Lipopolysaccharide Activates Distinct Signaling Pathways in Intestinal Epithelial Cell Lines Expressing Toll-Like Receptors1

By E. Cario, I. Rosenberg, S. Brandwein, P. Beck, H. Reinecker, D. Podolsky. Journal of Immunology, 2000

808 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/453268b9635d15674bc837dde7b4d50c5a039d15

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Fangqing Zhao
2. Qinghua Cui
3. E. Cario
4. M. Abreu
5. D. Podolsky

In Immunology

1. M. Abreu
2. J. Kuiper
3. E. Cario
4. T. V. van Berkel
5. E. V. van Amersfoort
6. D. Podolsky

In Surgery

1. M. Abreu

Citations in the corpus

• TLR Signaling in the Gut in Health and Disease1 (2005, background): “TLR expression in commonly used human-derived IEC lines TLRs SW480 Caco2 T84 HT-29 1 RNA, protein (9) RNA (low level) (8) RNA (8) RNA (8) 2 * (9), (36) RNA, protein (92), RNA (5), poorly responsive to ligands (6, 8), RNA, ( protein) poorly responsive to ligands (8), protein (92) RNA, poorly responsi”
• Gut microbiota dysbiosis contributes to the development of hypertension (2017, background): “The capacity to synthesize and export LPS of the gut microbiome in patients with colorectal carcinoma has been suggested to represent an important mechanism whereby inflammation contributes to tumor progression [5, 41, 42].”
• Differential Alteration in Intestinal Epithelial Cell Expression of Toll-Like Receptor 3 (TLR3) and TLR4 in Inflammatory Bowel Disease (2000, background): “We and colleagues have previously demonstrated that various intestinal epithelial cell lines constitutively express several members of a novel family of transmembrane receptors designated Toll-like receptors (TLRs) which may serve as a major link between innate and adaptive mucosal immune responses ”
• Chylomicrons promote intestinal absorption of lipopolysaccharides Published, JLR Papers in Press, September 24, 2008. (2009, background): “Although some LPS acquired by the intestinal epithelial cell remains associated with the cell membrane (37), significant amounts of LPS are internalized and directed to the Golgi, where most TLR4 resides (23).”
• Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock (2003, background): “on various other cell types including epithelial and endothelial cells (59, 118, 614); TLR2 is also present on hepatocytes (323).”
• Cutting Edge: Repurification of Lipopolysaccharide Eliminates Signaling Through Both Human and Murine Toll-Like Receptor 21 (2000, background): “Several groups, in fact, have demonstrated LPS signaling in the absence of TLR2 in various primary cells and cell lines (14, 15, 20, 21, 24, 25, 40).”
• Decreased Expression of Toll-Like Receptor-4 and MD-2 Correlates with Intestinal Epithelial Cell Protection Against Dysregulated Proinflammatory Gene Expression in Response to Bacterial Lipopolysaccharide1 (2001, methodology): “We used LPS at a concentration of 50 ng/ml for our studies compared with concentrations ranging from 5–100 mg/ml in other studies (40, 42, 43).”