ArticleAnnals of surgery2011
Parenteral nutrition impairs lymphotoxin β receptor signaling via NF-κB.
Article in Annals of surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Migration and invasion inhibitory protein inhibits M2 macrophage polarization to suppress colorectal cancer progression through the STING-NFκB2-IL10 axis.Cancer biology & medicine · 2026Article
- Lymphocyte homing disorder: a concealed driver of intestinal immune collapse in sepsis.Frontiers in immunology · 2026Review
- Article
- NF-κB Inducing Kinase Regulates Intestinal Immunity and Homeostasis.Frontiers in immunology · 2022Review
- Gastrointestinal immune and microbiome changes during parenteral nutrition.American journal of physiology. Gastrointestinal and liver physiology · 2017Review
- Lymphotoxin β receptor activation promotes bladder cancer in a nuclear factor-κB-dependent manner.Molecular medicine reports · 2015Article
- Parenteral nutrition decreases paneth cell function and intestinal bactericidal activity while increasing susceptibility to bacterial enteroinvasion.JPEN. Journal of parenteral and enteral nutrition · 2014Article
- IL-25 improves luminal innate immunity and barrier function during parenteral nutrition.Annals of surgery · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo determine effects of (1) parenteral nutrition (PN), (2) exogenous Lymphotoxin β receptor (LTβR) stimulation in PN animals, and (3) exogenous LTβR blockade in chow animals on NF-κB activation pathways and products: MAdCAM-1, chemokine (C-C motif) Ligand (CCL) 19, CCL20, CCL25, interleukin (IL)-4, and IL-10.
backgroundLT stimulates LTβR in Peyer's patches (PP) to activate NF-κB via the noncanonical pathway. The p100/RelB precursor yields p52/RelB producing MAdCAM-1, cytokines, and chemokines important in cell trafficking. TNFα, IL-1β, and bacterial products stimulate the inflammatory canonical NF-κB pathway producing p65/p50 and c-Rel/p50. PN decreases LTβR, MAdCAM-1, and chemokines in PP and lowers small intestinal IgA compared with chow.
methodsCanonical (p50 and p65) and noncanonical (p52 and Rel B) NF-κB proteins in PP were analyzed by TransAM NF-κB kit after 5 days of chow or PN, 2 days of LTβR stimulation or 3 days of LTβR blockade. MAdCAM-1, chemokines, and cytokines in PP were measured by ELISA after LTβR stimulation or blockade.
resultsPN significantly reduced all NF-κB proteins in PP compared with chow. Exogenous LTβR stimulation during PN increased p50, p52, Rel B, MAdCAM-1, IL-4, and IL-10 in PP, but not p65, CCL19, CCL20, or CCL25 compared with PN. LTβR blockade reduced noncanonical products (p52 and Rel B), MAdCAM-1, CCL19, CCL20, CCL25, IL-4, and IL-10 but had no effect on the inflammatory pathway (p50 and p65) compared with chow.
conclusionLack of enteral stimulation during PN decreases both canonical and noncanonical NF-κB pathways in PP. LTβR stimulation during PN feeding completely restores PP noncanonical NF-κB activity, MAdCAM-1, IL-4, IL-10, and partly the canonical pathway. LTβR blockade decreases the noncanonical NF-κB activity, MAdCAM-1, chemokines, and cytokines without effect on the canonical NF-κB activity in PP.
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Registered trials
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