Mesenchymal stem cells-derived extracellular vesicles in acute respiratory distress syndrome: a review of current literature and potential future treatment options

Trushil G Shah, Dan Predescu, Sanda Predescu, Trushil G Shah, Dan Predescu, Sanda Predescu

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening inflammatory lung condition associated with significant morbidity and mortality. Unfortunately, the current treatment for this disease is mainly supportive. Mesenchymal stem cells (MSCs) due to their immunomodulatory properties are increasingly being studied for the treatment of ARDS and have shown promise in multiple animal studies. The therapeutic effects of MSCs are exerted in part in a paracrine manner by releasing extracellular vesicles (EVs), rather than local engraftment. MSC-derived EVs are emerging as potential alternatives to MSC therapy in ARDS. In this review, we will introduce EVs and briefly discuss current data on EVs and MSCs in ARDS. We will discuss current literature on the role of MSC-derived EVs in pathogenesis and treatment of ARDS and their potential as a treatment strategy in the future.

Keywords: Acute lung injury; Acute respiratory distress syndrome; Extracellular vesicles; Mesenchymal stem cells.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Effects of MSC-derived EVs in ARDS. After an injury, MSCs are mobilized from their specific niches [bone marrow (BM), adipose tissue, etc.], and transit via the blood to the site of injury. They participate in the tissue repair process, either directly or in a paracrine manner by releasing EVs. Also, under disease conditions, LR-MSCs migrate into the alveolar space and function hand-in-hand with the type II epithelial cells in a paracrine manner by releasing EVs to achieve epithelial repair following injury. The EVs interact/are internalized into the target cells such as endothelial cells, monocytes, macrophages, and neutrophils. The net effects are decreased apoptosis, reduced levels of pro-inflammatory cytokines, improved barrier function and increased proliferation. The cellular crosstalk between the airway epithelium and vascular endothelium and how the behavior of endothelial and epithelial cells is affected by the EVs interaction are not understood. (LR-MSC: lung resident MSC; BM-MSC: bone marrow-derived MSC; EpiC: epithelial cells; EC: endothelial cells)

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