Escherichia coli in menstrual blood: An association with bacterial endotoxin and toll-like receptor 4 (TLR4)-mediated growth of endometriosis

2006 ◽  
Vol 71 (2) ◽  
pp. 152-153 ◽  
Author(s):  
K.N. Khan ◽  
M. Kitajima ◽  
K. Hiraki ◽  
A. Fujishita ◽  
T. Ishimaru ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Bacterial Endotoxin ◽  
Menstrual Blood ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Low-grade endotoxaemia enhances artery thrombus growth via Toll-like receptor 4: implication for myocardial infarction

2020 ◽  
Vol 41 (33) ◽  
pp. 3156-3165 ◽  
Author(s):  
Roberto Carnevale ◽  
Sebastiano Sciarretta ◽  
Valentina Valenti ◽  
Flavio di Nonno ◽  
Camilla Calvieri ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Escherichia Coli ◽  
Platelet Activation ◽  
Cathepsin G ◽  
Low Grade ◽  
Toll Like Receptor ◽  
Gut Permeability ◽  
Toll Like Receptor 4 ◽  
E Coli ◽  
St Elevation

Abstract Aims Low-grade endotoxaemia is detectable in human circulation but its role in thrombosis is still unclear. Methods and results We measured serum lipopolysaccharide (LPS) concentration, soluble P-selectin (sP-selectin), a marker of platelet activation, and zonulin, a marker of gut permeability, in peripheral circulation, coronary thrombi, and intracoronary blood of patients with ST-elevation myocardial infarction (STEMI, n = 50) and stable angina (SA) (n = 50), respectively, and in controls (n = 50). Experimental study was carried out in mice to assess if Escherichia coli-LPS (E. coli-LPS) possess thrombotic property. Coronary thrombi from STEMI showed higher concentrations of LPS, sP-selectin vs. intracoronary blood of SA and peripheral blood of controls (P < 0.001). Zonulin was higher in STEMI compared to the other two groups [4.57 (3.34–5.22); 2.56 (0.41–4.36); 1.95 (1.22–2.65) ng/mL; P < 0.001] and correlated with LPS (Rs = 0.585; P < 0.001). Escherichia coli DNA was positive in 34% of STEMI vs. 12% of SA and 4% of controls (P < 0.001). In a subgroup of 12 STEMI, immunohistochemical analysis of coronary thrombi showed positivity for leucocyte Toll-like receptor 4 (TLR4), cathepsin G, and LPS from E. coli in 100%, 80%, and 25% of samples, respectively. E. coli-LPS injected in mice to reach LPS concentrations like those detected in coronary thrombi was associated with enhanced artery thrombosis and platelet activation, an effect blunted by TLR4 inhibitor co-administration. In vitro study demonstrated that LPS from E. coli enhanced platelet aggregation via TLR4-mediated leucocyte cathepsin G activation. Conclusion ST-elevation myocardial infarction patients disclose an enhanced gut permeability that results in LPS translocation in human circulation and eventually thrombus growth at site of artery lesion via leucocyte–platelet interaction.

scholarly journals Toll-Like Receptors in Innate Immunity: Role of Bacterial Endotoxin and Toll-Like Receptor 4 in Endometrium and Endometriosis

2009 ◽  
Vol 68 (1) ◽  
pp. 40-52 ◽  
Author(s):  
Khaleque Newaz Khan ◽  
Michio Kitajima ◽  
Koichi Hiraki ◽  
Akira Fujishita ◽  
Ichiro Sekine ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Bacterial Endotoxin ◽  
Toll Like Receptor ◽  
Toll Like Receptors ◽  
Toll Like Receptor 4

scholarly journals 3-O-Deacylation of Lipid A by PagL, a PhoP/PhoQ-regulated Deacylase ofSalmonella typhimurium, Modulates Signaling through Toll-like Receptor 4

2004 ◽  
Vol 279 (19) ◽  
pp. 20044-20048 ◽  
Author(s):  
Kiyoshi Kawasaki ◽  
Robert K. Ernst ◽  
Samuel I. Miller
Keyword(s):  
Mass Spectrometry ◽  
Escherichia Coli ◽  
Host Defense ◽  
Lipid A ◽  
Virulence Gene ◽  
Mouse Cell ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Layer Chromatography ◽  
Human And Mouse

Toll-like receptor 4 (TLR4)-mediated responses, which are induced by the lipid A portion of lipopolysaccharide, are important for host defense against Salmonellae infection. A variety of different data indicate that the acylation state of lipid A can alter TLR4-mediated responses. TheS. typhimuriumvirulence gene product PhoP/PhoQ signals the presence of host microenvironments to regulate the expression of a lipid A 3-O-deacylase, PagL, and a lipid A palmitoyltransferase, PagP. We now demonstrate that 3-O-deacylation and palmitoylation of lipid A decreases its ability to induce TLR4-mediated signaling. Deacylated lipid A, deacylated and palmitoylated lipid A, palmitoylated lipid A, and unmodified lipid A species were purified fromEscherichia coliheterologously expressing PagL and/or PagP. The purified lipid A preparations showed spectra of a single lipid A species on mass spectrometry and gave a single band on thin layer chromatography. The activity of purified lipid A species was examined using human and mouse cell lines that express recombinant human TLR4. Compared with unmodified lipid A, the modified lipid A species are 30–100-fold less active in the ability to induce NF-κB-dependent reporter activation. These results suggest that the lipid A modifications reduce TLR4-signaling as part of Salmonellae adaptation to host environments.

TAK-242 SUPPRESSES TOLL-LIKE RECEPTOR 4-MEDIATED CYTOKINE PRODUCTION AND PROTECTS MICE FROM ESCHERICHIA COLI-INDUCED LETHALITY

2004 ◽  
Vol 32 (Supplement) ◽  
pp. A15
Author(s):  
Masayuki Ii ◽  
Mie Sunamoto ◽  
Naoko Matsunaga ◽  
Kazuyo Nakamura ◽  
Katsunori Takashima ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

Cloning and Expression of TLR4-EGFP Fusion Protein in HT-29 Cells and the Visualized Interaction between TLR4 and Enteropathogenic E.coli

2011 ◽  
Vol 138-139 ◽  
pp. 1168-1173
Author(s):  
Quan Xin Gao ◽  
Li Li Qi ◽  
Jin Bo Wang ◽  
Qing Cha Zhuang ◽  
Shi Jian Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Fluorescent Protein ◽  
Cloning And Expression ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Gene Encoding ◽  
Egfp Fusion Protein ◽  
Green Fluorescent ◽  
First Time ◽  
Ht 29

The aim of this study was to determine whether theEscherichia coli(EPEC) attached to cells by the TLR4. A fusion between gene encoding fluoresce-enhanced green fluorescent protein (EGFP) and Toll like receptor 4 (TLR4) was constructed and expressed inEscherichia coli. Then the pEGFP-N1-TLR4 fusion expression vector was transfected into HT-29 cells. The green fluoresce was observed at the plasma membrane of HT-29 cells under inverted fluorescent microscopes. In addition, the FITC stained EPEC was also observed adherence to the TLR4 of HT-29 cells.The results indicated that the EPEC adhered to cells by bonding to TLR4 protein. It is the first time that the TLR4 has been explained as an adhesion receptor.

TLR4 inactivation and rBPI21 block burn-induced myocardial contractile dysfunction

2002 ◽  
Vol 283 (4) ◽  
pp. H1645-H1655 ◽  
Author(s):  
James A. Thomas ◽  
May F. Tsen ◽  
D. Jean White ◽  
Jureta W. Horton
Keyword(s):  
Myocardial Contractility ◽  
Burn Injury ◽  
Bacterial Endotoxin ◽  
Critical Element ◽  
Contractile Dysfunction ◽  
Mutant Form ◽  
Rodent Models ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Myocardial Contractile

Both large burns and severe gram-negative sepsis are associated with acute myocardial contractile dysfunction. Because others have reported that burn injury may be followed by transient endotoxemia, we hypothesized that bacterial endotoxin induces contractile impairment after burn trauma. We tested this hypothesis in two rodent models. In each model, postburn myocardial contractility was assessed using Langendorff preparations of excised hearts. In the first model, mice expressing either a mutant form of or no Toll-like receptor 4 (TLR4), a critical element of the mammalian endotoxin receptor, were resistant to postburn myocardial contractile dysfunction. In the second model, starting 30 min or 4 h after burn injury, rats were infused with recombinant bactericidal/permeability-increasing protein (rBPI21), a protein that binds and neutralizes endotoxin. Hearts from rBPI21-treated animals were completely protected from postburn contractile impairment. Because burn-induced contractile dysfunction can be prevented either by blocking signaling through the endotoxin receptor or by neutralizing circulating LPS, bacterial endotoxin may contribute to impaired myocardial contractility after burn injury.

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