When should we stop inflammation?

Av Nadezhda Latysheva
Overingeniør ved TREC

Inflammation is the body’s natural defense against damaged cells, viruses, bacteria, etc. It aims to remove these harmful or foreign invaders and heal itself. There are two types of inflammation: acute and chronic. While acute inflammation starts quickly and generally disappears in a few days, chronic inflammation can last for months or years. Recently, brazilian researchers from Universidade Federal de Minas Gerais in Belo Horizonte have come up with a new approach to limit an unwanted long-drawn inflammatory reaction exploiting the body’s natural mechanisms.

Inflammation begins when pro-inflammatory hormones in the body call out for white blood cells to come and clear out infection and damaged tissue. Arteries dilate, blood flow increases, and capillaries become more permeable so that white blood cells, hormones and nutrients can move into the spaces between cells. White blood cells swarm the injured area and ingest germs, dead or damaged cells and other foreign materials to help heal the body.

Pro-inflammatory agents are matched by equally powerful, closely related anti-inflammatory compounds, which move in once the threat is neutralized to begin the healing process. This last stage of inflammation is called resolution. A failure to resolve inflammation can lead to a chronic or autoimmune disease.

In a recent issue of the journal Blood, Michelle Sugimoto and co-authors describe a new way inflammation resolution can be stimulated. They found that the enzyme called plasmin could facilitate the resolution process in mice. Plasmin is known to play a major role in the process of blood clot lysis (fibrinolysis). It dissolves the clot, thereby restoring blood flow in the damaged vessel when the healing is finished. The authors showed that plasmin helps white blood cells to switch to resolving modus so that they could send anti-inflammatory signals and start “cleaning up” products of inflammation (pus). They found that another protein called Annexin A1 would mark cells to be “cleaned up” and was necessary for plasmin action on the cells.

Nowadays inflammation is recognized as a critical component in the pathophysiology of venous thrombosis (blood clot). One could suggest that modulation of the activity of plasmin and other enzymes of the fibrinolytic system could be a new way to control inflammation without compromising the body’s protective functions in venous thrombosis.

Reference: Sugimoto AM, Ribeiro CLA, Costa CRB, Vago PJ, Lima MK, Carneiro SF, Ortiz OMM, Lima NLG, Carmo FAA, Rocha MR, Perez AD, Reis AC, Pinho V, Miles LA, Garcia CC, Teixeira MM and Sousa LP. Plasmin and plasminogen induce macrophage reprogramming and regulate key steps of inflammation resolution via annexin A1. Blood (2017).

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