What is it about?
Sepsis, a life-threatening condition caused by an excessive inflammatory response to infection, often leads to cardiac dysfunction, which increases the mortality rate. Current therapies are mainly supportive, but a greater understanding of cellular mechanisms during sepsis may lead to new therapeutic approaches. The present study investigates the role of a specific target (a receptor named formyl-peptide receptor 2; FPR2), highly expressed in myeloid cells. The study found that lack of FPR2 specifically in myeloid cells worsened cardiac dysfunction and clinical outcomes in a model of polymicrobial sepsis. This outcome was attributed to impaired ability of our body to deal with the infection, both locally and within the heart. This receptor mediates the action of a specific protein, termed Annexin A1, which helps our body to deal with infections: in mice lacking FPR2 in myeloid cells, Annexin A1 had limited beneficial effects in preserving cardiac function and controlling spread of the bugs. Mechanistically, this was consequent to inability to effect a macrophage phenotype switch, a fundamental phenomenon in resolution and tissue repair regulated by this endogenous protective axis centred on Annexin A1 and FPR2.
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Why is it important?
This study provides valuable insights into the cellular mechanisms showing the importance of engagement of a specific target, the receptor FPR2, in myeloid cells. It also highlights the potential of FPR2 activation as a therapeutic strategy for improving cardiac outcomes in sepsis, opening novel therapeutic development.
Read the Original
This page is a summary of: Formyl peptide receptor type 2 (FPR2) deficiency in myeloid cells amplifies sepsis-induced cardiac dysfunction, Journal of Innate Immunity, April 2023, Karger Publishers, DOI: 10.1159/000530284.
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