The mannose-sensitive hemagglutination pilus strain of Pseudomonas aeruginosa shift peritoneal milky spot macrophages towards an M1 phenotype to dampen peritoneal dissemination
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- 作者：Zhi-Feng Miao (1)
Ting-Ting Zhao (2)
Feng Miao (3)
Zhen-Ning Wang (1)
Ying-Ying Xu (2)
Xiao-Yun Mao (2)
Jian Gao (4)
Jian-Hua Wu (1)
Xing-Yu Liu (1)
Yi You (1)
Hao Xu (1)
Hui-Mian Xu (1) - 关键词：Peritoneal carcinomatosis ; Stomach cancer ; Peritoneal macrophage ; Immunotherapy ; PA ; MSHA ; Inflammatory cytokines
- 刊名：Tumor Biology
- 出版年：2014
- 出版时间：May 2014
- 年：2014
- 卷：35
- 期：5
- 页码：4285-4293
- 全文大小：
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Ting-Ting Zhao (2)
Feng Miao (3)
Zhen-Ning Wang (1)
Ying-Ying Xu (2)
Xiao-Yun Mao (2)
Jian Gao (4)
Jian-Hua Wu (1)
Xing-Yu Liu (1)
Yi You (1)
Hao Xu (1)
Hui-Mian Xu (1)
1. Department of Surgical Oncology, The First Affiliated Hospital of China Medical University, No.155 North Nanjing Street, Heping District, Shenyang, Liaoning Province, 110001, China
2. Department of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
3. Department of Digestion, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
4. Center of Laboratory Technology and Experimental Medicine, China Medical University, Shenyang, Liaoning Province, China - ISSN：1423-0380
文摘
Peritoneal dissemination (PD) of tumor cells is the most frequent pattern of gastric cancer recurrence and the leading cause of death. Peritoneal milky spots are deemed as the site of origin of gastric cancer PD wherein the main cellular components are macrophages. A vaccine derived from the mannose-sensitive hemagglutination pilus strain of Pseudomonas aeruginosa (PA-MSHA) has exhibit strong immune modulatory properties. In the present study, we tested the hypothesis whether the PA-MSHA vaccine activated peritoneal milky spot macrophages (PMSM) in a manner that would attenuate PD. It was observed that PA-MSHA activated PMSM towards a classical activation phenotype via a toll-like receptor4/9-dependent mechanism, which increased interleukin-12 levels and promoted the expression of co-stimulatory and antigen-presenting molecules like CD80, CD86, and MHC-II (P-lt;-.05). In addition, PA-MSHA-treated PMSM exhibited strong nonspecific antitumor effects in both contact-dependent and contact-independent modes of action (P-lt;-.05). In mice treated with PA-MSHA before inoculating gastric cancer cells, we noted alleviated PD toward the untreated mice. In conclusion, our findings demonstrated that PA-MSHA can stimulate PMSM towards an M1 phenotype and that activated PMSM inhibit gastric cancer growth and PD both in vitro and in vivo. The results of the current study provide a mechanistic insight that is relevant to the potential application of PA-MSHA in the treatment of gastric cancer-mediated PD.