Regulation of the immune response during infectious myocarditis

Abstract

Infectious myocarditis (IM) is a commonly undiagnosed condition that may cause several heart diseases, including dilated cardiomyopathy and chronic heart failure. The understanding of the physiopathology of myocardial inflammation is crucial for a timely diagnosis and for the control of the tissue damage, which may occur in some cases of IM. Of note, some experimental studies suggest that dilated cardiomyopathy could be a consequence of untreated IM. However, further research is required to address the molecular mechanisms that may link these two clinical entities. Here we review the mechanisms involved in the regulation at different levels of the immune response during IM, with a special focus on diagnostic and therapeutic perspectives of molecules that have been linked to the development of IM and the resulting chronic heart diseases.

Keywords::

• chronic heart disease
• immune response
• immunology
• inflammation
• myocarditis

Financial & competing interests disclosure

R Sesti-Costa is supported by a fellowship from Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (CNPQ), Brazil. GK Silva is supported by grant no. 2103/00579-9 from FAPESP, Brazil. PMM Guedes is supported by grant no. 5-2011 from FAPERN-PPP and a grant no. 470772/2012-3 from CNPQ, Brazil. JS Silva is also supported by funding from CNPQ and FAPESP, Brazil. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Infectious myocarditis (IM) is barely diagnosed and it may lead to dilated cardiomyopathy or chronic heart failure if it remains untreated.

• The immune response may provide valuable points that can be of help in the design of diagnostic and therapeutic approaches for IM and subsequent heart disorders.

• Expressions of innate immune receptors and the balance in macrophage subtypes M1/M2 are the key inducers of the inflammatory response during early IM.

• Treg is important in the control of exacerbated inflammation during myocarditis. These cells are usually counterbalanced by the development and expansion of Th1 or Th17 lymphocytes, which promote intense inflammation and tissue destruction.

Notes