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Lipopolysaccharide Assembly and Modifications in Gram-Negative Bacteria

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 4012

Special Issue Editors


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Guest Editor
Unit of Bacterial Genetics, Gdansk University of Technology, Narutowicza 11/12, 80-233 Gdansk, Poland
Interests: protein folding; heat shock response; peptidyl prolyl cis/trans isomerases; disulfide bond formation; RpoE sigma factor; two-component systems; envelope stress; transcription factors; lipopolysaccharide
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Unit of Bacterial Genetics, Gdansk University of Technology, Narutowicza 11/12, 80-233 Gdansk, Poland
Interests: heat shock proteins; envelope stress response; protein folding catalysts; prolyl isomerase; LPS biosynthesis; LPS assembly; LPS modifications; non-coding regulatory RNAs; proteases; phosphatases; kinases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The most defining feature of Gram-negative bacteria is the presence of an asymmetric outer membrane (OM), with phospholipids facing its inner leaflet and lipopolysaccharide (LPS) on the outer surface. LPS is generally essential, constituting the major component of OM and is the causative agent of sepsis. LPS is a complex glycolipid comprised of a hydrophobic membrane-anchored lipid A and a core oligosaccharide, which is linked to O-antigen in smooth-type bacteria, with the highly conserved lipid A part constituting the endotoxin principal. The biosynthesis of LPS and assembly requires more than 50 genes and many of them are essential and being unique to bacteria are targets for the discovery of new antibiotics. LPSs are potent activators of mammalian immune system. Bacteria often alter their LPS composition, due to changes in acylation, modifications of LPS core and lipid A part, which often confer antibiotic resistance or evade detection by immune system. Recent studies have unraveled novel essential components in the regulation of a tight balance between LPS and phospholipid content, LPS transport to the OM and role of cardiolipins. In this issue, diversity of LPS structure, its modifications, assembly of LPS and detection of LPS by host immune system will be covered.

Prof. Dr. Satish Raina
Dr. Gracjana Klein
Guest Editors

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Keywords

  • genetics and enzymology of LPS biosynthesis
  • assembly and transport of LPS
  • regulatory controls of LPS biosynthesis at LpxC
  • LPS assembly proteins
  • chemical structure and diversity of LPS
  • regulated modifications of LPS
  • LPS and virulence
  • recognition of LPS by immune system
  • antibiotic resistance and LPS composition
  • envelope stress
  • phospholipids and balance with LPS

Published Papers (2 papers)

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Research

17 pages, 4276 KiB  
Article
The Mechanism of Lipopolysaccharide’s Effect on Secretion of Endometrial Mucins in Female Mice during Pregnancy
by Dezhang Lu, Wenxiang Hu, Tian Tian, Mengran Wang, Mengru Zhou and Chenchen Wu
Int. J. Mol. Sci. 2022, 23(17), 9972; https://doi.org/10.3390/ijms23179972 - 01 Sep 2022
Cited by 1 | Viewed by 1329
Abstract
The main toxic component of endotoxins released from the death or dissolution of Gram-negative bacteria is lipopolysaccharide (LPS), which exists widely in the natural environment, and a large amount of endotoxin can significantly inhibit the reproductive performance of animals. A previous study showed [...] Read more.
The main toxic component of endotoxins released from the death or dissolution of Gram-negative bacteria is lipopolysaccharide (LPS), which exists widely in the natural environment, and a large amount of endotoxin can significantly inhibit the reproductive performance of animals. A previous study showed that endotoxins mainly damaged the physiological function of mucins in the endometrium, but the mechanism is not clear. In this study, the PI3K/Akt signaling pathway was not activated, and the NF-κB signaling pathway was inhibited by LPS treatment; the expression of occludin and E-cadherin proteins were decreased and ZO-1 protein expression was increased, because LPS can lead to the mucous layer becoming thinner, so that the embryonic survival rate is significantly reduced in early pregnancy. In middle and late pregnancy, LPS translocated to the epithelial cells of the uterus and the expression of claudin-1, JAMA, and E-cadherin proteins were decreased; at this time, a large number of glycosaminoglycan particles were secreted by endometrial gland cells through the PI3K/Akt/NF-κB signaling pathway that was activated after LPS treatment, However, there was no significant difference between the survival rates of fetal mice in the LPS (+) and LPS (-) groups. Glycosaminoglycan particles and mucins are secreted by gland cells, which can protect and maintain the pregnancy in the middle and late gestational periods. Full article
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18 pages, 4598 KiB  
Article
LPS Response Is Impaired by Urban Fine Particulate Matter
by Natália de Souza Xavier Costa, Gabriel Ribeiro Júnior, Adair Aparecida dos Santos Alemany, Luciano Belotti, Marcela Frota Cavalcante, Susan Ribeiro, Mariana Matera Veras, Esper Georges Kallás, Paulo Hilário Nascimento Saldiva, Marisa Dolhnikoff and Luiz Fernando Ferraz da Silva
Int. J. Mol. Sci. 2022, 23(7), 3913; https://doi.org/10.3390/ijms23073913 - 01 Apr 2022
Cited by 2 | Viewed by 1981
Abstract
Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury [...] Read more.
Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1β, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure. Full article
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