Abstract | BACKGROUND: OBJECTIVE AND METHODS: RESULTS: Peripheral blood mononuclear cells from Global initiative for chronic Obstructive Lung Disease ( GOLD) D patients produced more CCL5 and TNF-α, and less IL-10 compared to GOLD A-C patients. SB203580 treatment suppressed CCL5 and TNF-α and stimulated IL-10 production; however, the effect of SB203580 on IL-10 was lower in the COPD group. Culture of MH-S cells with COPD serum showed a significant increase in CCL5 and a significant decrease in IL-10 compared to healthy serum. This effect was not suppressed with SB203580 treatment. CONCLUSION:
COPD serum has a potent proinflammatory effect on pulmonary cells. Inhibition of p38 phoshorylation had a limited effect in restoring impaired lymphocyte function and suppressing inflammation induced by COPD serum, implying important p38-independent inflammatory mechanisms in COPD.
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Authors | Aihong Meng, Xiaopeng Zhang, Siyu Wu, Mingxia Wu, Jing Li, Xixin Yan, Kamilla Kopec-Harding, Jiakai Wu |
Journal | International journal of chronic obstructive pulmonary disease
(Int J Chron Obstruct Pulmon Dis)
Vol. 11
Pg. 909-17
( 2016)
ISSN: 1178-2005 [Electronic] New Zealand |
PMID | 27199554
(Publication Type: Journal Article, Video-Audio Media)
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Chemical References |
- Anti-Inflammatory Agents
- CCL5 protein, human
- Chemokine CCL5
- Cytokines
- IL10 protein, human
- Imidazoles
- Inflammation Mediators
- Protein Kinase Inhibitors
- Pyridines
- Tumor Necrosis Factor-alpha
- Interleukin-10
- p38 Mitogen-Activated Protein Kinases
- SB 203580
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Topics |
- Aged
- Anti-Inflammatory Agents
(pharmacology)
- Case-Control Studies
- Cell Line
- Chemokine CCL5
(blood)
- Cytokines
(blood)
- Female
- Humans
- Imidazoles
(pharmacology)
- Inflammation Mediators
(blood)
- Interleukin-10
(blood)
- Macrophages, Alveolar
(drug effects, enzymology, immunology)
- Male
- Middle Aged
- Phosphorylation
- Protein Kinase Inhibitors
(pharmacology)
- Pulmonary Disease, Chronic Obstructive
(blood, diagnosis, immunology)
- Pyridines
(pharmacology)
- Signal Transduction
(drug effects)
- Tumor Necrosis Factor-alpha
(blood)
- p38 Mitogen-Activated Protein Kinases
(antagonists & inhibitors, metabolism)
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