Therapy with granulocyte colony-stimulating factor in the chronic stage, but not in the acute stage, improves experimental autoimmune myocarditis in rats via nitric oxide

Shimada, Keisuke; Okabe, Taka-aki; Mikami, Yu; Hattori, Miki; Fujita, Masatoshi; Kishimoto, Chiharu

doi:10.1016/j.yjmcc.2010.02.003

Cited by 14 publications

(17 citation statements)

References 48 publications

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“…After 2 days and 7 days, the ESR concentration was decreased but the values are still higher than control. This elevation in total leukocytes is in harmony with the results of Shimada et al 10 in their model of myocarditis. Also, these results were matched with those of Kang et al 11 which showed that the initial laboratory tests in patients with myocarditiscan show leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate, and increased levels of cardiac troponins or of the creatinine kinase MB isoenzyme.…”

supporting

confidence: 90%

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

Kholoud¹,

Iman²,

Rasha³

et al. 2014

Afr H. Sci.

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Background:Myocarditis is an uncommon disease that presents with a wide range of symptoms in children and adults. It is histologically characterized by varying degrees of myocardialnecrosis, edema and cellular infiltration myocardial inflammation is a nonspecificresponse to many triggers such as bacterial infection, cardio toxic agents, ormechanical injury. Objective: This study was carried out to investigate the experimental Streptococcus faecalis induction of myocarditis and its effect on some blood parameters, inflammatory markers and histopathological changes in male albino rats. Methods: Rats were infected by intraperitoneal injection of 10 8 CFU/ ml of Streptococcus faecalis and sacrificed after one, two and seven days post infection. Biochemical analyses of blood were carried out to investigate the serum biomarkers of inflammation, liver function tests, cardiac enzymes & kidney function tests. Results: All biochemical analyses showed statistically significant increase in the measured parameters due to bacterial infections except for blood urea which appear to be normal. A significant positive correlation was observed between lactate dehydrogenase enzyme (LDH) with creatinine (r =0.778, P<0.01). In the 7 days group, there were significant positive correlations between aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (r=0.675, P<0.05), erythrocyte sedimentation rate (ESR) with Urea (r=0.659, P<0.05) and alkaline phosphatase (ALP) with C-reactive protein (CRP) (r=0.765, p<0.01). Conclusion: Many of these biomarkers will provide important new insights into pathophysiology and aid in the diagnosis and management of cardiovascular patients.

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supporting

confidence: 90%

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

Kholoud¹,

Iman²,

Rasha³

et al. 2014

Afr H. Sci.

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“…The long-term treatment with NOS inhibitor did not have a protection in mutant SOD1 mice which argues for the role of NO solely as a proinflammatory mediator in ALS [65]. NO was recently shown to be involved in GCSF-mediated regeneration in chronic myocardial disease [66]. …”

Section: Discussionmentioning

confidence: 99%

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis

Pollari

Savchenko

Jaronen

et al. 2011

J Neuroinflammation

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BackgroundGranulocyte colony stimulating factor (GCSF) is protective in animal models of various neurodegenerative diseases. We investigated whether pegfilgrastim, GCSF with sustained action, is protective in a mouse model of amyotrophic lateral sclerosis (ALS). ALS is a fatal neurodegenerative disease with manifestations of upper and lower motoneuron death and muscle atrophy accompanied by inflammation in the CNS and periphery.MethodsHuman mutant G93A superoxide dismutase (SOD1) ALS mice were treated with pegfilgrastim starting at the presymptomatic stage and continued until the end stage. After long-term pegfilgrastim treatment, the inflammation status was defined in the spinal cord and peripheral tissues including hematopoietic organs and muscle. The effect of GCSF on spinal cord neuron survival and microglia, bone marrow and spleen monocyte activation was assessed in vitro.ResultsLong-term pegfilgrastim treatment prolonged mutant SOD1 mice survival and attenuated both astro- and microgliosis in the spinal cord. Pegfilgrastim in SOD1 mice modulated the inflammatory cell populations in the bone marrow and spleen and reduced the production of pro-inflammatory cytokine in monocytes and microglia. The mobilization of hematopoietic stem cells into the circulation was restored back to basal level after long-term pegfilgrastim treatment in SOD1 mice while the storage of Ly6C expressing monocytes in the bone marrow and spleen remained elevated. After pegfilgrastim treatment, an increased proportion of these cells in the degenerative muscle was detected at the end stage of ALS.ConclusionsGCSF attenuated inflammation in the CNS and the periphery in a mouse model of ALS and thereby delayed the progression of the disease. This mechanism of action targeting inflammation provides a new perspective of the usage of GCSF in the treatment of ALS.

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“…126,127 Treating animals with G-CSF has been reported to ameliorate cardiac inflammation in EAM. 128…”

Section: Neutrophilsmentioning

confidence: 99%

Control of inflammatory heart disease by CD4⁺ T cells

Barin

Čiháková

2013

Annals of the New York Academy of Sciences

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This review focuses on autoimmune myocarditis and its sequela, inflammatory dilated cardiomyopathy (DCMI), and the inflammatory and immune mechanisms underlying the pathogenesis of these diseases. Several mouse models of myocarditis and DCMI have improved our knowledge of the pathogenesis of these diseases, informing more general problems of cardiac remodeling and heart failure. CD4(+) T cells are critical in driving the pathogenesis of myocarditis. We discuss in detail the role of T helper cell subtypes in the pathogenesis of myocarditis, the biology of T cell-derived effector cytokines, and the participation of other leukocytic effectors in mediating disease pathophysiology. We discuss interactions between these subsets in both suppressive and collaborative fashions. These findings indicate that cardiac inflammatory disease, and autoimmunity in general, may be more diverse in divergent effector mechanisms than has previously been appreciated.

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Therapy with granulocyte colony-stimulating factor in the chronic stage, but not in the acute stage, improves experimental autoimmune myocarditis in rats via nitric oxide

Cited by 14 publications

References 48 publications

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis

Control of inflammatory heart disease by CD4⁺ T cells

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Therapy with granulocyte colony-stimulating factor in the chronic stage, but not in the acute stage, improves experimental autoimmune myocarditis in rats via nitric oxide

Cited by 14 publications

References 48 publications

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

The effect of experimental streptococcus infection in myocarditis on some biochemical and inflammatory markers in albino rats

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis

Control of inflammatory heart disease by CD4+ T cells

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Product

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Control of inflammatory heart disease by CD4⁺ T cells