ArticleWorld journal of gastroenterology2014
ATG16L1 and NOD2 polymorphisms enhance phagocytosis in monocytes of Crohn's disease patients.
Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- NOD2-Related Multisystem Inflammatory Disorders and Recent Advances.Current rheumatology reports · 2026Review
- Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy.Clinical and molecular hepatology · 2024Article
- Origin and Function of Monocytes in Inflammatory Bowel Disease.Journal of inflammation research · 2024Review
- Autophagic reprogramming of bone marrow-derived macrophages.Immunologic research · 2023Article
- IBD-associated G protein-coupled receptor 65 variant compromises signalling and impairs key functions involved in inflammation.Cellular signalling · 2022Article
- Association between variants of the autophagy related gene ATG16L1 in inflammatory bowel diseases and clinical statues.Gastroenterology and hepatology from bed to bench · 2019Article
- Genetic deficiency of NOD2 confers resistance to invasive aspergillosis.Nature communications · 2018Article
- Glucocorticoids Impair Phagocytosis and Inflammatory Response Against Crohn's Disease-Associated Adherent-InvasiveFrontiers in immunology · 2018Article
- NOD2 and inflammation: current insights.Journal of inflammation research · 2018Review
- Understanding the regulation of pattern recognition receptors in inflammatory diseases - a 'Nod' in the right direction.Immunology · 2017Review
- Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate if the presence of relevant genetic polymorphisms has effect on the effectual clearance of bacteria by monocytes and granulocytes in patients with Crohn's disease (CD).
methodsIn this study, we assessed the differential responses in phagocytosis by measuring the phagocytic activity and the percentage of active phagocytic monocytes and granulocytes in inflammatory bowel disease patients as well as healthy controls. As both autophagy related like 1 (ATG16L1) and immunity-related guanosine triphosphatase gene are autophagy genes associated with CD and more recently nucleotide-binding ligomerization domain-containing protein 2 (NOD2) has been identified as a potent inducer of autophagy we genotyped the patients for these variants and correlated this to the phagocytic reaction. The genotyping was done with restriction fragment length polymorphisms analysis and the phagocytosis was determined with the pHrodo™ Escherichia coli Bioparticles Phagocytosis kit for flowcytometry.
resultsIn this study, we demonstrate that analysis of the monocyte and granulocyte populations of patients with CD and ulcerative colitis showed a comparable phagocytic activity (ratio of mean fluorescence intensity) between the patient groups and the healthy controls. CD patients show a significantly higher phagocytic capacity (ratio mean percentage of phagocytic cells) compared to healthy controls (51.91% ± 2.85% vs 37.67% ± 7.06%, P = 0.05). The extend of disease was not of influence. However, variants of ATG16L1 (WT: 2.03 ± 0.19 vs homozygoot variant: 4.38 ± 0.37, P < 0.009) as well as NOD2 (C-ins) (heterozygous variant: 42.08 ± 2.94 vs homozygous variant: 75.58 ± 4.34 (P = 0.05) are associated with the phagocytic activity in patients with CD.
conclusionMonocytes of CD patients show enhanced phagocytosis associated with the presence of ATG16L1 and NOD2 variants. This could be part of the pathophysiological mechanism resulting in the disease.
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