ArticleScientific reports2016
Deficiency in Toll-interacting protein (Tollip) skews inflamed yet incompetent innate leukocytes in vivo during DSS-induced septic colitis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Yuyang Decoction Regulates Macrophage Polarization and Repairs the Intestinal Mucosal Barrier via the TLRs/Tollip Signaling Pathway.Journal of inflammation research · 2025Article
- Transcriptome sequencing and experiments reveal the effect of formyl peptide receptor 2 on liver homeostasis.World journal of gastroenterology · 2023Article
- The beneficial effects of commensal E. coli for colon epithelial cell recovery are related with Formyl peptide receptor 2 (Fpr2) in epithelial cells.Gut pathogens · 2023Article
- Contributions of the microbiota to the systemic inflammatory response.Microbiota and host · 2023Article
- Integrated Single Cell and Bulk RNA-Seq Analysis Revealed Immunomodulatory Effects of Ulinastatin in Sepsis: A Multicenter Cohort Study.Frontiers in immunology · 2022Article
- Bile acids as inflammatory mediators and modulators of intestinal permeability.Frontiers in immunology · 2022Review
- Neutrophil extracellular trap formation index predicts occurrences of deep surgical site infection after laparotomy.Annals of translational medicine · 2021Article
- Article
- Chrysin Derivative CM1 and Exhibited Anti-Inflammatory Action by Upregulating Toll-Interacting Protein Expression in Lipopolysaccharide-Stimulated RAW264.7 Macrophage Cells.Molecules (Basel, Switzerland) · 2021Article
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Toll-like receptors in sepsis-associated cytokine storm and their endogenous negative regulators as future immunomodulatory targets.International immunopharmacology · 2020Review
- Toll-Interacting Protein Regulates Immune Cell Infiltration and Promotes Colitis-Associated Cancer.iScience · 2020Article
- Discovery of Selenocysteine as a Potential Nanomedicine Promotes Cartilage Regeneration With Enhanced Immune Response by Text Mining and Biomedical Databases.Frontiers in pharmacology · 2020Article
- The Contribution of Chemoattractant GPCRs, Formylpeptide Receptors, to Inflammation and Cancer.Frontiers in endocrinology · 2020Review
- Enhanced Neutrophil Immune Homeostasis Due to Deletion of PHLPP.Frontiers in immunology · 2019Article
- Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation.Journal of leukocyte biology · 2018Review
- Suppression of Neutrophil Antimicrobial Functions by Total Particulate Matter From Cigarette Smoke.Frontiers in immunology · 2018Article
- Regulation of inflammation by members of the formyl-peptide receptor family.Journal of autoimmunity · 2017Review
- Programming and memory dynamics of innate leukocytes during tissue homeostasis and inflammation.Journal of leukocyte biology · 2017Review
- Toll-Interacting Protein in Resolving and Non-Resolving Inflammation.Frontiers in immunology · 2017Review
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Functionally compromised neutrophils contribute to adverse clinical outcomes in patients with severe inflammation and injury such as colitis and sepsis. However, the ontogeny of dysfunctional neutrophil during septic colitis remain poorly understood. We report that the dysfunctional neutrophil may be derived by the suppression of Toll-interacting-protein (Tollip). We observed that Tollip deficient neutrophils had compromised migratory capacity toward bacterial product fMLF due to reduced activity of AKT and reduction of FPR2, reduced potential to generate bacterial-killing neutrophil extra-cellular trap (NET), and compromised bacterial killing activity. On the other hand, Tollip deficient neutrophils had elevated levels of CCR5, responsible for their homing to sterile inflamed tissues. The inflamed and incompetent neutrophil phenotype was also observed in vivo in Tollip deficient mice subjected to DSS-induced colitis. We observed that TUDCA, a compound capable of restoring Tollip cellular function, can potently alleviate the severity of DSS-induced colitis. In humans, we observed significantly reduced Tollip levels in peripheral blood collected from human colitis patients as compared to blood samples from healthy donors. Collectively, our data reveal a novel mechanism in Tollip alteration that underlies the inflamed and incompetent polarization of neutrophils leading to severe outcomes of colitis.
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