|
| Source | Injury model | Cell delivery route | Finding and mechanism of action | Reference |
|
| Acute respiratory distress syndrome (ARDS)/acute lung injury/pneumonia |
|
| Bone marrow-derived MSCs | Murine model in LPS-induced ALI (i.t) | i.t
mBM-MSCs 5 × 105 cells
1 h/4 h/24 h after injury | Both functional and survival advantages with histological improvement in the severity of lung injury without engrafting through to stem cell chemoattractants | [58] |
| Rodent model in endotoxin-induced ALI (i.v) | i.v
rBM-MSCs 7.1 × 106 cells
2 h after injury | The beneficial effect of MSCs overexpressing HO-1 might be achieved through the engraftment of differentiated MSCs in lung through secretion of paracrine factors | [61] |
| Rodent model in paraquat poisoning-induced ALI (i.p) | i.v
rBM-MSCs 1 × 106 cells
6 h after injury | Inhibit the release of inflammatory mediator, lung edema, and lipid peroxidation | [62] |
| Rodent model in LPS-induced ALI (i.t) | Intrapleural delivery
rBM-MSCs 1 × 106 cells immediately after injury | Attenuate the severity of ALI by mediating paracrine/endocrine repair mechanism than by the cell engraftment mechanism | [63] |
| Murine model in LPS-induced ALI (i.t) | i.t
mBM-MSC MVs
12 h after injury | The therapeutic properties of MSCs can be recapitulated by the MV that MSCs actively secrete in culture through KGF | [64] |
| Murine model in LPS- or CLP-induced ALI (i.p) | i.t
hBM-MSCs 2 × 106 cells
24 h after injury | MSCs therapy at day 1 reduces lung inflammation and remodeling for each type of initial insult triggering extrapulmonary ARDS; MSCs increase MMP8 and decreaseTIMP1; MSCs shift macrophage | [65] |
|
| Adipose tissue-derived MSCs | Rodent model in IR-induced ALI | i.v
mASCs 4.8 × 106 cells
1 h and 6 h after injury | Autologous ASCs suppress inflammatory response and oxidative stress (increased NAD(P)H, HO-1) as well as enhancement of angiogenesis (VCAM1, ICAM-1) | [66] |
| Rodent model in LPS-induced ALI (i.v) | i.v
hASCs 2 × 106 cells
30 min after injury | Decrease inflammatory cytokine levels in serum and lung as well as reduce alveolar inflammatory cell infiltration in the lung and protected multiorgan injury | [67] |
| Murine model in LPS-induced ALI (i.t) | O.A
mASCs or hASCs 7.5 × 105 cells
4 h after injury | Attenuates neutrophil influx and inflammation due to the increased production of IL-10 | [68] |
|
| Umbilical cord-derived MSCs | Murine model in LPS-induced ALI (i.t) | i.t
hUC-MSCs 1 × 106 cells
3-4 h after injury | Several clinical advantages that provide expansion of CD4+CD25+Foxp3+Treg cells, balancing anti- and proinflammatory factors as well as bacterial clearance | [60] |
| Rodent model in LPS-induced ALI (i.t) | i.v
hUC-MSCs 5 × 105 cells
1 h after injury | Reduces TNF-α, IL-1β, and IL-6 but not IL-10 as well as oxidative stress | [59] |
|
| MSCs from other tissues | Murine model in LPS-induced ALI (i.t) | i.v
human orbital fat-derived MSCs 3 × 105 cells
20 min after injury | Systemic orbital fat-derived stem/stromal cells are effective in modulating inflammation | [69] |
|
| Chronic obstructive pulmonary disease (COPD)/emphysema |
|
| Bone marrow-derived MSCs | Rodent model in CS-induced emphysema (6 m) | i.t or i.v
rBM-MSCs 6 × 105-6 cells and rBMMSC-CM 0.3 mL
5 w after injury | Increased VEGF-A and inhibited the apoptosis (Bax, Bcl-2) of lung alveolar cells; TNF-α-mediated VEGF-A secretion by VEGF
The effectiveness of MSC-CM was similar to that of BMCs and MSCs, supporting a paracrine mechanism as well as decreasing apoptosis
May recover lung fibroblast from CS-induced damage through inhibition of caspase-3, induction of proliferation, and restoration of lung fibroblast repair function via PI3K/Akt pathway | [70–72] |
| Rodent model in CS-induced emphysema (11 w) | i.t
rBM-MSCs or hBM-MSCs 6 × 106 cells
after injury | A therapeutic potential in parenchymal repair by increased levels of growth factors and decreased cell apoptosis through VEGF, VEGF receptor, and TGFβ-1
Relieve airway inflammation through inhibition of COX-2/PGE2 in alveolar macrophages, mediated by the p38 MAPK and ERK pathway | [73, 74] |
|
| Adipose tissue-derived MSCs | Murine model in PPE-induced emphysema (i.t) | i.t
mASCs 5 × 105 cells
2 w after injury | ASCs ameliorate damage of alveolar structure through the release of soluble humoral factor (HGF, EGF, and SLP1) | [75] |
|
