country | edition | language |
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2013-01-01 |