Lipopolysaccharide as a Drug Target
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".
Deadline for manuscript submissions: 31 October 2025 | Viewed by 16
Special Issue Editor
2. Groningen Research Institute for Asthma and COPD (GRIAC), University Medical Center Groningen, University of Groningen, 9713 AV Groningen, The Netherlands
Interests: chronic inflammatory disorders; cyclic nucleotides; Epac; asthma; COPD; fibrosis; Alzheimer’s disease, Parkinson disease; air pollution
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Special Issue Information
Dear Colleagues,
Of the various surface proteins and polysaccharides that can act as pathogen-associated molecular patterns (PAMPs), lipopolysaccharide (LPS) stands out as a highly potent inducer of inflammatory responses. As such, LPS has been linked to both obstructive lung disorders (e.g., COPD, asthma, IPF, post-COVID) and neurodegenerative disorders (e.g., Alzheimer’s disease, Parkinson’s disease). Owing to its structural diversity, the precise response triggered by LPS varies greatly, which contributes to the complex relationship between lipopolysaccharides and chronic inflammatory diseases. As an endotoxin, LPS is primarily released following bacterial lysis and can subsequently associate with environmental particles such as (house) dust and air pollutants (e.g., cigarette smoke). The ubiquitous presence of LPS in household and occupational environments has been linked to the development of chronic inflammatory disorders. Furthermore, bacterial infections may lead to tissue injury, inflammation, and tissue remodeling, indicating that exposure to LPS may be particularly dangerous for already vulnerable patients (i.e., those with existing diseases).
Acute responses to LPS are initiated following its recognition by Toll-like receptors (e.g., TLR4) expressed on immune cells, which also require LPS-binding protein (LBP) and CD14. Subsequently, TLR4 triggers two (non-distinct) signaling cascades: (1) activation of interferon regulatory factors (IRFs) and the release of type 1 interferons (IFNs), which are essential for the innate immune response to bacterial infections, via TIR domain-containing adaptor molecule 1 (TICAM1/TRIF). Alongside this signaling, Tumor necrosis factor (TNF) I, a critical mediator, is released in response to LPS stimulation. TNF is initially generated in its transmembrane form (mTNF-α) and converted to its soluble form (sTNF-α) by specific metalloproteinases such as TNF-α-converting enzyme. TNF can exert its effects via TNF receptor (TNFR) 1 and 2, which have opposing functions.
We welcome studies that focus on potential innovative breakthroughs to finding a cause, treatment, and cure of LPS-driven (neuro)inflammation. Suitable topics include, but are not limited to, the following: identification of novel targets to diminish defects in immune cells, defects in sensing neuroinflammation, and the decline in both tissue barriers and mitochondria. Research may employ pharmacological screening platforms, animal models, organoids and iPSC-derived brain cells, and spatial transcriptomics. Special focus may lie on the interplay between LPS and TNF.
Prof. Dr. Martina Schmidt
Guest Editor
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Keywords
- tissue barriers
- neuroinflammation
- macrophages
- microglia
- organoids
- scaffolds
- infections
- cry-EM
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