Propionibacterium acnes (PA) is a gram-positive anaerobic bacterium implicated as a putative etiologic agent of sarcoidosis. To characterize the pulmonary immune response to PA, C57BL/6 and BALB/c mice were intraperitoneally sensitized and intratracheally challenged with heat-killed bacteria. C57BL/6 mice challenged with PA developed a cellular immune response characterized by elevations in Th1 cytokines/chemokines, increased numbers of lymphocytes and macrophages in lung lavage fluid, and peribronchovascular granulomatous inflammation composed of T- and B-lymphocytes and epithelioid histiocytes. T-lymphocytes in the lung lavage fluid showed a marked CD4+ cell predominance. In contrast, C57BL/6 mice challenged with Staphylococcus epidermidis (SE), another gram-positive commensal of human skin, and BALB/c mice challenged with PA, showed only a modest induction of Th1 cytokines, less pulmonary inflammation, and no granulomatous changes in the lung. Enhancement of Toll-like receptor expression was seen in PA-exposed C57BL/6 mice within 24 h after exposure, suggesting that induction of innate immunity by PA contributes to the robust, polarized Th1 immune response elicited by this bacterium. These findings suggest that PA-induced pulmonary inflammation may be a useful model for testing the contributions of both bacterial and host factors in the development, maintenance, and resolution of granulomatous inflammation in the lung.
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http://dx.doi.org/10.1165/rcmb.2005-0285OC | DOI Listing |
Fluids Barriers CNS
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Laboratory for Therapeutic and Diagnostic Antibodies, KU Leuven - University of Leuven, O&N II Herestraat 49 box 820, 3000, Leuven, Belgium.
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Department of Cardiology, Nanjing Drum Tower Hospital, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, 358 Zhongshan Road, 210008 Nanjing, China; Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, 358 Zhongshan Road, 210008 Nanjing, China. Electronic address:
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Department of Biochemistry, Cancer Biology, Neuroscience, and Pharmacology, School of Medicine, Meharry Medical College, 1005 D.B. Todd Jr. Blvd, Nashville, TN, USA.
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College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
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Pathol Res Pract
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Clinical Pharmacy & Pharmacology Research Institute, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Health Commission Key Laboratory of Basic Research in Sphingolipid Metabolism Related Diseases, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China; China-USA Lipids in Health and Disease Research Center, Guilin Medical University,Guilin 541001, China; Laboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin 541001, China. Electronic address:
Given the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (Her-2) in triple-negative breast cancer (TNBC) cells, the efficacy of targeted therapies is limited. In this study, we uncovered that triptolide (TP) effectively suppresses the migration and invasiveness of MDA-MB-231 cells by activating autophagic pathways. Western blotting analysis revealed that TP significantly reduced the expression levels of p62 protein, while simultaneously markedly increasing the expression levels of LC3B-II, BNIP3, BNIP3L, ATG5, and ULK1 proteins, strongly suggesting an enhancement of autophagic activity in the cells.
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