Innate Immune Responses to Lipopolysaccharide Stimulation
Summary
Lipopolysaccharide (LPS), the endotoxin component of Gram-negative bacterial cell walls, is a potent activator of the mammalian innate immune system. Detection of LPS occurs primarily through the co-receptor CD14 and the Toll-like receptor 4 (TLR4)–MD-2 complex, leading to recruitment of adaptor proteins such as MyD88 and TRIF. Downstream signalling cascades converge on transcription factors including NF-κB and IRFs to drive rapid expression of pro-inflammatory cytokines (for example, tumour necrosis factor and interleukin-6), chemokines and type I interferons. Concurrently, LPS engagement triggers metabolic reprogramming in myeloid cells, enhancing glycolysis and mitochondrial reactive oxygen species to sustain antimicrobial functions. Phagocytic uptake of bacteria is amplified by upregulation of surface receptors and the release of extracellular vesicles bearing pattern-recognition molecules. Regulation of LPS responses involves soluble binding proteins, negative feedback loops (such as endotoxin tolerance) and anti-inflammatory mediators, which together balance pathogen clearance with prevention of excessive tissue damage. This finely tuned system underlies susceptibility to sepsis, chronic inflammatory disorders and the design of immunomodulatory therapies.
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Innate Immune Responses to Lipopolysaccharide Stimulation publication trend
The graph below shows the total number of articles in innate immune responses to lipopolysaccharide stimulation across all publications each year (not limited to Nature Index journals).
Technical terms
Lipopolysaccharide (LPS): A glycolipid endotoxin from Gram-negative bacteria that activates innate immune signalling.
CD14: A glycosylphosphatidylinositol-anchored co-receptor that presents LPS to TLR4.
Toll-like receptor 4 (TLR4): A membrane-spanning pattern-recognition receptor that initiates inflammatory signalling upon LPS binding.
NF-κB: A transcription factor family central to expression of pro-inflammatory genes.
MyD88/TRIF: Adaptor proteins that mediate TLR4-dependent signalling pathways leading to distinct transcriptional programmes.
References
- Apoptotic Cell-Derived CD14(+) Microparticles Promote the Phagocytic Activity of Neutrophilic Precursor Cells in the Phagocytosis of Apoptotic Cells. Cells (2023).
- Non-ionic surfactant vesicles exert anti-inflammatory effects through inhibition of NFκB. Journal of Inflammation (2024).
- Enhanced Mouse Susceptibility to Endotoxin Shock after Plasmodium yoelii Infection Is Correlated with Increased Serum Levels of Lipopolysaccharide Soluble Receptors. International Journal of Molecular Sciences (2023).
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