A locus for eosinophilia in the MES rat is on Chromosome 19

Li, Guixin; Guo, Zhanjun; Higuchi, Kenichi; Kawakubo, Masatomo; Matsumoto, Kiyoshi; Mori, Masayuki

doi:10.1007/s00335-004-2454-5

Cited by 8 publications

(11 citation statements)

References 15 publications

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“…In our previous study, we observed that the blood eosinophil count in (ACI × MES)F 1 × MES backcross rats homozygous for the mutant Cyba mes gene sacrificed at 12 weeks of age was significantly lower than in parental MES rats of the same age [14]. The reason for this difference was unclear.…”

Section: Hematologic and Histological Examinationmentioning

confidence: 95%

“…Eosinophil-related gastroenteritis or aortitis are also observed. The primary cause of eosinophilia in MES rats is a loss-of-function mutation in the gene for cytochrome b(-245), alpha polypeptide (Cyba; also known as p22 phox ), which is an essential component of the superoxide-generating NADPH oxidase complex [14,19,20]. In a previous study, we bred and characterized a congenic rat strain in which the mutant Cyba mes gene was introduced into the background of a BN strain (BN.MESCyba mes ) [37].…”

Section: Introductionmentioning

confidence: 99%

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Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

et al. 2011

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Abstract:The Matsumoto Eosinophilia Shinshu (MES) rat strain develops hereditary blood eosinophilia due to the mutant Cyba mes gene. In contrast, BN.MES-Cyba mes congenic rats, in which the mutant Cyba mes gene introduced into the background of the BN strain, have a normal blood eosinophil level despite showing robust proliferation of eosinophils in the bone marrow. However, the congenic rats manifest focal necrosis with eosinophilic infiltration in the liver, a phenotype rarely observed in the original MES rat strain. To elucidate the genetic basis for the strain differences, (MES × BN.MES-Cyba mes )F 2 rats were bred, and genetic analyses of phenotypes for eosinophilia were performed. Blood and bone marrow eosinophil levels in the F 2 rats showed broad distributions, suggesting that the traits were under the influence of multiple genes. Genetic association studies revealed that BN-derived marker loci on chromosomes 9 and 5 were responsible for the increase in eosinophil level in the bone marrow, decrease in blood eosinophil level, and the induction of focal necrosis with eosinophilic infiltration in the liver. The BN-derived allele of the marker gene on chromosome 1 was responsible for the decrease of both bone marrow and blood eosinophil levels. These data suggest the existence of genes characterizing/distinguishing the eosinophilic phenotypes of MES and BN.MES-Cyba mes on these chromosomes, and form the basis for positional cloning studies of the genes. These studies will advance the understanding of the mechanisms involved in eosinophil mobilization from the bone marrow and recruitment to the organs.

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Section: Hematologic and Histological Examinationmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

et al. 2011

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“…In a previous study, we performed chromosomal mapping of the gene(s) associated with eosinophilia in MES rats by breeding (ACI × MES) × MES backcross progeny [2]. Blood eosinophil counts in the 328 backcrosses showed a broad distribution.…”

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confidence: 99%

“…Fifty-five rats with low eosinophil and neutrophil numbers and devoid of enlarged mediastinal lymph nodes were categorized as a normal group (Group 3). Genetic linkage analysis between abnormal phenotypes and microsatellite marker loci using the chi square test revealed that the major locus for eosinophilia (eosinophilia 1; eos1) was located in the telomeric region of the q arm of chromosome 19 [2]. Significant deviations in homozygosity of the MES allele were observed in the abnormal rats (Groups 1 and 2) at marker loci including D19Rat2 (Table 1).…”

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confidence: 99%

A Third Locus for Eosinophilia on Chromosome 1 of the MES Rats

2006

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Matsumoto Eosinophilia Shinshu (MES) is a rat strain that spontaneously develops eosinophilia and eosinophil-related inflammatory lesions in many organsThe etiology of the majority of idiopathic HES cases and the mechanisms of eosinophilopoiesis remain poorly understood.Matsumoto Eosinophilia Shinshu (MES) is a rat strain that develops eosinophilia spontaneously [3][4][5][6]8]. In these rats a marked increase in peripheral blood eosinophils (>500/µl) occurs at about 9 weeks of age, with eosinophilia progressing with age until the number of eosinophils eventually exceeds the level that is characteristic of human hypereosinophilia (>1,500/µl). The abnormal eosinophilic proliferation takes place in the bone marrow and is associated with enlargement of the mesenteric lymph nodes. This enlargement is the result of infiltration of eosinophils into the lymph nodes, Eosinophil is a type of white blood cell that plays an important role in the innate immune system, especially in counteracting parasitic infections. The normal range for blood eosinophils is 40-400/µl in humans and 15-120/µl in rats. The term eosinophilia refers to conditions in which abnormally high numbers of eosinophils are found in either blood (600-1,500/µl) or tissues [1]. Eosinophilia may occur in a number of diseased conditions, which include parasitic infections, allergies, collagen vascular diseases, and neoplastic disorders. Another morbid condition distinct from these secondary eosinophilias, idiopathic hypereosinophilic syndrome (idiopathic HES), is a condition in which eosinophilia persists without any apparent etiology [7].

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“…Eosinophil-related gastroenteritis and aortitis are also observed. The primary cause of eosinophilia in MES rats is a loss-of-function mutation in the gene for cytochrome b(-245), alpha polypeptide (Cyba; also known as p22 phox ), which is an essential component of the superoxide-generating NADPH oxidase complex [11,14,15]. As animal models for eosinophilia, three transgenic mouse strains overexpressing IL-5 with different genetic backgrounds have been developed [5,10,27].…”

Section: Introductionmentioning

confidence: 99%

BN.MES-Cybames Congenic Rats Manifest Focal Necrosis with Eosinophilic Infiltration in the Liver without Blood Eosinophilia

et al. 2010

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Abstract:The Matsumoto Eosinophilia Shinshu (MES) rat strain develops hereditary blood eosinophilia and eosinophil-related inflammatory lesions in organs due to the mutant Cyba mes gene. We hypothesized that a new eosinophilia model with a different phenotype could be established by changing the genetic background of rats. We bred and characterized a congenic strain, in which the mutant Cyba mes gene was introduced into the background of a BN strain (BN.MES-Cyba mes ). The congenic rats showed robust proliferation of eosinophils in the bone marrow. Nonetheless, blood eosinophil levels of the rats remained within the normal range. In addition, the rats manifested focal necrosis with eosinophilic infiltration in the liver, a phenotype rarely observed in the original MES rat strain. These results imply the presence of genetic polymorphisms between MES and BN strains which modulate the mobilization of eosinophils to the peripheral circulation and organs. The newly established BN.MES-Cyba mes congenic rat strain, together with the original MES strain, will provide useful models for elucidating the molecular genetic mechanisms involved in the development and trafficking of eosinophils.

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A locus for eosinophilia in the MES rat is on Chromosome 19

Cited by 8 publications

References 15 publications

Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

A Third Locus for Eosinophilia on Chromosome 1 of the MES Rats

BN.MES-Cybames Congenic Rats Manifest Focal Necrosis with Eosinophilic Infiltration in the Liver without Blood Eosinophilia

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