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Journal articles on the topic 'Lipopolysaccharide'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2024

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1

Annenkov, Alexander Y., and Flora S. Baranova. "Lipopolysaccharide-Dependent and Lipopolysaccharide-Independent Pathways of Monocyte Desensitisation to Lipopolysaccharides." Journal of Leukocyte Biology 50, no. 3 (September 1991): 215–22. http://dx.doi.org/10.1002/jlb.50.3.215.

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2

Bahrani, K., and James D. Oliver. "Studies on the lipopolysaccharide of a virulent and an avirulent strain of Vibrio vulnificus." Biochemistry and Cell Biology 68, no. 2 (February 1, 1990): 547–51. http://dx.doi.org/10.1139/o90-078.

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Vibrio vulnificus is a marine bacterium associated with both primary septicemias and wound infections in humans. The lipopolysaccharides of a virulent and an avirulent strain of Vibrio vulnificus were compared with respect to their chemical constituents and electrophoretic characteristics. 2-Keto-3-deoxyoctonic acid, a normal constituent of the lipopolysaccharide of typical Enterobacteriaceae, was not found in the lipopolysaccharide of either strain. Hexadecenoate (C16:1) was the predominant fatty acid of the lipid A moiety of the lipopolysaccharides and of the membrane phospholipids of both strains. Hydroxy fatty acids composed 44% of the total fatty acids of the lipid A of the avirulent and 40% of those in the virulent strain. In addition, odd-numbered fatty acids were detected in both lipopolysaccharides. The electrophoretic profile was similar for both strains, but demonstrated no "ladder-like" pattern characteristic of "smooth" lipopolysaccharides. The result of this study showed no significant differences between the lipopolysaccharides of the virulent and avirulent strains of Vibrio vulnificus. The possible role for lipopolysaccharide in pathogenesis of Vibrio vulnificus infections is discussed.Key words: Vibrio, lipopolysaccharide, pathogenesis.

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3

Nakazawa, Nobuhiro, Takehiko Yokobori, Makoto Sohda, Nobuhiro Hosoi, Takayoshi Watanabe, Yuki Shimoda, Munenori Ide, et al. "Significance of Lipopolysaccharides in Gastric Cancer and Their Potential as a Biomarker for Nivolumab Sensitivity." International Journal of Molecular Sciences 24, no. 14 (July 22, 2023): 11790. http://dx.doi.org/10.3390/ijms241411790.

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Lipopolysaccharides are a type of polysaccharide mainly present in the bacterial outer membrane of Gram-negative bacteria. Recent studies have revealed that lipopolysaccharides contribute to the immune response of the host by functioning as a cancer antigen. We retrospectively recruited 198 patients with gastric cancer who underwent surgery. The presence of lipopolysaccharides was determined using immunohistochemical staining, with the intensity score indicating positivity. The relationship between lipopolysaccharides and CD8, PD-L1, TGFBI (a representative downstream gene of TGF-β signaling), wnt3a, and E-cadherin (epithelial–mesenchymal transition marker) was also investigated. Thereafter, we identified 20 patients with advanced gastric cancer receiving nivolumab and investigated the relationship between lipopolysaccharides and nivolumab sensitivity. After staining for lipopolysaccharides in the nucleus of cancer cells, 150 negative (75.8%) and 48 positive cases (24.2%) were found. The lipopolysaccharide-positive group showed increased cancer stromal TGFBI expression (p < 0.0001) and PD-L1 expression in cancer cells (p = 0.0029). Lipopolysaccharide positivity was significantly correlated with increased wnt3a signaling (p = 0.0028) and decreased E-cadherin expression (p = 0.0055); however, no significant correlation was found between lipopolysaccharide expression and overall survival rate (p = 0.71). In contrast, high TGFBI expression in the presence of LPS was associated with a worse prognosis than that in the absence of LPS (p = 0.049). Among cases receiving nivolumab, the lipopolysaccharide-negative and -positive groups had disease control rates of 66.7% and 11.8%, respectively (p = 0.088). Lipopolysaccharide positivity was associated with wnt3a, TGF-β signaling, and epithelial–mesenchymal transition and was considered to tend to promote therapeutic resistance to nivolumab.

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4

Su, Grace L. "Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 2 (August 1, 2002): G256—G265. http://dx.doi.org/10.1152/ajpgi.00550.2001.

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Endogenous gut-derived bacterial lipopolysaccharides have been implicated as important cofactors in the pathogenesis of liver injury. However, the molecular mechanisms by which lipopolysaccharides exert their effect are not entirely clear. Recent studies have pointed to proinflammatory cytokines such as tumor necrosis factor-α as mediators of hepatocyte injury. Within the liver, Kupffer cells are major sources of proinflammatory cytokines that are produced in response to lipopolysaccharides. This review will focus on three important molecular components of the pathway by which lipopolysaccharides activate Kupffer cells: CD14, Toll-like receptor 4, and lipopolysaccharide binding protein. Within the liver, lipopolysaccharides bind to lipopolysaccharide binding protein, which then facilitates its transfer to membrane CD14 on the surface of Kupffer cells. Signaling of lipopolysaccharide through CD14 is mediated by the downstream receptor Toll-like receptor 4 and results in activation of Kupffer cells. The role played by these molecules in liver injury will be examined.

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5

Fuke, Nobuo, Shojiro Sawada, Takahiro Ito-Sasaki, Kumi Y. Inoue, Yusuke Ushida, Ikuo Sato, Tomokazu Matsue, Hideki Katagiri, Hiroyuki Ueda, and Hiroyuki Suganuma. "Relationship between Plasma Lipopolysaccharide Concentration and Health Status in Healthy Subjects and Patients with Abnormal Glucose Metabolism in Japan: A Preliminary Cross-Sectional Study." J 6, no. 4 (November 30, 2023): 605–26. http://dx.doi.org/10.3390/j6040040.

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Lipopolysaccharides are components of Gram-negative bacteria. The relationship between blood lipopolysaccharide levels and health status has mainly been investigated in Europe, and there is a lack of information about Asia, particularly Japan. This study aimed to investigate the relationship between blood lipopolysaccharide levels and health status in the Japanese. We conducted two cross-sectional studies in 36 healthy subjects (Study 1) and 36 patients with abnormal glucose metabolism (AGM; Study 2). The plasma lipopolysaccharide concentration in healthy subjects was positively correlated with body mass index. The plasma lipopolysaccharide concentration in AGM patients was obviously higher than that in healthy subjects. Furthermore, in AGM patients, the plasma lipopolysaccharide concentration was positively correlated with C-peptide, fasting plasma glucose levels, triglycerides, and stage of diabetic nephropathy. The plasma lipopolysaccharide concentration was also negatively correlated with 20/(C-peptide × fasting plasma glucose), an indicator of insulin resistance, and high-density lipoprotein cholesterol. In particular, the correlation between plasma lipopolysaccharide concentration and triglycerides in AGM patients was maintained in multiple regression analyses adjusted for age, sex, or body mass index. These results suggest a possible role of lipopolysaccharides in obesity in healthy subjects and in the deterioration of triglyceride metabolism in AGM patients in the Japanese population.

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6

Sonesson, Anders, Erik Jantzen, Torill Tangen, and Ulrich Zähringer. "Lipopolysaccharides of Legionella erythra and Legionella oakridgensis." Canadian Journal of Microbiology 40, no. 8 (August 1, 1994): 666–71. http://dx.doi.org/10.1139/m94-105.

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The chemical composition of lipopolysaccharides from Legionella erythra and Legionella oakridgensis was analysed. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed both lipopolysaccharides to have a smooth-type character. The polysaccharide part of both lipopolysaccharides contained D-mannose, D-glucose, D-glycero-D-mannoheptose, L-glycero-D-manno-heptose, 2-keto-3-deoxyoctonic acid, L-fucosamine, D-glucosamine, and glucosamine phosphate. In addition, L-rhamnose, glycerol phosphate, and glucose phosphate were identified in the polysaccharide part of L. erythra lipopolysaccharide. The main sugar identified in the lipid A part of both lipopolysaccharides, 2,3-diamino-2,3-dideoxy-D-glucose, was found to be substituted with a complex fatty acid composition including at least 16 different amide-linked 3-hydroxy fatty acids. Both lipopolysaccharides contained nonhydroxy fatty acids and the uncommon 27-oxo-octacosanoic acid, 29-oxotriacontanoic acid, and 27-hydroxyoctacosanoic acid. The lipopolysaccharide of L. oakridgensis also contained 29-hydroxytriacontanoic acid. The dioic long-chain acids heptacosane-1,27-dioic acid and nonacosane-1,29-dioic acid were only present in the lipopolysaccharide of L. erythra.Key words: taxonomy, long-chain fatty acids, chemical analysis, 2,3-diamino-2,3-dideoxy-D-glucose.

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7

Xiaoting Wang and Xinglei Xiao. "Galangin inhibits lipopolysaccharide-induced inflammation and stimulates osteogenic differentiation of bone marrow mesenchymal stem cells via regulation of AKT/mTOR signaling." Allergologia et Immunopathologia 51, no. 1 (January 1, 2023): 133–39. http://dx.doi.org/10.15586/aei.v51i1.741.

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Background: Bone marrow mesenchymal stem cells (BMSCs), with the abilities of multidirec-tional differentiation and self-renewal, have been widely used in bone repair and regeneration of inflammation-stimulated oral diseases. Galangin is a flavonoid isolated from Alpinia officinarum, exerts anti-obesity, antitumor, and anti-inflammation pharmacological effects. The roles of galangin in lipopolysaccharide-induced inflammation and osteogenic differentiation of BMSCs were investigated. Methods: BMSCs were isolated from rat bone marrow and identified by flow cytometry. The isolated BMSCs were treated with 1 μg/mL lipopolysaccharides or cotreated with lipopolysaccharides and different concentrations of galangin. Cell viability and apoptosis were detected by MTT (tetrazolium component) and flow cytometry. ELISA was used to detect inflammation. Alizarin red staining was used to investigate osteogenic differentiation. Results: The rat BMSCs showed negative rate of CD34, and positive rate of CD29 and CD44. Lipopolysaccharides treatment reduced cell viability of BMSCs, and promoted the cell apoptosis. Incubation with galangin enhanced cell viability of lipopolysaccharide-stimulated BMSCs, and suppressed the cell apoptosis. Galangin decreased levels of TNF-α, IL-1β, and IL-6 in lipo-polysaccharide-stimulated BMSCs through down-regulation of NF-κB phosphorylation (p-NF-κB). Galangin up-regulated expression of osteo-specific proteins, collagen type I alpha 1 (COL1A1), osteopontin (OPN), and runt-related transcription factor 2 (RUNX2), to promote the osteogenic differentiation of lipopolysaccharide-stimulated BMSCs. Protein expression of p-AKT and p-mTOR in lipopolysaccharide-stimulated BMSCs were increased by galangin treatment. Galangin exerted an anti-inflammatory effect against lipopolysaccharide-stimulated BMSCs and promoted osteogenic differentiation through the activation of AKT/ mTOR signaling.

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8

Tian, Juan, Tao Han, and Minjuan Pan. "Friedelin Protects Against Alveolar Epithelial Cells Apoptosis in Lps-Induced Acute Pneumonia in Neonatal Rats by Suppressing NF-κB Activation." Current Topics in Nutraceutical Research 19, no. 1 (July 14, 2020): 58–63. http://dx.doi.org/10.37290/ctnr2641-452x.19:58-63.

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Neonatal pneumonia is caused by inflammation mediated by lipopolysaccharide from gram negative bacteria. This type of pneumonia is characterized by inflammatory and apoptotic responses. In this study, we have examined the effect of friedelin on lipopolysaccharide-induced pneumonia and the role of nuclear factor kappa B in this process. Also, using the human pulmonary alveolar epithelial cells as a model we examined the effect of lipopolysaccharide on the cell apoptosis and its protection by friedelin. The results show that friedelin prevented lipopolysaccharide-induced acute pneumonia in neonatal rats and cellular apoptosis by suppressing the nuclear factor kappa B signaling pathway. In summary, this study shows that the friedelin exhibits a remarkable protective effect on lung tissues exposed to lipopolysaccharides.

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9

Ranjan, Manish, Devanshi Khokhani, Sanjeeva Nayaka, Suchi Srivastava, Zachary P. Keyser, and Ashish Ranjan. "Genomic diversity and organization of complex polysaccharide biosynthesis clusters in the genus Dickeya." PLOS ONE 16, no. 2 (February 11, 2021): e0245727. http://dx.doi.org/10.1371/journal.pone.0245727.

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The pectinolytic genus Dickeya (formerly Erwinia chrysanthemi) comprises numerous pathogenic species which cause diseases in various crops and ornamental plants across the globe. Their pathogenicity is governed by complex multi-factorial processes of adaptive virulence gene regulation. Extracellular polysaccharides and lipopolysaccharides present on bacterial envelope surface play a significant role in the virulence of phytopathogenic bacteria. However, very little is known about the genomic location, diversity, and organization of the polysaccharide and lipopolysaccharide biosynthetic gene clusters in Dickeya. In the present study, we report the diversity and structural organization of the group 4 capsule (G4C)/O-antigen capsule, putative O-antigen lipopolysaccharide, enterobacterial common antigen, and core lipopolysaccharide biosynthesis clusters from 54 Dickeya strains. The presence of these clusters suggests that Dickeya has both capsule and lipopolysaccharide carrying O-antigen to their external surface. These gene clusters are key regulatory components in the composition and structure of the outer surface of Dickeya. The O-antigen capsule/group 4 capsule (G4C) coding region shows a variation in gene content and organization. Based on nucleotide sequence homology in these Dickeya strains, two distinct groups, G4C group I and G4C group II, exist. However, comparatively less variation is observed in the putative O-antigen lipopolysaccharide cluster in Dickeya spp. except for in Dickeya zeae. Also, enterobacterial common antigen and core lipopolysaccharide biosynthesis clusters are present mostly as conserved genomic regions. The variation in the O-antigen capsule and putative O-antigen lipopolysaccharide coding region in relation to their phylogeny suggests a role of multiple horizontal gene transfer (HGT) events. These multiple HGT processes might have been manifested into the current heterogeneity of O-antigen capsules and O-antigen lipopolysaccharides in Dickeya strains during its evolution.

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10

Jang, Soyoung, Soyeon Jang, Jiwon Ko, Eungyung Kim, Hyejin Hyung, Ji Yeong Park, Su-Geun Lim, Sijun Park, Myoung Ok Kim, and Zae Young Ryoo. "Protection of Neuronal Cells from Lipopolysaccharide-Induced Systemic Inflammation by Gossypetin." CURRENT TOPICS IN NUTRACEUTICAL RESEARCH 21, no. 2 (April 7, 2023): 138–43. http://dx.doi.org/10.37290/ctnr2641-452x.21:138-143.

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Systemic inflammation caused by infection, surgery, or injury can lead to cognitive decline. Lipopolysaccharides are known as toll-like receptor 4 ligands, which are common to the cell walls of gram-negative bacteria. Activation of toll-like receptor 4 leads to the production of proinflammatory cytokines that subsequently mediate systemic inflammation. Furthermore, induc¬tion of systemic inflammation by lipopolysaccharide injection in mice can affect the brain, including cognitive functions. To investigate the neuroprotective role of gossypetin in systemic inflammation, a mouse hippocampal cell line (HT22) and mice were challenged with lipopolysaccharide. The increase in proinflammatory cytokines and reactive oxygen species caused by lipopolysaccharide treatment in HT22 cells was decreased by gossypetin treatment. To evaluate the protective function against memory impairment, gossypetin was orally administered to C57BL/6J mice receiving lipopolysaccharide injec¬tion. Lipopolysaccharide-induced memory deficit was observed in lipopolysaccharide-only treated group in Y-maze test. However, the group treated with gossypetin and lipopolysaccharide had a diminution in cognitive impairment. Consistent with the behavioral test results, the proinflammatory cytokines were also relatively downregulated in the gossypetin-treated mouse group. To sum up, gossypetin can be protect the neuron cells from inflammation in vitro and prevent the cognitive impairment in mice in vivo.

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11

Kim, Yun Jeong, Eun-Ra Jang, Jong Chan Lee, Seong Jun Seo, Min Won Lee, and Chung Soo Lee. "Diarylheptanoid Hirsutenoxime Inhibits Toll-Like Receptor 4-Mediated NF-κB Activation Regulated by Akt Pathway in Keratinocytes." American Journal of Chinese Medicine 38, no. 06 (January 2010): 1207–22. http://dx.doi.org/10.1142/s0192415x10008573.

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Microbial products, including lipopolysaccharides, may be involved in the pathogenesis of inflammatory skin diseases. We examined the effect of hirsutenoxime on the Toll-like receptor 4-mediated activation of Akt and nuclear factor (NF)-κB in lipopolysaccharide-stimulated keratinocytes. Hirsutenoxime, a cell signaling Akt inhibitor, and Bay 11-7085, an inhibitor of NF-κB activation, attenuated the lipopolysaccharide-induced expression of Toll-like receptor 4, activation of NF-κB and Akt, and the production of chemokines and reactive oxygen/nitrogen species. Hirsutenoxime may reduce the Toll-like receptor 4 expression-mediated NF-κB activation, which is regulated by the Akt pathway in keratinocytes exposed to lipopolysaccharides. This effect may reduce the skin inflammatory response.

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12

Preston, Martin A., and J. L. Penner. "Characterization of cross-reacting serotypes of Campylobacter jejuni." Canadian Journal of Microbiology 35, no. 2 (February 1, 1989): 265–73. http://dx.doi.org/10.1139/m89-040.

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Some strains of Campylobacter jejuni react with more than one reference antiserum from the serotyping scheme based on heat-stable lipopolysaccharide antigens. To investigate the molecular basis of these cross-reactions, lipopolysaccharides from the reference strains for serotypes 4, 13, 16, 43, and 50 and isolates recovered during two different outbreaks of C. jejuni enteritis were analyzed by passive haemagglutination and sodium dodecyl sulphate – polyacrylamide gel electrophoresis coupled with silver staining or immunoblotting. The results showed that lipopolysaccharides from the reference strains and the isolates reacted with antisera prepared against heterologous strains in various combinations and that both silver-stainable, low Mr and non-silver-stainable, high Mr lipopolysaccharide components provided the antigenic determinants associated with the cross-reactions. There were strain-to-strain differences in the structural and antigenic properties of these macromolecules and shared antigenic determinants were not always provided by a common structure. Analysis of the silver-stained lipopolysaccharide profiles, outer membrane protein patterns, and chromosomal DNA restriction patterns indicated that strains with the same lipopolysaccharide profile could have the same outer membrane protein pattern and the same DNA restriction pattern. These results provided evidence for the presence of clones within this antigenic complex and implicated antigenic variation in some strains as the phenomenon responsible for the multiplicity of cross-reactions.Key words: Campylobacter, serotypes, cross-reaction.

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13

Haifeng, Liu, Zhang Fan, Wu Huiming, Wang Qinglai, Zhang Kuixian, and Zeng Xiaoshuai. "Polydatin Alleviates Lipopolysaccharide-Triggered Inflammatory Injury Through Up-Regulating miR-125b in Chondrogenic ATDC5 Cells." Current Topics in Nutraceutical Research 18, no. 1 (November 12, 2019): 108–14. http://dx.doi.org/10.37290/ctnr2641-452x.18:108-114.

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Osteoarthritis is a bone-joint disease prevalent in older people characterized by joint inflammation. In traditional Chinese medicine, polydatin plays an important anti-inflammatory role. This study analyzed the potential effects and possible internal mechanisms of polydatin on osteoarthritis. First, lipopolysaccharide-induced osteoarthritis injury was established in chondrogenic ATDC5 cells. Lipopolysaccharides significantly stimulated inflammatory injuries in ATDC5 cells as exemplified by a decrease in cell viability and an increase in inflammatory cytokine secretions including interleukin-6, tumor necrosis factor-a, and interleukin-1. Moreover, lipopolysacchrides also increased Cleaved caspase-3 and Cleaved Poly (ADP-ribose) polymerase to promote cell apoptosis. Second, polydatin showed significant protective effects against lipopolysaccharide-induced inflammatory injury, again exemplified by increased cell viability, decreased inflammatory cytokines, Cleaved caspase-3, and Cleaved poly (ADP-ribose) polymerase. Lastly, miR-125b and its binding target Rho-Associated Coiled-Coil Containing Protein Kinase 1 were closely associated with regulatory effects of polydatin against lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries. Polydatin alleviated lipopolysaccharide-stimulated inflammatory injuries via the down-regulation of miR-125b. The present study concludes that polydatin plays an anti-inflammatory role in lipopolysaccharide-stimulated ATDC5 cell inflammatory injuries via the down-regulation of miR-125b.

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14

Minka, S., and M. Bruneteau. "Isolement et caractérisation chimique des lipopolysaccharides de type R dans une souche hypovirulente de Yersinia pestis." Canadian Journal of Microbiology 44, no. 5 (May 1, 1998): 477–81. http://dx.doi.org/10.1139/w98-029.

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The lipopolysaccharides LPS I and LPS II, isolated from the hypovirulent EV40 strain of Yersinia pestis, are composed only of type R lipopolysaccharides. This type consists of two forms, a and b, depending on their solubility pattern in a solvent mixture containing varying proportions of chloroform, methanol, hexane, and hydrochloric acid. LPS I consists of one subtype, RIb, while LPS II consists of two subtypes, RIIa and RIIb. Analysis by gel electrophoresis shows that the mass of these lipopolysaccharide forms are in the vicinity of 2000-3000 Da. The RIb and RIIb subtypes, which are found in the majority of lipopolysaccharide I and II fractions, are composed of ketoses and amines that are similar to those occurring in LPS I and LPS II. In contrast, the two subtypes RIIa and RIIb are different both in terms of the composition of lipid A and the extent of its substitution. Certain fractions of RIIa contain only lipid A and 3-deoxy-D-manno-octulosonic acid (KDO), while other fractions of RIIb possess a lipid A, which is not substituted by arabinose. The whole set of these R-type lipopolysaccharide forms are excellent models for the study of the role of the primary structure of the polysaccharide region, and for the effect of lipid A substitution on the biological activity of bacterial lipopolysaccharides.Key words: Yersinia pestis, hypovirulence, lipopolysaccharides, R type.[Journal translation]

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15

Ageldinov, R. A., A. I. Levashova, V. S. Kokhan, and M. S. Nesterov. "Methodical aspects of lipopolysaccharides obtaining and characterization from Escherichia coli cells." Journal Biomed 17, no. 3E (October 26, 2021): 14–16. http://dx.doi.org/10.33647/2713-0428-17-3e-14-16.

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In this study, a procedure was applied to purify lipopolysaccharides from Escherichia coli based on a hot phenolic extraction protocol. The purity of the extracted lipopolysaccharides was assessed by HPLC-UV. Pyrogenic activity was determined using the Limulus Amebocyte Lysate test and used to monitor the functionality of the purified lipopolysaccharides. HPLC analysis showed a high degree of purity comparable to commercial lipopolysaccharide. Pyrogenic activity confirmed the functional activity of purified lipopolysaccharides. The presented protocol can be used to isolate lipopolysaccharides with high purity and functional activity.

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16

Ingalls, Robin R., Holger Heine, Egil Lien, Atsutoshi Yoshimura, and Douglas Golenbock. "LIPOPOLYSACCHARIDE RECOGNITION, CD14, AND LIPOPOLYSACCHARIDE RECEPTORS." Infectious Disease Clinics of North America 13, no. 2 (June 1999): 341–53. http://dx.doi.org/10.1016/s0891-5520(05)70078-7.

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17

Mutharia, Lucy W., Bonnie T. Raymond, Teri R. Dekievit, and Roselynn M. W. Stevenson. "Antibody specificities of polyclonal rabbit and rainbow trout antisera against Vibrio ordalii and serotype 0:2 strains of Vibrio anguillarum." Canadian Journal of Microbiology 39, no. 5 (May 1, 1993): 492–99. http://dx.doi.org/10.1139/m93-070.

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Polyclonal rabbit antisera raised against Vibrio ordalii and serotype 02 strains of Vibrio anguillarum showed extensive cross-reactivity with lipopolysaccharide from these bacterial pathogens of fish when tested in western immunoblot analysis. Results with absorbed polyclonal antisera indicated that lipopolysaccharide molecules from these strains had both common and strain-specific antigenic determinants, which allowed the antisera to be used to differentiate between V. ordalii and serotype 02 strains of V. anguillarum. Unlike rabbits, the immune response in rainbow trout to serotype 02 common antigenic epitopes was dependent on the source of the immunizing lipopolysaccharide antigens. Serum from fish immunized with V. ordalii antigens reacted more extensively with serotype 02 common antigens. In contrast, fish anti-V. anguillarum 02 serum did not interact with O antigens from the V. ordalii strains. Lipopolysaccharide from V. anguillarum serotype 02 and 02a strains showed identical antibody binding properties when interacted with rabbit or fish antiserum to either V. anguillarum 02 or V. ordalii. Lipopolysaccharide from V. anguillarum 02b strains did not interact with the tested rabbit or fish polyclonal sera. The results from this study suggest that fish and rabbits recognise different antigenic determinants in lipopolysaccharide from V. ordalii and serotpye 02 V. anguillarum strains; that V. ordalii and serotype 02 strains of V. anguillarum should be regarded as distinct serotype 02 subgroups based on the strain-specific antigenic determinants; and finally that the serological classification of V. anguillarum serotype 02b strains should be reexamined.Key words: antigenic heterogeneity, lipopolysaccharides, fish immune response.not available

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18

Lin, Miao-Fang, Christie Williams, Michael V. Murray, and Philip A. Ropp. "Removal of lipopolysaccharides from protein–lipopolysaccharide complexes by nonflammable solvents." Journal of Chromatography B 816, no. 1-2 (February 2005): 167–74. http://dx.doi.org/10.1016/j.jchromb.2004.11.029.

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19

Fabio, José L. Di, Jean-Robert Brisson, and Malcolm B. Perry. "Structural analysis of the three lipopolysaccharides produced by Salmonella madelia (1,6,14,25)." Biochemistry and Cell Biology 67, no. 2-3 (February 1, 1989): 78–85. http://dx.doi.org/10.1139/o89-012.

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Salmonella madelia reported to express the O-antigenic factors 1, 6, 14, and 25, defined in the Kauffmann–White classification system, was found to produce three different homogeneous lipopolysaccharides, which differed in having three structurally distinct O-polysaccharide components. The O-polysaccharide fraction obtained by mild acetic acid hydrolysis of the S. madelia lipopolysaccharide was analyzed by chemical composition, nitrous acid deamination, periodate oxidation, methylation, and 1H and 13C nuclear magnetic resonance methods and was demonstrated to be composed of three polysaccharides, PS(I), PS(II), and PS(III), which had the structures of repeating oligosaccharide units:[Formula: see text]Key words: Salmonella madelia, lipopolysaccharide, structure, analysis, nuclear magnetic resonance.

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20

Putnins, Edward E., Ali-Reza Sanaie, Qiang Wu, and James D. Firth. "Induction of Keratinocyte Growth Factor 1 Expression by Lipopolysaccharide Is Regulated by CD-14 and Toll-Like Receptors 2 and 4." Infection and Immunity 70, no. 12 (December 2002): 6541–48. http://dx.doi.org/10.1128/iai.70.12.6541-6548.2002.

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ABSTRACT Periodontal disease is a chronic inflammatory condition that is associated with increased concentrations of gram-negative pathogenic bacteria and epithelial cell proliferation. Regulation of this proliferation is poorly understood but is most likely controlled by locally expressed growth factors. Keratinocyte growth factor 1, an epithelium-specific growth factor, is expressed by gingival fibroblasts, and its expression is regulated in a concentration-dependent manner by lipopolysaccharide. In this study, induction of keratinocyte growth factor 1 protein expression was dependent on gingival fibroblast expression of membrane CD14 (mCD14) and Toll-like receptors 2 and 4. Lipopolysaccharides from Escherichia coli and Porphyromonas gingivalis induced membrane expression of CD14 at 1, 3, and 24 h. Specifically, lipopolysaccharide induced low mCD14 expression gingival fibroblasts to express mCD14 at a level consistent with that of high mCD14 expression cells. Functional studies with specific blocking antibodies for CD14 and Toll-like receptors 2 and 4 implicated all of these molecules in signal transduction. The rapid decrease in cell membrane expression of Toll-like receptors 2 and 4 after treatment with lipopolysaccharide was consistent with receptor internalization, and blocking of either of these receptors completely inhibited keratinocyte growth factor 1 protein expression. The transcription factors AP-1 and NF-κB were involved in lipopolysaccharide induction of keratinocyte growth factor 1 mRNA and protein expression. These results suggest that lipopolysaccharide may induce proliferation of periodontal epithelial cells by upregulating keratinocyte growth factor 1 expression via the CD14 and Toll-like receptor signaling pathway.

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21

Zou, Chang Hua, Yuriy A. Knirel, Jürgen H. Helbig, Ulrich Zähringer, and Clifford S. Mintz. "Molecular Cloning and Characterization of a Locus Responsible for O Acetylation of the O Polysaccharide of Legionella pneumophila Serogroup 1 Lipopolysaccharide." Journal of Bacteriology 181, no. 13 (July 1, 1999): 4137–41. http://dx.doi.org/10.1128/jb.181.13.4137-4141.1999.

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ABSTRACT Complementation experiments, Tn5 mutagenesis, and DNA sequencing were used to identify a locus (lag-1) that participates in acetylation of Legionella pneumophilaserogroup 1 lipopolysaccharide. Nuclear magnetic resonance analyses of lipopolysaccharides from mutant and complemented strains suggest thatlag-1 is responsible for O acetylation of serogroup 1 O polysaccharide.

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22

Rivera, M., L. E. Bryan, R. E. Hancock, and E. J. McGroarty. "Heterogeneity of lipopolysaccharides from Pseudomonas aeruginosa: analysis of lipopolysaccharide chain length." Journal of Bacteriology 170, no. 2 (1988): 512–21. http://dx.doi.org/10.1128/jb.170.2.512-521.1988.

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23

Raetz, Christian R. H., and Chris Whitfield. "Lipopolysaccharide Endotoxins." Annual Review of Biochemistry 71, no. 1 (June 2002): 635–700. http://dx.doi.org/10.1146/annurev.biochem.71.110601.135414.

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24

Kosma, Paul. "Chlamydial lipopolysaccharide." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1455, no. 2-3 (October 1999): 387–402. http://dx.doi.org/10.1016/s0925-4439(99)00061-7.

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Lynn, William A., and Douglas T. Golenbock. "Lipopolysaccharide antagonists." Immunology Today 13, no. 7 (January 1992): 271–76. http://dx.doi.org/10.1016/0167-5699(92)90009-v.

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Varbanets, L. D. "SEROLOGICAL AND BIOLOGICAL ACTIVITY OF LIPOPOLYSACCHARIDE." Biotechnologia Acta 8, no. 1 (March 23, 2015): 32–38. http://dx.doi.org/10.15407/biotech8.01.032.

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Varbanets, L. D. "SEROLOGICAL AND BIOLOGICAL ACTIVITY OF LIPOPOLYSACCHARIDE." Biotechnologia Acta 8, no. 1 (March 23, 2015): 56–62. http://dx.doi.org/10.15407/biotech8.01.056.

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Gamble, L., L. J. Quinton, K. I. Happel, P. Zhang, G. J. Bagby, and S. Nelson. "The Lipopolysaccharide Binding Protein Response to Intratracheal Lipopolysaccharide." Journal of Investigative Medicine 53, no. 1_part_5 (January 2005): 328. http://dx.doi.org/10.1177/1081558905053001918.

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Gamble, L., L. J. Quinton, K. I. Happel, P. Zhang, G. J. Bagby, and S. Nelson. "The Lipopolysaccharide Binding Protein Response to Intratracheal Lipopolysaccharide." Journal of Investigative Medicine 53, no. 1_part_5 (January 2005): 297. http://dx.doi.org/10.1177/1081558905053001746.

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Nagy, Laura, Péter Urbán, Lilla Makszin, Viktor Sándor, Anikó Kilár, Hajnalka Ábrahám, Beáta Albert, Béla Kocsis, and Ferenc Kilár. "The Effect of Mutation in Lipopolysaccharide Biosynthesis on Bacterial Fitness." Cells 11, no. 20 (October 16, 2022): 3249. http://dx.doi.org/10.3390/cells11203249.

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This paper presents the genome sequence of a Shigella sonnei mutant strain (S. sonnei 4351) and the effect of mutation in lipopolysaccharide biosynthesis on bacterial fitness. Lipopolysaccharides are the major component of the outer leaflet of the Gram-negative outer membrane. We report here a frameshift mutation of the gene gmhD in the genome of S. sonnei 4351. The mutation results in a lack of epimerization of the core heptose while we also found increased thermosensitivity, abnormal cell division, and increased susceptibility to erythromycin and cefalexin compared to the S. sonnei 4303. Comparative genomic analysis supplemented with structural data helps us to understand the effect of specific mutations on the virulence of the bacteria and may provide an opportunity to study the effect of short lipopolysaccharides.

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Souza, L. de, and M. C. Koury. "Isolation and biological activities of endotoxin from Leptospira interrogans." Canadian Journal of Microbiology 38, no. 4 (April 1, 1992): 284–89. http://dx.doi.org/10.1139/m92-047.

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Endotoxins extracted with ethylenediaminetetraacetate (EDTA) from Leptospira interrogans serovars icterohaemorrhagiae and canicola and Leptospira biflexa serovar patoc were tested for various biological activities characteristic of endotoxins. The presence of lipopolysaccharide biological activity was demonstrated by the Limulus amoebocyte lysate test, pyrogenicity in rabbits, complement interaction inhibiting the erythrocyte lysis, and chicken-embryo lethality. The lipopolysaccharides did not induce the local Shwartzman reaction. The lipopolysaccharides of serovars icterohaemorrhagiae and canicola were immunogenic in rabbits and were cytotoxic to chicken-embryo fibroblasts. Key words: Leptospira, endotoxin.

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Brock-Utne, J. G., and S. L. Gaffin. "Endotoxins and Anti-endotoxins (Their Relevance to the Anaesthetist and the Intensive Care Specialist)." Anaesthesia and Intensive Care 17, no. 1 (February 1989): 49–55. http://dx.doi.org/10.1177/0310057x8901700111.

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Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.

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Beynon, Linda M., and Malcolm B. Perry. "Structure of the lipopolysaccharide O-antigen of Pseudomonas cepacia serotype A." Biochemistry and Cell Biology 71, no. 9-10 (September 1, 1993): 417–20. http://dx.doi.org/10.1139/o93-061.

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The O-antigenic polysaccharides of the lipopolysaccharides produced by three isolates of Pseudomonas cepacia serogroup A were analysed by composition, methylation, periodate oxidation, and two-dimensional nuclear magnetic resonance methods. They were found to be identical linear unbranched polymers of a repeating trisaccharide unit containing 2-acetamido-2-deoxy-D-galactose and L-rhamnose residues (2:1) and have the structure[Formula: see text]Key words: lipopolysaccharide, Pseudomonas cepacia, O-antigen.

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Kumar, G. Seshu, M. V. Jagannadham, and M. K. Ray. "Low-Temperature-Induced Changes in Composition and Fluidity of Lipopolysaccharides in the Antarctic Psychrotrophic Bacterium Pseudomonas syringae." Journal of Bacteriology 184, no. 23 (December 1, 2002): 6746–49. http://dx.doi.org/10.1128/jb.184.23.6746-6749.2002.

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ABSTRACT The Antarctic psychrotrophic bacterium Pseudomonas syringae was more sensitive to polymyxin B at a lower (4°C) temperature of growth than at a higher (22°C) temperature. The amount of hydroxy fatty acids in the lipopolysaccharides (LPS) also increased at the lower temperature. These changes correlated with the increase in fluidity of the hydrophobic phase of lipopolysaccharide aggregates in vitro.

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Grundt, Inger K., and Harald Nyland. "Effects of Polyunsaturated Fatty Acids on Glial Cell Activation. A Study Using Primary Cultures." Alternatives to Laboratory Animals 22, no. 3 (May 1994): 201–6. http://dx.doi.org/10.1177/026119299402200311.

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The aim of this study was to examine the effects of essential fatty acids (gammalinolenic acid [18:3 n-6; GLA] and alpha-linolenic acid [18:3 n-3; Lin]) on the activation of glial cells, using lipopolysaccharides as the activating agent. Primary cultures of mixed glial cells from rat brain were used as the model. The morphological activation of microglia was the most significant response to the exposure. This activation was followed by an increase in 5’-nucleotidase (5’-NT) activity. The 5’-NT activity was increased by GLA or Lin alone to 250–350% of the control value and further increased by co-incubation with lipoteichoic acid (a lipopolysaccharide) to 500–600% of the control value. The lipopolysaccharide-induced activation of glial cells was also followed by an augmented release of prostaglandin E2. GLA increased the release of prostaglandin E2 in a dose-dependent manner, whereas Lin had no effect on its release. The results show that this model system is useful for studies on factors affecting the activation of glial cells. GLA and Lin did not reverse glial activation induced by lipopolysaccharides under these experimental conditions.

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Gamble, L., L. J. Quinton, K. I. Happel, P. Zhang, G. J. Bagby, and S. Nelson. "249 THE LIPOPOLYSACCHARIDE BINDING PROTEIN RESPONSE TO INTRATRACHEAL LIPOPOLYSACCHARIDE." Journal of Investigative Medicine 53, no. 1 (January 1, 2005): S297.1—S297. http://dx.doi.org/10.2310/6650.2005.00006.248.

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Gamble, L., L. J. Quinton, K. I. Happel, P. Zhang, G. J. Bagby, and S. Nelson. "421 THE LIPOPOLYSACCHARIDE BINDING PROTEIN RESPONSE TO INTRATRACHEAL LIPOPOLYSACCHARIDE." Journal of Investigative Medicine 53, no. 1 (January 1, 2005): S328.3—S328. http://dx.doi.org/10.2310/6650.2005.00006.420.

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OHNO, Naohito, and David C. MORRISON. "Lipopolysaccharide interactions with lysozyme differentially affect lipopolysaccharide immunostimulatory activity." European Journal of Biochemistry 186, no. 3 (December 1989): 629–36. http://dx.doi.org/10.1111/j.1432-1033.1989.tb15253.x.

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Lei, Chunyang, Zhaohui Qiao, Yingchun Fu, and Yanbin Li. "Colorimetric detection of lipopolysaccharides based on a lipopolysaccharide-binding peptide and AuNPs." Analytical Methods 8, no. 45 (2016): 8079–83. http://dx.doi.org/10.1039/c6ay02371a.

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Heumann, D., J. D. Baumgartner, H. Jacot-Guillarmod, and M. P. Glauser. "Antibodies to Core Lipopolysaccharide Determinants: Absence of Cross-reactivity with Heterologous Lipopolysaccharides." Journal of Infectious Diseases 163, no. 4 (April 1, 1991): 762–68. http://dx.doi.org/10.1093/infdis/163.4.762.

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Yu, Xiaoying, Saddam Hussein, Lijia Li, Qingyu Liu, Zhibin Ban, and Hailong Jiang. "Effect of Dihydroquercetin on Energy Metabolism in LPS-Induced Inflammatory Mice." BioMed Research International 2022 (July 4, 2022): 1–25. http://dx.doi.org/10.1155/2022/6491771.

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This study investigated the effects and alterations of dihydroquercetin on the growth performance, nutriment metabolism, antioxidant and immune function, and energy substrate utilization in lipopolysaccharide-challenged mice. A total of 0, 50, and 200 mg/kg of dihydroquercetin were intragastrically administered once a day for 21 days. After the pretreatment with dihydroquercetin, each group was subjected to a lipopolysaccharide challenge (except for the control group). After lipopolysaccharide injection, food intake, body weight, metabolic indexes of blood and liver nutrients, blood inflammatory factors, and liver oxidative stress indexes were measured at 6, 12, 24, and 48 h, respectively. Indirect calorimetry analysis was performed by respiratory gas analysis for 48 h to calculate the energy substrate metabolism of carbohydrate, fat, and protein. Urinary nitrogen excretion was measured to evaluate the urinary protein metabolism to calculate the substrate utilization. The results showed that dihydroquercetin pretreatment can significantly increase the weight gain and average food intake and decrease the mortality rate in lipopolysaccharide-induced inflammation mice. Furthermore, dihydroquercetin pretreatment can alleviate the negative effects of lipopolysaccharides by increasing levels of superoxide dismutase and glutathione peroxidase and by decreasing the malondialdehyde and serum inflammatory cytokines (interleukin-1β, nuclear factor κB, and interleukin-6). Dihydroquercetin pretreatment also can relieve nutrient metabolic disorder by increasing blood glucose, serum total protein, and liver glycogen levels and reducing serum and liver triglycerides, serum cholesterol, serum lactate dehydrogenase, and serum urea nitrogen levels. Meanwhile, it increases the relative utilization of carbohydrate, reducing relative utilization of protein and lipid, alleviating the change in energy metabolism pattern from glucose-predominant to lipid-predominant caused by lipopolysaccharide stimulation. In addition, the degree of metabolic pattern transformation depends on the dose of dihydroquercetin supplement. Finally, according to principal component analysis, we found that the inflammation was strongest in the mice at 24 h and was subsequently relieved in the LPS-stimulated group, whereas in the dihydroquercetin-pretreated group, the inflammation was initially relieved. To summarize, dihydroquercetin pretreatment can improve energy metabolism disorder and attenuate the negative effects of lipopolysaccharide challenge in mice from the initial stage of inflammation.

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Brovarska, O. S., L. D. Varbanets, G. V. Gladka, A. D. German, and O. B. Tashyrev. "Lipopolysaccharide of Pseudomonas mandelii, Isolated from Antarctica." Mikrobiolohichnyi Zhurnal 83, no. 4 (August 17, 2021): 24–34. http://dx.doi.org/10.15407/microbiolj83.04.024.

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Representatives of the Pseudomonas mandelii species are able to exist and multiply in places where the temperature is constantly low. The optimum growth temperature for P. mandelii is 25–30°C, although this bacterium can grow at 4°C but not at 37°C. Therefore, P. mandelii is an excellent example of psychrotolerant bacterium which like psychrophilic bacteria is characterized by a number of structural and functional adaptations that facilitate survival at low temperatures. To understand these microorganisms’ role in Antarctica the characterization of its biopolymers is vital. One of these biopolymers is lipopolysaccharide (LPS), composition and structure of which are diagnostically significant. This determines the aim of the work – to isolate lipopolysaccharides from the cells of Antarctic strain of P. mandelii, grown at different temperatures, to characterize them chemically, and to study their functional and biological activity. Methods. The object of the study was Pseudomonas sp. U1, isolated from moss on Galindez Island in Antarctica. Lipopolysaccharides were extracted from dried cells by 45% phenol water solution at 65–68°С by Westphal and Jann method. The amount of carbohydrates was determined by phenol-sulfuric method. Carbohydrate content was determined in accordance to the calibration curve, which was built using glucose as a standard. The content of nucleic acids was determined by Spirin, protein − by Lowry method. Serological activity of LPS was investigated by double immunodiffusion in agar using the method of Ouchterlony. Polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS-PAAG electrophoresis) was performed according to Laemmli. Results. As a result of phylogenetic analysis (programs ClustalX 2.1, Tree view, Mega v. 6.00) it was shown that the Antarctic bacterial strain Pseudomonas sp. U1 associated with green moss has a 99.4% homology with the type strain from the GenBank database NR024902 P. mandelii CIP 105273T. According to these data and proximity to the corresponding cluster of species, the studied isolate can be identified as P. mandelii. A characteristic feature of LPS isolated from P. mandelii cells, grown at different temperatures (20°C and 4°C) is their heterogeneity. This is evidenced by the data of the monosaccharide composition, electrophoretic distribution, which showed that P. mandelii produces S- and SR-forms of LPS, differed in the length of the O-specific polysaccharide chains. The R-form of LPS is also present, which does not contain an O-specific polysaccharide chains. Structural heterogeneity is also inherent in LPS lipid A. This is evidenced by the data of the fatty acid composition. In LPS grown at 4°C no unsaturated fatty acids were found, while such ones are synthesized in LPS of other bacteria grown in the cold, in response to a decrease in growth temperature. The study of the immunochemical properties of LPS was carried out using polyclonal O-antisera as antibodies, and LPS as antigens indicated that in homologous systems LPS exhibited serological activity. LPS obtained from P. mandelii U1 cells, grown at 20°C, had a complex antigenic composition and gave two clear lines of precipitation at a concentration of 1 mg/mL. LPS obtained from P. mandelii U1 cells, grown at 4°C, gave one line, which indicates their serological homogeneity. Conclusions. For the first time lipopolysaccharides were isolated from cells of P. mandelii U1, grown at 4°C and 20°С. A characteristic feature of these LPS is their heterogeneity. This is evidenced by the data of the monosaccharide and fatty acid composition, electrophoretic distribution, which showed that P. mandelii produces S- and SR-forms of LPS, differed in the length of the O-specific polysaccharide chains. LPS, obtained from cells, grown at different temperatures, are differed by serological activity.

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Tirsoaga, Alina, Alexey Novikov, Minou Adib-Conquy, Catherine Werts, Catherine Fitting, Jean-Marc Cavaillon, and Martine Caroff. "Simple Method for Repurification of Endotoxins for Biological Use." Applied and Environmental Microbiology 73, no. 6 (January 19, 2007): 1803–8. http://dx.doi.org/10.1128/aem.02452-06.

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ABSTRACT A method for obtaining highly purified endotoxin (lipopolysaccharide [LPS]) in a few hours by repurification of commercial or laboratory preparations was devised. It avoids the use of phenol, which is not suitable for phenol-soluble lipopolysaccharides nor for some industrial purposes. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and matrix-assisted laser desorption ionization mass spectrometry analysis confirmed the integrity of the purified LPSs. The purified products did not activate Toll-like receptor 2 (TLR2), nuclear oligomerization domain 1 (NOD1), or NOD2 but did activate TLR4. Applied to different lipopolysaccharides, the method also improved their mass spectra, thus facilitating their structural analysis.

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Er, Ayse, Ibrahim Aydin, and Burak Dik. "Effect of Anti-TNF-α on the Development of Offspring and Pregnancy Loss During Pregnancy in Rats." Acta Scientiae Veterinariae 44, no. 1 (March 19, 2018): 6. http://dx.doi.org/10.22456/1679-9216.80901.

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Background: Etanercept binds soluble tumor necrosis factor-alpha (TNF-α) and is classified as pregnancy risk category B. Increase in TNF-α level causes preterm labour or miscarriage. Lipopolysaccharides trigger preterm birth and abortion via producing of pro-inflammatory cytokines. Cytokines are divided into two groups as pro-inflammatory and anti-inflammatory. TNF-α is a pro-inflammatory cytokine, whereas interleukin (IL)-10 is an anti-inflammatory cytokine. IL-10 predominant in normal pregnancy while TNF-α characterize in abortion and recurrent abortion. The aim of this study was to determine the effect of etanercept on the development of offspring and lipopolysaccharide-induced pregnancy loss.Materials, Methods & Results: Twenty-eight female and 7 male Wistar rats (5-6 months old) were used in this study. The rats were fed a standard pelleted diet and tap water ad libitum. After female rats were caged with males for 1 day, the presence of a vaginal plug was designated as day 0 of pregnancy. Twenty-eight pregnant Wistar rats were divided into 4 equal groups, as follows: control (0.3 mL of Normal Saline Solution intravenously on day 10 of pregnancy); etanercept (0.8 mg kg-1/day intraperitoneally on days 9 and 10 of pregnancy); lipopolysaccharide (160 µg kg-1 intravenously on day 10 of pregnancy); and etanercept + lipopolysaccharide. Blood samples were obtained from the tail vein on day 10 of pregnancy (3 h after lipopolysaccharide administration). All animals were followed during pregnancy. Pregnancy rates and offspring characteristics were determined. TNF-α and IL-10 levels were measured using an ELISA reader. Etanercept alone did not have any negative effects, and etanercept did not prevent (P < 0.05) lipopolysaccharide-induced pregnancy loss. Higher TNF-α and IL-10 levels were measured (P < 0.05) in the etanercept + lipopolysaccharide group compared to other groups.Discussion: It is well known that use of etanercept does not increase pregnacy loss. In this study, higher pregnancy rates were determined in the control and etanercept groups than the lipopolysaccharide and etanercept + lipopolysaccharide groups. The proportion of fetal deaths in lipopolysaccharide administered pregnant subjects was decreased by the use of anti-TNF-α agents. While the concentrations of TNF-α are low in the onset of pregnancy period, the concentrations of TNF-α increases a peak level during the onset of labour. Embryonic resorption is affected by Th1 cytokines (TNF-α and lL-2) and low-dose lipopolysaccharide without any affecting mother survival, and in the early pregnancy term, the implantation area of embryo is enormously sensitive to these molecules. In the current study, etanercept increased the concentration of TNF-α and the concentration of IL-10 when compared to the lipopolysaccharide group. IL-10 has a protective role, while TNF-α is an abortive factor during pregnancy. Thus, etanercept did not prevent pregnancy loss. This finding may have reflected an insufficient dose of etanercept. Adverse effects did not occur in the offspring of the etanercept or control groups, and there was no difference between the two groups statistically. Adverse pregnancy outcomes such as stillbirth, low birth weight, spontaneous abortion and herediter malformations are not associated with TNF-α inhibitors. In conclusion, etanercept does not pose a major teratogenic risk and has no preventive effects with respect to infection-dependent pregnancy loss.

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Hicks, Greg, and Zongchao Jia. "Structural Basis for the Lipopolysaccharide Export Activity of the Bacterial Lipopolysaccharide Transport System." International Journal of Molecular Sciences 19, no. 9 (September 10, 2018): 2680. http://dx.doi.org/10.3390/ijms19092680.

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Gram-negative bacteria have a dense outer membrane (OM) coating of lipopolysaccharides, which is essential to their survival. This coating is assembled by the LPS (lipopolysaccharide) transport (Lpt) system, a coordinated seven-subunit protein complex that spans the cellular envelope. LPS transport is driven by an ATPase-dependent mechanism dubbed the “PEZ” model, whereby a continuous stream of LPS molecules is pushed from subunit to subunit. This review explores recent structural and functional findings that have elucidated the subunit-scale mechanisms of LPS transport, including the novel ABC-like mechanism of the LptB2FG subcomplex and the lateral insertion of LPS into the OM by LptD/E. New questions are also raised about the functional significance of LptA oligomerization and LptC. The tightly regulated interactions between these connected subcomplexes suggest a pathway that can react dynamically to membrane stress and may prove to be a valuable target for new antibiotic therapies for Gram-negative pathogens.

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Mayeux, Philip R. "PATHOBIOLOGY OF LIPOPOLYSACCHARIDE." Journal of Toxicology and Environmental Health 51, no. 5 (August 1997): 415–35. http://dx.doi.org/10.1080/00984109708984034.

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Kaufmann, Stefan, Karin Ilg, Alireza Mashaghi, Marcus Textor, Bernard Priem, Markus Aebi, and Erik Reimhult. "Supported Lipopolysaccharide Bilayers." Langmuir 28, no. 33 (August 9, 2012): 12199–208. http://dx.doi.org/10.1021/la3020223.

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Hood, D. W., J. C. Richards, and E. R. Moxon. "Haemophilus influenzae lipopolysaccharide." Biochemical Society Transactions 27, no. 4 (August 1, 1999): 493–98. http://dx.doi.org/10.1042/bst0270493.

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Brade, H., W. Brabetz, L. Brade, O. Hoist, S. Löbau, M. Lucakova, U. Mamat, A. Rozalski, K. Zych, and P. Kosma. "Review: Chlamydial lipopolysaccharide." Journal of Endotoxin Research 4, no. 1 (February 1997): 67–84. http://dx.doi.org/10.1177/096805199700400108.

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Barber, C. M. "Allergy to lipopolysaccharide?" Allergy 56, no. 8 (August 2001): 797. http://dx.doi.org/10.1034/j.1398-9995.2001.056008797.x.

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