scholarly journals The lipopolysaccharide from Escherichia coli O127:B8 induces inflammation and motility disturbances in rabbit ileum

2017 ◽  
Vol 25 (2) ◽  
pp. 185
Author(s):  
Laura Grasa ◽  
Sergio Gonzalo ◽  
Alba De Martino ◽  
María Divina Murillo
Keyword(s):  
Escherichia Coli ◽  
Mrna Expression ◽  
Intestinal Inflammation ◽  
Organ Bath ◽  
Toll Like Receptor ◽  
Rabbit Ileum ◽  
Toll Like Receptor 4 ◽  
E Coli ◽  
Mucosal Layer ◽  
Spontaneous Contractions

<p>The aim of this work was to evaluate the effects of lipopolysaccharide (LPS) from <em>Escherichia coli </em>O127:B8 on the expression of toll-like receptor 4 (TLR4), the histology, and motor function in rabbit ileum. Rabbits were injected intravenously with saline or LPS (100 μg/kg, 2 h). The mRNA expression and localization of TLR4 were determined by reverse transcriptase-PCR and immunofluorescence, respectively. Histological damage induced by LPS was evaluated in sections of ileum stained with haematoxylin and eosin. Contractility studies of ileum were performed in an organ bath. The mRNA expression of TLR4 decreased in the muscular but not in the mucosal layer of rabbits treated with LPS. TLR4 was localised in both the mucosal and muscular layers of rabbit ileum. LPS induced intestinal inflammation and altered the spontaneous contractions and the serotonin-, acetylcholine- and KCl-induced contractions. In conclusion, LPS from <em>E. coli </em>O127:B8 induced a decrease in the mRNA expression of TLR4, an inflammatory response, and changes in the contractility of rabbit ileum.</p>

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 &lt; 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 &lt; 0.001] and correlated with LPS (Rs = 0.585; P &lt; 0.001). Escherichia coli DNA was positive in 34% of STEMI vs. 12% of SA and 4% of controls (P &lt; 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 Escherichia coli Nissle 1917 Distinctively Modulates T-Cell Cycling and Expansion via Toll-Like Receptor 2 Signaling

2005 ◽  
Vol 73 (3) ◽  
pp. 1452-1465 ◽  
Author(s):  
Andreas Sturm ◽  
Klaus Rilling ◽  
Daniel C. Baumgart ◽  
Konstantinos Gargas ◽  
Tay Abou-Ghazalé ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
T Cells ◽  
T Cell ◽  
Peripheral Blood ◽  
Intestinal Inflammation ◽  
Toll Like Receptor ◽  
E Coli ◽  
Toll Like Receptor 2 ◽  
Cell Cycling

ABSTRACT Although the probiotic Escherichia coli strain Nissle 1917 has been proven to be efficacious for the treatment of inflammatory bowel diseases, the underlying mechanisms of action still remain elusive. The aim of the present study was to analyze the effects of E. coli Nissle 1917 on cell cycling and apoptosis of peripheral blood and lamina propria T cells (PBT and LPT, respectively). Anti-CD3-stimulated PBT and LPT were treated with E. coli Nissle 1917-conditioned medium (E. coli Nissle 1917-CM) or heat-inactivated E. coli Nissle 1917. Cyclin B1, DNA content, and caspase 3 expression were measured by flow cytometry to assess cell cycle kinetics and apoptosis. Protein levels of several cell cycle and apoptosis modulators were determined by immunoblotting, and cytokine profiles were determined by cytometric bead array. E. coli Nissle 1917-CM inhibits cell cycling and expansion of peripheral blood but not mucosal T cells. Bacterial lipoproteins mimicked the effect of E. coli Nissle 1917-CM; in contrast, heat-inactivated E. coli Nissle 1917, lipopolysaccharide, or CpG DNA did not alter PBT cell cycling. E. coli Nissle 1917-CM decreased cyclin D2, B1, and retinoblastoma protein expression, contributing to the reduction of T-cell proliferation. E. coli Nissle 1917 significantly inhibited the expression of interleukin-2 (IL-2), tumor necrosis factor α, and gamma interferon but increased IL-10 production in PBT. Using Toll-like receptor 2 (TLR-2) knockout mice, we further demonstrate that the inhibition of PBT proliferation by E. coli Nissle 1917-CM is TLR-2 dependent. The differential reaction of circulating and tissue-bound T cells towards E. coli Nissle 1917 may explain the beneficial effect of E. coli Nissle 1917 in intestinal inflammation. E. coli Nissle 1917 may downregulate the expansion of newly recruited T cells into the mucosa and limit intestinal inflammation, while already activated tissue-bound T cells may eliminate deleterious antigens in order to maintain immunological homeostasis.

scholarly journals Toll-Like Receptor 4/Stem Cell Antigen 1 Signaling Promotes Hematopoietic Precursor Cell Commitment to Granulocyte Development during the Granulopoietic Response to Escherichia coli Bacteremia

2013 ◽  
Vol 81 (6) ◽  
pp. 2197-2205 ◽  
Author(s):  
Xin Shi ◽  
Robert W. Siggins ◽  
William L. Stanford ◽  
John N. Melvan ◽  
Marc D. Basson ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Bone Marrow ◽  
Stem Cell ◽  
Precursor Cell ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Content Type ◽  
E Coli ◽  
Hematopoietic Precursor

ABSTRACTIn response to severe bacterial infection, bone marrow hematopoietic activity shifts toward promoting granulopoiesis. The underlying cell signaling mechanisms remain obscure. To study the role of Toll-like receptor 4 (TLR4)/stem cell antigen-1 (Sca-1) signaling in this process, bacteremia was induced in mice by intravenous injection ofEscherichia coli. A subgroup of animals also received intravenous 5-bromo-2-deoxyuridine (BrdU). In a separate set of experiments, bone marrow lineage-negative (lin−) stem cell growth factor receptor-positive (c-kit+) Sca-1−cells containing primarily common myeloid progenitors were culturedin vitrowithout or withE. colilipopolysaccharide (LPS). In genotypic background control mice, bacteremia significantly upregulated Sca-1 expression by lin−c-kit+cells, as reflected by a marked increase in BrdU-negative lin−c-kit+Sca-1+cells in the bone marrow. In mice with the TLR4 gene deletion, this bacteremia-evoked Sca-1 response was blocked.In vitro, LPS induced a dose-dependent increase in Sca-1 expression by cultured marrow lin−c-kit+Sca-1−cells. LPS-induced upregulation of Sca-1 expression was regulated at the transcriptional level. Inhibition of c-Jun N-terminal kinase/stress-activated protein kinase (JNK) activity with the specific inhibitor SP600125 suppressed LPS-induced upregulation of Sca-1 expression by marrow lin−c-kit+Sca-1−cells. Engagement of Sca-1 with anti-Sca-1 antibodies enhanced the expression of Sfpi1 spleen focus-forming virus (SFFV) proviral integration 1 (PU.1) in marrow lin−c-kit+Sca-1−cells cultured with LPS. Sca-1 null mice failed to maintain the marrow pool of granulopoietic cells following bacteremia. These results demonstrate that TLR4/Sca-1 signaling plays an important role in the regulation of hematopoietic precursor cell programming and their enhancement of granulocyte lineage commitment in response toE. colibacteremia.

scholarly journals Porphyromonasgingivalis Lipopolysaccharide Antagonizes Escherichiacoli Lipopolysaccharide at Toll-Like Receptor 4 in HumanEndothelialCells

2003 ◽  
Vol 71 (12) ◽  
pp. 6799-6807 ◽  
Author(s):  
Stephen R. Coats ◽  
Robert A. Reife ◽  
Brian W. Bainbridge ◽  
Thu-Thao T. Pham ◽  
Richard P. Darveau
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Adaptor Protein ◽  
Dominant Negative ◽  
Toll Like Receptor ◽  
Human Endothelial Cells ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
E Coli ◽  
Signaling Complex

ABSTRACT E. coli lipopolysaccharide (LPS) induces cytokine and adhesion molecule expression via the toll-like receptor 4 (TLR4) signaling complex in human endothelial cells. In the present study, we investigated the mechanism by which Porphyromonas gingivalis LPS antagonizes E. coli LPS-dependent activation of human endothelial cells. P. gingivalis LPS at 1 μg/ml inhibited both E. coli LPS (10 ng/ml) and Mycobacterium tuberculosis heat shock protein (HSP) 60.1 (10 μg/ml) stimulation of E-selectin mRNA expression in human umbilical vein endothelial cells (HUVEC) without inhibiting interleukin-1 beta (IL-1β) stimulation. P. gingivalis LPS (1μ g/ml) also blocked both E. coli LPS-dependent and M. tuberculosis HSP60.1-dependent but not IL-1β-dependent activation of NF-κB in human microvascular endothelial (HMEC-1) cells, consistent with antagonism occurring upstream from the TLR/IL-1 receptor adaptor protein, MyD88. Surprisingly, P. gingivalis LPS weakly but significantly activated NF-κB in HMEC-1 cells in the absence of E. coli LPS, and the P. gingivalis LPS-dependent agonism was blocked by transient expression of a dominant negative murine TLR4. Pretreatment of HUVECs with P. gingivalis LPS did not influence the ability of E. coli LPS to stimulate E-selectin mRNA expression. Taken together, these data provide the first evidence that P. gingivalis LPS-dependent antagonism of E. coli LPS in human endothelial cells likely involves the ability of P. gingivalis LPS to directly compete with E. coli LPS at the TLR4 signaling complex.

Differential expression of Toll-like receptor 4 signaling pathway genes in Escherichia coli F18-resistant and – sensitive Meishan piglets

2016 ◽  
Vol 19 (2) ◽  
pp. 303-308 ◽  
Author(s):  
Y. Liu ◽  
L.N. Gan ◽  
W.Y. Qin ◽  
S.Y. Sun ◽  
G.Q. Zhu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Lymph Nodes ◽  
Signaling Pathway ◽  
Expression Profiles ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
E Coli ◽  
Significant Difference ◽  
Spleen And Lymph Nodes

Abstract The Toll-like receptor 4 (TLR4) signaling pathway is an important inflammatory pathways associated with the progression of numerous diseases. The aim of the present study was to investigate the relationship between TLR4 signaling and resistance to Escherichia coli F18 in locally weaned Meishan piglets. Using a real-time PCR approach, expression profiles were determined for key TLR4 signaling pathway genes TLR4, MyD88, CD14, IFN-α, IL-1β and TNF-α in the spleen, thymus, lymph nodes, duodenum and jejunum of E. coli F18-resistant and -sensitive animals. TLR4 signaling pathway genes were expressed in all the immune organs and intestinal tissues, and the expression was generally higher in the spleen and lymph nodes. TLR4 transcription was higher in the spleen of sensitive piglets (p<0.05), but there was no significant difference in TLR4 mRNA levels in other tissues. Similarly, CD14 transcription was higher in lymph nodes of sensitive animals (p<0.05) but not in other tissues. IL-1β expression was higher in the spleen and in the duodenum of resistant piglets (p<0.05, p<0.01, respectively), and there were no significant differences in other tissues. There were also no significant differences in the expression of MyD88, TNF-α and IFN-α between sensitive and resistant piglets (p>0.05). These results further confirm the involvement of the TLR4 signaling pathway in resistance to E. coli F18 in Meishan weaned piglets. The resistance appeared to be mediated via downregulation of TLR4 and CD14, and upregulation of MyD88 that may promote the release of cytokines TNF-α, IL-1β, IFN-α and other inflammatory mediators which help to fight against E. coli F18 infection.

scholarly journals Francisella tularensis LPS induces the production of cytokines in human monocytes and signals via Toll-like receptor 4 with much lower potency than E. coli LPS

2006 ◽  
Vol 18 (5) ◽  
pp. 785-795 ◽  
Author(s):  
Ana I Dueñas ◽  
Mónica Aceves ◽  
Antonio Orduña ◽  
Ramón Díaz ◽  
Mariano Sánchez Crespo ◽  
...  
Keyword(s):  
Francisella Tularensis ◽  
Human Monocytes ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
E Coli

scholarly journals Streptomycin-Induced Inflammation Enhances Escherichia coli Gut Colonization Through Nitrate Respiration

mBio ◽  
2013 ◽  
Vol 4 (4) ◽  
Author(s):  
Alanna M. Spees ◽  
Tamding Wangdi ◽  
Christopher A. Lopez ◽  
Dawn D. Kingsbury ◽  
Mariana N. Xavier ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Microbial Community ◽  
Intestinal Inflammation ◽  
Anaerobic Bacteria ◽  
Nitrate Respiration ◽  
Colonization Resistance ◽  
Content Type ◽  
E Coli ◽  
Gut Colonization ◽  
Facultative Anaerobic Bacteria

ABSTRACTTreatment with streptomycin enhances the growth of human commensalEscherichia coliisolates in the mouse intestine, suggesting that the resident microbial community (microbiota) can inhibit the growth of invading microbes, a phenomenon known as “colonization resistance.” However, the precise mechanisms by which streptomycin treatment lowers colonization resistance remain obscure. Here we show that streptomycin treatment rendered mice more susceptible to the development of chemically induced colitis, raising the possibility that the antibiotic might lower colonization resistance by changing mucosal immune responses rather than by preventing microbe-microbe interactions. Investigation of the underlying mechanism revealed a mild inflammatory infiltrate in the cecal mucosa of streptomycin-treated mice, which was accompanied by elevated expression ofNos2, the gene that encodes inducible nitric oxide synthase. In turn, this inflammatory response enhanced the luminal growth ofE. coliby nitrate respiration in aNos2-dependent fashion. These data identify low-level intestinal inflammation as one of the factors responsible for the loss of resistance toE. colicolonization after streptomycin treatment.IMPORTANCEOur intestine is host to a complex microbial community that confers benefits by educating the immune system and providing niche protection. Perturbation of intestinal communities by streptomycin treatment lowers “colonization resistance” through unknown mechanisms. Here we show that streptomycin increases the inflammatory tone of the intestinal mucosa, thereby making the bowel more susceptible to dextran sulfate sodium treatment and boosting theNos2-dependent growth of commensalEscherichia coliby nitrate respiration. These data point to the generation of alternative electron acceptors as a by-product of the inflammatory host response as an important factor responsible for lowering resistance to colonization by facultative anaerobic bacteria such asE. coli.

Sign in / Sign up

Export Citation Format

Share Document