Key result
Induction of experimental autoimmune myocarditis in rats significantly increased the percentage area of arginase 1 immunoreactivity (M2 macrophages) in cardiac lesions to 16.1% compared to 2.5% in controls.
Absolute Event Rate: 16.1% vs 2.5%
p-value: p=<0.01
Alternatively activated M2 macrophages (arginase-1 positive) are significantly increased in the early stages of experimental autoimmune myocarditis, suggesting they may play a role in modulating cardiac inflammation.
M2 macrophage increase may modulate early myocarditis inflammation; hypothesis-generating and requires human validation before clinical consideration.
To better understand the role of macrophages in early stages of experimental autoimmune myocarditis (EAM), we compared the expression of inducible nitric oxide synthase (iNOS) and arginase-1, markers for classically activated M1 and alternatively activated M2 macrophages, respectively, in the hearts of EAM-affected and control rats.Immunohistochemical evidence revealed that both iNOS-positive and arginase 1-positive macrophages were found in EAM lesions, while some cells were co-localized with both markers.This finding suggests that the increased level of arginase-1, which is partly from M2 macrophages, contributes to the modulation of EAM, possibly through the reduction of nitric oxide in the lesion.
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Oh et al. (2013) studied Experimental autoimmune myocarditis. Cardiac myosin immunization (EAM induction) vs. CFA-immunized control was evaluated on Percentage area of arginase 1 immunoreactivity (p=<0.01). Induction of experimental autoimmune myocarditis in rats significantly increased the percentage area of arginase 1 immunoreactivity (M2 macrophages) in cardiac lesions to 16.1% compared to 2.5% in controls.
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