Related Experiment Video
Updated: May 11, 2026

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Low dose LPS does not increase TLR4 expression on monocytes in a human in vivo model
Philipp Lichte1, Jan-Sebastian Grigoleit2, Eva Maria Steiner3
1Department of Orthopaedic Trauma Surgery, Medical School of the RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany; Department of Trauma Surgery, University Essen Medical School, Hufelandstrasse 55, 45122 Essen, Germany.
Low-dose lipopolysaccharide (LPS) stimulation in humans increased CD11b expression on monocytes but not Toll-like receptor 4 (TLR4) expression. This suggests CD11b, not TLR4, is key for early inflammatory recognition.
Area of Science:
- Immunology
- Cell Biology
- Inflammation Research
Background:
- Toll-like receptor 4 (TLR4) recognizes lipopolysaccharides (LPS) and is crucial for inflammatory responses.
- CD11b, expressed on monocytes, mediates leukocyte adhesion and migration during inflammation.
Purpose of the Study:
- To investigate the in vivo expression of TLR4 and CD11b on human monocytes following low-dose LPS stimulation.
- To understand the early molecular changes in monocytes during an induced inflammatory response.
Main Methods:
- A double-blind, randomized crossover study involving 16 healthy males.
- Administration of low-dose LPS or saline, followed by analysis of vital signs, blood counts, cytokines, and monocyte surface marker expression (TLR4, CD11b).
Main Results:
- LPS induced a transient inflammatory response, including increased body temperature, leukocyte count, and pro- and anti-inflammatory cytokines.
- Significant upregulation of CD11b expression on monocytes was observed.
- No detectable change in TLR4 expression on circulating monocytes occurred.
Conclusions:
- Early changes in TLR4 expression are not consistently observed on human monocytes after low-dose LPS exposure.
- Increased CD11b expression on monocytes may be sufficient for enhanced recognition and signaling in the early inflammatory phase.

