Abstract:
:Lipopolysaccharide (LPS), the major outer surface membrane component of Gram-negative bacteria, is one of the main etiological factors in the pathogenesis of several lung diseases, such as chronic obstructive pulmonary disease. The respiratory epithelium and the macrophages comprise the dynamic interface between the outside environment and the host response to bacterial infection via cytokine secretion. In the present study, the mechanisms of LPS induced‑inflammatory response in human lung cells and macrophages were investigated. The effects of LPS exposure on cytokine production, inflammation‑related transcription factors and intracellular signaling pathway activation were assessed in human lung mucoepidermoid carcinoma H292 cells and human macrophage THP‑1 cells. The results demonstrated that LPS markedly increased the expression of interleukin (IL)‑6, IL‑8, tumor necrosis factor (TNF)‑α, matrix metallopeptidase (MMP)‑9 and tissue inhibitor of metalloproteinases‑1 in H292 cells, while it increased the production of IL‑6, IL‑8 and TNF‑α in differentiated THP‑1 cells. In addition, LPS exposure activated nuclear factor (NF)‑κB and activator protein (AP)‑1 signaling in H292 cells, while it activated NF‑κB and signal transducer and activator of transcription (STAT) 3 signaling in THP‑1 cells. Furthermore, treatment with NF‑κB, AP‑1 or STAT3 inhibitors significantly decreased the LPS‑mediated expression of IL‑8 and TNF‑α in these cells, suggesting that these pathways might serve crucial roles in LPS‑induced cytokine expression. In conclusion, LPS stimulation of H292 and THP‑1 cells induced cytokine expression and NF‑κB, mitogen‑activated protein kinase and Janus kinase/STAT3 pathway activation with subsequent nuclear translocation of NF‑κB, AP‑1 and STAT3, which demonstrated potential of the use of NF‑κB, AP‑1 and STAT3 in therapies for conditions and diseases associated with chronic inflammation.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Liu X,Yin S,Chen Y,Wu Y,Zheng W,Dong H,Bai Y,Qin Y,Li J,Feng S,Zhao Pdoi
10.3892/mmr.2018.8542subject
Has Abstractpub_date
2018-04-01 00:00:00pages
5484-5491issue
4eissn
1791-2997issn
1791-3004journal_volume
17pub_type
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