RGD Reference Report - Advanced intercross line mapping suggests that ncf1 (ean6) regulates severity in an animal model of guillain-barre syndrome.

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Advanced intercross line mapping suggests that ncf1 (ean6) regulates severity in an animal model of guillain-barre syndrome.
Authors:	Huberle, A Beyeen, AD Ockinger, J Ayturan, M Jagodic, M De Graaf, KL Fissolo, N Marta, M Olofsson, P Hultqvist, M Holmdahl, R Olsson, T Weissert, R
Citation:	Huberle A, etal., J Immunol. 2009 Apr 1;182(7):4432-8.
RGD ID:	2306769
Pubmed:	PMID:19299744 (View Abstract at PubMed)
DOI:	DOI:10.4049/jimmunol.0803847 (Journal Full-text)
We here present the first genetic fine mapping of experimental autoimmune neuritis (EAN), the animal model of Guillain-Barre syndrome, in a rat advanced intercross line. We identified and refined a total of five quantitative trait loci on rat chromosomes 4, 10, and 12 (RNO4, RNO10, RNO12), showing linkage to splenic IFN-gamma secretion and disease severity. All quantitative trait loci were shared with other models of complex inflammatory diseases. The quantitative trait locus showing strongest linkage to clinical disease was Ean6 and spans 4.3 Mb on RNO12, harboring the neutrophil cytosolic factor 1 (Ncf1) among other genes. Polymorphisms in Ncf1, a member of the NADPH oxidase complex, have been associated with disease regulation in experimental arthritis and encephalomyelitis. We therefore tested the Ncf1 pathway by treating rats with a NADPH oxidase complex activator and ameliorated EAN compared the oil-treated control group. By proving the therapeutic effect of stimulating the NADPH oxidase complex, our data strongly suggest the first identification of a gene regulating peripheral nervous system inflammation. Taken together with previous reports, our findings suggest a general role of Ncf1 and oxidative burst in pathogenesis of experimental autoimmune animal models.

Annotation Click to see Annotation Detail View

Disease Annotations

Body Weight Changes (IDA)

Experimental Autoimmune Neuritis (IAGP)

Guillain-Barre syndrome (IAGP)

Muscle Weakness (IAGP)

Phenotype Annotations

Mammalian Phenotype

abnormal interferon-gamma secretion (IDA)

demyelination (IDA)

increased activated T cell number (IDA)

increased T cell proliferation (IDA)

muscle weakness (IAGP,IDA)

weight loss (IAGP,IDA)

Objects Annotated

QTLs

Ean2 (Experimental allergic neuritis QTL 2)

Ean3 (Experimental allergic neuritis QTL 3)

Ean4 (Experimental allergic neuritis QTL 4)

Ean5 (Experimental allergic neuritis QTL 5)

Ean6 (Experimental allergic neuritis QTL 6)

Strains

Kini:DA,PVG-G12 (NA)

Objects referenced in this article

QTL	Cia27	Collagen induced arthritis QTL 27	Rattus norvegicus
QTL	Cia3	Collagen induced arthritis QTL 3	Rattus norvegicus
QTL	Eae18a	Experimental allergic encephalomyelitis QTL 18a	Rattus norvegicus
QTL	Eae5	Experimental allergic encephalomyelitis QTL 5	Rattus norvegicus
QTL	Oia3	Oil induced arthritis QTL 3	Rattus norvegicus
QTL	Oia4	Oil induced arthritis QTL 4	Rattus norvegicus
QTL	Pia4	Pristane induced arthritis QTL 4	Rattus norvegicus

Additional Information

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Advanced intercross line mapping suggests that ncf1 (ean6) regulates severity in an animal model of guillain-barre syndrome.

Mammalian Phenotype