IL-8 analogue CXCL8 (3-72) K11R/G31P, modulates LPS-induced inflammation via AKT1-NF-kβ and ERK1/2-AP-1 pathways in THP-1 monocytes.

Authors:
Mr Williams Walana, Mr
Mr Williams Walana, Mr
Universitiy for Development Studies
Mr
Microbiology and Immunology
Tamale , Northern Region | Ghana
Jing-Jing Wang
Jing-Jing Wang
Fudan University
China
Dr. Sylvanus Kampo, Ph.D., M.med., CRA., RN.
Dr. Sylvanus Kampo, Ph.D., M.med., CRA., RN.
First Affiliated Hospital of Dalian Medical University.
Ph.D. Student
Anesthesiology
Dalian , Liaoning | China
Mahmoud Al-Azab
Mahmoud Al-Azab
Dalian Medical University
PhD candidate
Rheumatology
Dalian, liaoning | China
Abdalkhalig Elkhider
Abdalkhalig Elkhider
Dalian Medical University
Dr. Eugene Dogkotenge Kuugbee, PhD
Dr. Eugene Dogkotenge Kuugbee, PhD
University for Development Studies
Lecturer
Microbiology, Biochemistry and molecular biology
Tamale, Northern Region | Ghana

Hum Immunol 2018 Nov 17;79(11):809-816. Epub 2018 Aug 17.

Department of Immunology, Dalian Medical University, Dalian, Liaoning, China. Electronic address:

IL-8 is elevated during inflammation, and it initiates cascade of down-stream reactions. Its antagonist, CXCL8 (3-72) K11R/G31P (G31P), represses inflammatory reactions via competitive binding to CXC chemokine family, preferentially G protein-couple receptors (GPCRs) CXCR1/2. This study reports the effect of G31P on the transcription profile of lipopolysaccharide (LPS) induced inflammation in THP-1 monocytes ex-vivo. LPS (1 µg/ml) induced elevation of IL-8 was significantly reduced by G31P (20 µg/ml and 30 µg/ml), with relatively increased inhibition of CXCR2 than CXCR1. Transcription of IL-1β, IL-6, and TNF-α were significantly inhibited, while IL-10 remained relatively unchanged. G31P treatment also had repressing effect on the inflammatory associated enzymes COX-2, MMP-2, and MMP-9. Significant restriction of c-Fos, and NF-kβ mRNA expression was observed, while that of c-Jun was marginally elevated. Conversely, SP-1 mRNA expression was seen to increase appreciably by G31P treatment. While the translation of pAKT, pERK1/2, and p65- NF-kβ were down-regulated by the G31P following THP-1 cells stimulation with LPS, reactive oxygen species (ROS) expression was on the positive trajectory. Collectively, the IL-8 analogue, G31P, modulates the inflammatory profile of LPS induced inflammation in THP-1 monocytes via AKT1-NF-kβ and ERK1/2-AP-1 pathways.

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http://dx.doi.org/10.1016/j.humimm.2018.08.007DOI Listing

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November 2018
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