Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes.
By S. Creely, P. McTernan, C. Kusminski, F. Fisher, N. D. Silva, M. Khanolkar, M. Evans, A. Harte, Satish Kumar, Sudhesh Kumar. American Journal of Physiology. Endocrinology and Metabolism, 2007
1,038 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/1d1a3da22fc7571248d14b6d4ebfc46567d82937
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In Epidemiology
- Patrice D Cani
- N. Delzenne
- O. Osborn
- Jerrold M. Olefsky
- S. Ghosh
- Curtis Huttenhower
- F. Bäckhed
- Nicola Segata
In Immunology
- Jerrold M. Olefsky
- C. Andersen
- M. Fernández
- S. Ghosh
- Kelsey E. Murphy
- F. Bäckhed
- Patrice D Cani
- O. Osborn
Citations in the corpus
- Understanding the Holobiont: How microbial metabolites affect human health and shape the immune system (2017, background): “Similarly, Chang et al. demonstrated that butyrate limits the secretion of pro-inflammatory cytokines from LPS-stimulated macrophages in the colonic lamina propria.”
- Human Intestinal Barrier Function in Health and Disease (2016, background): “This relationship between fatty acid ingestion and metabolic endotoxemia has been confirmed in multiple independent studies.98–100 Furthermore, it has been shown that metabolic endotoxemia increases adipose tissue markers of inflammation such as TNF-α and IL-6, as well as insulin resistance in healt”
- Intestinal Barrier Dysfunction, LPS Translocation, and Disease Development (2020, background): “Even in humans, obese phenotype is associated with endotoxemia, establishing the critical role of gut-derived LPS in the development of metabolic diseases [56, 57].”
- Impact of Obesity and Metabolic Syndrome on Immunity. (2016, background): “The LPS-neutralizing properties of HDL may be particularly important in obesity and MetS, where blood LPS levels are often found to be elevated (114, 115).”
- Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Disease (2012, background): “One mechanism that may explain microbial-induced obesity associated with metabolic syndrome and T2D, is endotoxemia which is characterized by excess circulating LPS which triggers systemic inflammation [81,82].”
- INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “As an additional aspect of Tlr4-mediated inflammation, it has been reported that obesity is associated with gastrointestinal dysbiosis in which LPS derived from gastrointestinal-tract microflora leaks into the systemic circulation (Brun et al., 2007; Creely et al., 2007).”
- Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease (2009, neutral): “n 17 18 14 21 Sex (M) 3/14 2/16 NS 3/11 2/19 NS Age 44 (34-53) 41 (32-54) NS 46(32-54) 40 (32-53 NS BMI 24.”
- Targeting gut microbiota in obesity: effects of prebiotics and probiotics (2011, background): “Moreover, Creely and colleagues demonstrated that metabolic endotoxemia is a factor associated with the development of type 2 diabetes mellitus”
- Canonical Nlrp3 inflammasome links systemic low grade inflammation to functional decline in aging (2013, neutral): “, 2012) and prior studies have reported circulating LPS as a potential cause of inflammation in metabolic syndrome (Creely et al., 2007), we also investigated if caspase-11 is involved in ‘‘inflammaging’’ process through potential interaction with gut-derived LPS.”
- Intestinal microbiota in patients with nonalcoholic fatty liver disease (2013, neutral): “ALP (U/L) 65 (49-98) 64 (42-105) 77 (37-114)”
- The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “In obesity, LPS derived from the gut microflora can leak into the circulation, resulting in higher serum LPS concentration”