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Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused by Pseudomonas aeruginosa via Inhibiting Overproduction of Prostaglandin E2.
Stem Cells. 2015 Jul; 33(7):2331-42.SC

Abstract

RATIONALE

New strategies for treating Pseudomonas aeruginosa pulmonary infection are urgently needed. Adipose tissue-derived mesenchymal stem cells (ASCs) may have a potential therapeutic role in P. aeruginosa-induced pulmonary infection.

METHODS

The therapeutic and mechanistic effects of ASCs on P. aeruginosa pulmonary infection were evaluated in a murine model of P. aeruginosa pneumonia.

RESULTS

ASCs exhibited protective effects against P. aeruginosa pulmonary infection, evidenced by reduced bacterial burdens, inhibition of alveolar neutrophil accumulation, decreased levels of myeloperoxidase, macrophage inflammatory protein-2 and total proteins in broncho-alveolar lavage fluid (BALF), and attenuated severity of lung injury. ASCs had no effects on BALF and serum levels of keratinocyte growth factor or Ang-1. ASCs had no effects on the levels of insulin growth factor 1 (IGF-1) in BALF, but increased IGF-1 levels in serum. ASCs inhibited the overproduction of prostaglandin E2 (PGE2) by decreasing the expression of cyclooxygenase-2 (COX2) and enhancing the expression of 15-PGDH. In addition, the addition of exogenous PGE2 with ASCs abolished many of the protective effects of ASCs, and administrating PGE2 alone exacerbated lung infection. By inhibiting production of PGE2 , ASCs improved phagocytosis and the bactericidal properties of macrophages. Furthermore suppressing PGE2 signaling by COX2 inhibition or EP2 inhibition exhibited protective effects against pulmonary infection as well.

CONCLUSIONS

In a murine model of P. aeruginosa pneumonia, ASCs exhibited protective effects by inhibiting production of PGE2 , which subsequently improved phagocytosis and the bactericidal properties of macrophages. ASCs may provide a new strategy for managing pulmonary infection caused by P. aeruginosa.

Authors+Show Affiliations

Department of Pulmonary Medicine, Huadong Hospital and d, Fudan University, Shanghai, People's Republic of China.Department of Pulmonary Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.Department of Pulmonary and Critical Care Medicine, University of California, San Francisco, USA.Department of Pulmonary Medicine, Huadong Hospital and d, Fudan University, Shanghai, People's Republic of China.Department of Pulmonary Medicine, Huadong Hospital and d, Fudan University, Shanghai, People's Republic of China.Department of Pulmonary Medicine, Huadong Hospital and d, Fudan University, Shanghai, People's Republic of China.Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.Department of Pulmonary Medicine, Huadong Hospital and d, Fudan University, Shanghai, People's Republic of China. Department of Pulmonary Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25788456

Citation

Mao, Yan-Xiong, et al. "Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused By Pseudomonas Aeruginosa Via Inhibiting Overproduction of Prostaglandin E2." Stem Cells (Dayton, Ohio), vol. 33, no. 7, 2015, pp. 2331-42.
Mao YX, Xu JF, Seeley EJ, et al. Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused by Pseudomonas aeruginosa via Inhibiting Overproduction of Prostaglandin E2. Stem Cells. 2015;33(7):2331-42.
Mao, Y. X., Xu, J. F., Seeley, E. J., Tang, X. D., Xu, L. L., Zhu, Y. G., Song, Y. L., & Qu, J. M. (2015). Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused by Pseudomonas aeruginosa via Inhibiting Overproduction of Prostaglandin E2. Stem Cells (Dayton, Ohio), 33(7), 2331-42. https://doi.org/10.1002/stem.1996
Mao YX, et al. Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused By Pseudomonas Aeruginosa Via Inhibiting Overproduction of Prostaglandin E2. Stem Cells. 2015;33(7):2331-42. PubMed PMID: 25788456.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adipose Tissue-Derived Mesenchymal Stem Cells Attenuate Pulmonary Infection Caused by Pseudomonas aeruginosa via Inhibiting Overproduction of Prostaglandin E2. AU - Mao,Yan-Xiong, AU - Xu,Jin-Fu, AU - Seeley,Eric J, AU - Tang,Xiao-Dan, AU - Xu,Lu-Lu, AU - Zhu,Ying-Gang, AU - Song,Yuan-Lin, AU - Qu,Jie-Ming, Y1 - 2015/05/13/ PY - 2014/10/20/received PY - 2015/02/19/accepted PY - 2015/3/20/entrez PY - 2015/3/20/pubmed PY - 2016/4/14/medline KW - Adipose tissue-derived mesenchymal stem cells KW - Prostaglandin E2 KW - Pseudomonas aeruginosa KW - Pulmonary infection SP - 2331 EP - 42 JF - Stem cells (Dayton, Ohio) JO - Stem Cells VL - 33 IS - 7 N2 - RATIONALE: New strategies for treating Pseudomonas aeruginosa pulmonary infection are urgently needed. Adipose tissue-derived mesenchymal stem cells (ASCs) may have a potential therapeutic role in P. aeruginosa-induced pulmonary infection. METHODS: The therapeutic and mechanistic effects of ASCs on P. aeruginosa pulmonary infection were evaluated in a murine model of P. aeruginosa pneumonia. RESULTS: ASCs exhibited protective effects against P. aeruginosa pulmonary infection, evidenced by reduced bacterial burdens, inhibition of alveolar neutrophil accumulation, decreased levels of myeloperoxidase, macrophage inflammatory protein-2 and total proteins in broncho-alveolar lavage fluid (BALF), and attenuated severity of lung injury. ASCs had no effects on BALF and serum levels of keratinocyte growth factor or Ang-1. ASCs had no effects on the levels of insulin growth factor 1 (IGF-1) in BALF, but increased IGF-1 levels in serum. ASCs inhibited the overproduction of prostaglandin E2 (PGE2) by decreasing the expression of cyclooxygenase-2 (COX2) and enhancing the expression of 15-PGDH. In addition, the addition of exogenous PGE2 with ASCs abolished many of the protective effects of ASCs, and administrating PGE2 alone exacerbated lung infection. By inhibiting production of PGE2 , ASCs improved phagocytosis and the bactericidal properties of macrophages. Furthermore suppressing PGE2 signaling by COX2 inhibition or EP2 inhibition exhibited protective effects against pulmonary infection as well. CONCLUSIONS: In a murine model of P. aeruginosa pneumonia, ASCs exhibited protective effects by inhibiting production of PGE2 , which subsequently improved phagocytosis and the bactericidal properties of macrophages. ASCs may provide a new strategy for managing pulmonary infection caused by P. aeruginosa. SN - 1549-4918 UR - https://www.unboundmedicine.com/medline/citation/25788456/Adipose_Tissue_Derived_Mesenchymal_Stem_Cells_Attenuate_Pulmonary_Infection_Caused_by_Pseudomonas_aeruginosa_via_Inhibiting_Overproduction_of_Prostaglandin_E2_ L2 - https://doi.org/10.1002/stem.1996 DB - PRIME DP - Unbound Medicine ER -