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Review
. 2017 Nov 18;18(11):2449.
doi: 10.3390/ijms18112449.

Can Youthful Mesenchymal Stem Cells from Wharton's Jelly Bring a Breath of Fresh Air for COPD?

Andrzej M Janczewski  1 , Joanna Wojtkiewicz  2   3   4 , Ewa Malinowska  5 , Anna Doboszyńska  6
Affiliations
Review

Can Youthful Mesenchymal Stem Cells from Wharton's Jelly Bring a Breath of Fresh Air for COPD?

Andrzej M Janczewski et al. Int J Mol Sci. .

Abstract

Chronic obstructive pulmonary disease (COPD) is a major global cause of morbidity and mortality, projected to become the 3rd cause of disease mortality worldwide by 2020. COPD is characterized by persistent and not fully reversible airflow limitation that is usually progressive and is associated with an abnormal chronic inflammatory response of the lung to noxious agents including cigarette smoke. Currently available therapeutic strategies aim to ease COPD symptoms but cannot prevent its progress or regenerate physiological lung structure or function. The urgently needed new approaches for the treatment of COPD include stem cell therapies among which transplantation of mesenchymal stem cells derived from Wharton's jelly (WJ-MSCs) emerges as a promising therapeutic strategy because of the unique properties of these cells. The present review discusses the main biological properties of WJ-MSCs pertinent to their potential application for the treatment of COPD in the context of COPD pathomechanisms with emphasis on chronic immune inflammatory processes that play key roles in the development and progression of COPD.

Keywords: Wharton’s jelly; anti-inflammatory effects; chronic obstructive pulmonary disease; immunomodulation; mesenchymal stem cells; therapeutic applications.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Effects of MSCs on generation, maturation, and proliferation of monocyte-derived immature (iDC) and mature dendritic cells (mDC) mediated via prostaglandin E2 (PGE2), transforming growth factor-β (TGF-β), interleukin (IL)-6; stimulation of T regulatory cells (Tregs) via PGE2, TGF-β, IL-10, cell-cell contact; inhibition of T helper (Th) cells subtype 1 (Th1) via PGE2; stimulation of Th17 cells via PGE2; macrophage differentiation via PGE2; multifaceted regulation of neutrophils via IL-6; downregulation of T cells induction, proliferation and function via PGE2, TGF-β, IL-1β, IL-6, IL-10, interferon-γ (INF-γ), indoleamine-pyrrole 2,3-dioxygenase (IDO), hepatocyte growth factor (HGF), nitric oxide (NO), cell–cell contact; inhibition of natural killer (NK) cells via PGE2, TGF-β, INF-γ, cell–cell contact; inhibition of B cells via INF-γ, chemokine (C-C motif) ligand 2 (CCL2); dash arrow: cell differentiation; solid arrow: stimulation; T-bar: inhibition.
See this image and copyright information in PMC

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