Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-2-28
pubmed:abstractText
Subjects from Sardinia, Italy, are relatively homogeneous compared to Swedes. Although ethnically distant, both populations have similarly high multiple sclerosis (MS) incidence rates. Pro- and anti-inflammatory cytokines and their receptors, signalling molecules and other immune response-associated factors might influence MS pathogenesis, though definite proof is missing. The study of populations with similar MS incidence but different genetic and environmental background could make possible the definition of factors that relate to such background differences. We selected untreated female MS patients from Sassari, Sardinia, and Stockholm, Sweden, and corresponding sex- and age-matched healthy controls (HC), to study blood mononuclear cells (MNC) for mRNA expression of 20 immune response-related genes considered relevant in MS, employing real-time PCR. Higher expression of IL-12p40 mRNA was confined to MS from both Sassari and Stockholm, compared to corresponding HC. MS patients from Sassari, but not Stockholm, expressed higher TNF-alpha compared to corresponding HC. MS patients from Stockholm, but not Sassari, expressed higher IL-6. Indoleamine 2,3 dioxygenase (IDO), a molecule necessary in tolerance induction, was lower in MS from Stockholm compared to corresponding HC. This was not observed in Sassari. No differences were detected for other members of the IL-12 family, other Th1 and Th2 cytokines, and the signalling molecules Stat 4 and 6. The results corroborate a pro-inflammatory state in MS as reflected by high expression of IL-12, TNF-alpha and IL-6, although the extent of expression of TNF-alpha, IL-6 and IDO differs between strictly matched MS patients from different high-incidence areas. This might result from genetic and/or environmental differences. They may account for some of the discrepancies regarding immune response-related molecules previously reported in MS. In conclusion, a pro-inflammatory state exists in MS patients from Sassari as well as Stockholm. The changes of pro-inflammatory and other immune response-related variables differ however between the two MS populations. This may be attributed to the genetic and/or environmental background.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/IL18R1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Indoleamine-Pyrrole 2,3,-Dioxygenase, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18 Receptor alpha..., http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytokine, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-10, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-12, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-18, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT4 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT4 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta, http://linkedlifedata.com/resource/pubmed/chemical/Tryptophan Oxygenase, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1352-4585
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
16-23
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15732262-Adult, pubmed-meshheading:15732262-Cytokines, pubmed-meshheading:15732262-DNA-Binding Proteins, pubmed-meshheading:15732262-Female, pubmed-meshheading:15732262-Genetic Heterogeneity, pubmed-meshheading:15732262-Humans, pubmed-meshheading:15732262-Indoleamine-Pyrrole 2,3,-Dioxygenase, pubmed-meshheading:15732262-Interleukin-10, pubmed-meshheading:15732262-Interleukin-12, pubmed-meshheading:15732262-Interleukin-18, pubmed-meshheading:15732262-Interleukin-18 Receptor alpha Subunit, pubmed-meshheading:15732262-Interleukin-4, pubmed-meshheading:15732262-Interleukin-6, pubmed-meshheading:15732262-Italy, pubmed-meshheading:15732262-Middle Aged, pubmed-meshheading:15732262-Multiple Sclerosis, pubmed-meshheading:15732262-Receptors, Cytokine, pubmed-meshheading:15732262-Receptors, Interleukin, pubmed-meshheading:15732262-Receptors, Interleukin-10, pubmed-meshheading:15732262-Receptors, Interleukin-12, pubmed-meshheading:15732262-Receptors, Interleukin-18, pubmed-meshheading:15732262-Receptors, Interleukin-6, pubmed-meshheading:15732262-Receptors, Tumor Necrosis Factor, pubmed-meshheading:15732262-STAT4 Transcription Factor, pubmed-meshheading:15732262-STAT6 Transcription Factor, pubmed-meshheading:15732262-Sweden, pubmed-meshheading:15732262-Trans-Activators, pubmed-meshheading:15732262-Transforming Growth Factor beta, pubmed-meshheading:15732262-Tryptophan Oxygenase, pubmed-meshheading:15732262-Tumor Necrosis Factor-alpha
pubmed:year
2005
pubmed:articleTitle
Immunological heterogeneity of multiple sclerosis in Sardinia and Sweden.
pubmed:affiliation
Neurotec Department, Karolinska Institute, Stockholm, Sweden. yu-min.huang@neurotec.ki.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't