Inhibitory Effect of Toll-Like Receptor 4 on Fusion between Phagosomes and Endosomes/Lysosomes in Macrophages
Open accessAbstract
Toll-like receptor 4 (TLR4) of macrophages recognizes LPS of Gram-negative bacteria in cooperation with CD14, which is also involved in the recognition of apoptotic cells. In this study we asked whether TLR4 plays a role in the phagocytic clearance of apoptotic cells by macrophages. Macrophages were prepared from peritoneal fluid of thioglycolate-treated mice carrying either a wild-type or a disrupted TLR4-encoding gene and were examined for their ability to phagocytose apoptotic mouse thymocytes, apoptotic Jurkat T cells, Ig-opsonized mouse thymocytes, Ig-opsonized zymosan particles, and latex beads. Both populations of macrophages equally expressed CD14 on their surfaces and showed almost equal activities of binding to and engulfing all these targets. However, apoptotic thymocytes, apoptotic Jurkat cells, and opsonized thymocytes disappeared more rapidly in TLR4-deficient macrophages than in wild-type macrophages, and the fusion between endosomes/lysosomes and phagosomes containing any target cells or particles was accelerated in mutant macrophages. Activation of the transcription factor NF-κB appeared not to occur in wild-type macrophages after engulfment, and the rate of apoptotic cell degradation in wild-type macrophages remained the same regardless of the activation of NF-κB. Finally, immunohistochemical analyses showed that ectopically expressed TLR4 was associated with phagosomes in a macrophage-derived cell line. All these results collectively indicate that TLR4 negatively regulates the degradation of engulfed cells in macrophages via a pathway independent of NF-κB.
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An inflammatory environment can hinder efferocytosis of apoptotic corpses, limited by TLR4 signals and TNF-α.
“An inflammatory environment can also hinder efferocytosis of apoptotic corpses limited by TLR4 signals and TNF-α (139–141).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [141]
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- Authors
- Shiratsuchi, A., Watanabe, I., Takeuchi, O., Akira, S., & Nakanishi, Y.
- Affiliations
- Kanazawa University (JP)
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Corresponding author
- Shiratsuchi, Akiko
- Nakanishi, Yoshinobu
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-02
- Volume
- 172
- Issue
- 4
- Pages
- 2039-2047
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1944631098
- Cited by
- 112
- References
- 52
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 4 · 2022: 3 · 2020: 4 · 2019: 5 · 2018: 2 · 2017: 5 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 7 · 2012: 6
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- TLR4, macrophages, phagosome-lysosome fusion, efferocytosis, CD14, NF-κB, phagocytosis, zymosan, latex beads
- MeSH terms
- Ammonium Chloride, Animals, Cell Line, Humans, Immunosuppressive Agents, Intracellular Fluid, Lysosomes, Macrophages, Membrane Glycoproteins, Mice, Inbred C57BL, Phagocytosis, Phagosomes, Receptors, Cell Surface, Endosomes, T-Lymphocytes, NF-kappa B, Apoptosis, Mice, Knockout, Macrolides, Jurkat Cells, Toll-Like Receptors, Toll-Like Receptor 4, Mice
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