LPS-Induced Inflammatory Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 10 May 2026 | Viewed by 708

Special Issue Editors


E-Mail Website
Guest Editor
1. Sino-UK Joint Laboratory of Brain Function and Injury of Henan Province, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China
2. A4245-Transplantation, Immunology and Inflammation, Faculty of Medicine, University of Tours, Tours, France
3. School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK
Interests: ROS-sensitive calcium channels; oxidative stress calcium signaling; neuroinflammation; stroke; neurodegeneration; depression
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
Interests: LPS; endotoxemia; sepsis; LPS signaling; lung inflammation; lung injury; Hsp90; drug resistance; cancer

Special Issue Information

Dear Colleagues,

Lipopolysaccharide (LPS), a key component of the outer membrane of Gram-negative bacteria, is a potent inducer of inflammation and has been widely used as a model to study inflammatory diseases. LPS triggers the activation of Toll-like receptor 4 (TLR4) and the release of pro-inflammatory cytokines, oxidative stress, and immune dysregulation, contributing to the pathogenesis of conditions such as sepsis, acute lung injury, neuroinflammation, and metabolic disorders. Despite significant progress in understanding LPS-induced signaling pathways, effective therapeutic strategies to mitigate excessive inflammation remain elusive. This Special Issue aims to gather cutting-edge research and reviews on the molecular mechanisms underlying LPS-induced inflammation, novel anti-inflammatory targets, biomarker discovery, and potential therapeutic interventions. By addressing these aspects, this issue will provide valuable insights into the development of targeted therapies for inflammatory diseases driven by bacterial endotoxins.

Dr. Lin-Hua Jiang
Dr. Pankaj Kumar
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipopolysaccharide (LPS)
  • endotoxemia
  • inflammation
  • LPS signaling
  • acute lung injury
  • inflammatory cytokines
  • therapeutic targets

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

33 pages, 26227 KB  
Article
Engineered CCR2 Cell Membrane-Wrapped Cepharanthine Liposomes for Potential Targeted Attenuation of Acute Lung Injury
by Yifan Qing, Wenbo Zhao, Liangliang Xue, Yu Luo, Yuhao Gao, Xiang Sun, Fan Li, Linxuan Dai, Jing Mo, Guoqing Xu, Zenghao Bi, Suleixin Yang, Woo Tiam Hee, Jie Li and Liang Leng
Cells 2026, 15(3), 292; https://doi.org/10.3390/cells15030292 - 4 Feb 2026
Abstract
Severe respiratory inflammation or viral infections can lead to acute lung injury (ALI), a disease characterized by diffuse inflammatory injury of the pulmonary epithelium and endothelium. Cepharanthine (CEP) is reported as a promising drug candidate due to its antiviral properties. However, CEP exhibits [...] Read more.
Severe respiratory inflammation or viral infections can lead to acute lung injury (ALI), a disease characterized by diffuse inflammatory injury of the pulmonary epithelium and endothelium. Cepharanthine (CEP) is reported as a promising drug candidate due to its antiviral properties. However, CEP exhibits poor solubility and low bioavailability. Therefore, we developed a novel liposome, named CEP@LP-MCCR2, which integrates the advantages of cell membranes and lipid materials, to achieve effective accumulation of CEP in inflamed lungs. It exhibits a 1.73-fold increase in lung accumulation at 24 h in vivo, a 4.56-fold increase in cellular uptake in MLE-12 cells. CEP@LP-MCCR2 is equipped with a CCR2-overexpressed surface, enabling it to selectively neutralize elevated levels of CCL2, which is related to ALI, thereby reducing macrophage infiltration, thereby reducing the spread of inflammation, such as a reduction in levels of key pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). CEP@LP-MCCR2 could suppress M1 macrophage polarization, which led to a marked decrease in iNOS and an increase in Arg1. It upregulated the expression of junctional proteins E-cadherin and Occludin, indicating potential recovery of the pulmonary epithelial barrier. RNA sequencing analysis implied the potential of CEP@LP-MCCR2 to inactivate the TNF/NF-κB signaling axis. Full article
(This article belongs to the Special Issue LPS-Induced Inflammatory Diseases)
Back to TopTop