LPS Subtypes Activate Inflammatory Signaling Through CD-14 and TLR-4 in Human Monocytic Cells


	Research Journal of Immunology
	Year: 2020 \| Volume: 13 \| Issue: 1 \| Page No.: 1-9 DOI: 10.3923/rji.2020.1.9

LPS Subtypes Activate Inflammatory Signaling Through CD-14 and TLR-4 in Human Monocytic Cells

Waleed Alabdulmonem

, Zafar Rasheed, Abdullah S.M. Aljohani, Mohsen Almakrami, Hussain Al Ssadh

and Nelson Fernandez

Abstract: Background and Objective: The cellular component of innate immunity relies on cluster of differentiation (CD) 14 and toll-like receptor (TLR)-4 to combat harmful pathogens. This study was undertaken to investigate the effect of lipopolysaccharide (LPS) subtypes smooth (O55:B5) and LPS rough (EH100) on the expression of CD14 and TLR-4 in human leukemia macrophage-derived THP-1 cells. Materials and Methods: Monocyte to macrophage differentiation was achieved in THP-1 cells by phorbol-12-myristate-13-acetate (PMA) treatment. Surface expression of CD14 and TLR-4 were determined by flow cytometry after treatment with LPS subtypes. TNF-α was measured by ELISA. Confocal microscopy was used to determine co-localization of CD14 and TLR-4 receptors on THP-1 cell surface. Results: Treatment of THP-1 cells with LPS subtypes significantly increased the expression of CD14 and TLR-4 receptors (p<0.05). Higher levels of TNF-α were released in LPS-subtypes stimulated cells but the differences in the levels of TNF-α in differentiated and undifferentiated cells still unclear. Co-localization showed positive correlation between CD14 and TLR-4 receptors (r>0.83). Conclusion: This study revealed that monocyte to macrophage differentiation in THP-1 cells increases the surface expression of CD14 and TLR-4 receptors and also leads overproduction of TNF-α.

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How to cite this article:

Waleed Alabdulmonem, Zafar Rasheed, Abdullah S.M. Aljohani, Mohsen Almakrami, Hussain Al Ssadh and Nelson Fernandez, 2020. LPS Subtypes Activate Inflammatory Signaling Through CD-14 and TLR-4 in Human Monocytic Cells. Research Journal of Immunology, 13: 1-9.

DOI: 10.3923/rji.2020.1.9

URL: https://scialert.net/abstract/?doi=rji.2020.1.9

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