Relationship between levels of angiogenic and lymphangiogenic factors and the endoscopic, histological and clinical activity, and acute-phase reactants in patients with inflammatory bowel disease

Algaba, Alicia; Linares, Pablo M.; Fernández-Contreras, M.E.; Ordóñez, A. Fernández; Trápaga, J.; Guerra, Iván; Chaparro, María; Poza, Gema de la; Gisbert, Javier P.; Bermejo, Fernando

doi:10.1016/j.crohns.2013.04.005

Cited by 28 publications

(36 citation statements)

References 43 publications

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“…Lymphangiogenesis occurs in several pathologic circumstances varying from benign conditions as tissue repair , arthritis (Schwarz et al 2010;Zhang et al 2007), and inflammatory bowel diseases (Algaba et al 2013) or associated with various neoplasia (Cueni and Detmar 2008;Proulx et al 2013;Schoppmann et al 2013) (Fig. 1).…”

Section: Lymphangiogenesis: Step By Step From Friendship To Hostilitymentioning

confidence: 99%

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Cimpean

Raica

2015

Arch. Immunol. Ther. Exp.

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Several papers about lymphangiogenesis and inflammation focused on the detailed and complicated descriptions of the molecular pathways accompanying both non-tumor and tumor inflammatory-induced lymphatic vessel development. Many authors are tempted to present inflammatory-induced lymphangiogenesis in pathologic conditions neglecting the role of inflammatory cells during embryonic lymphatic vessel development. Some of the inflammatory cells are largely characterized in inflammatory-induced lymphangiogenesis, while others as mast cells, eosinophils, or plasma cells are less studied. No phenotypic characterization of inflammation-activated lymphatic endothelial cell is available in this moment. Another paradox is related to the existence of few papers regarding lymphangiogenesis inside lymphoid organs and for their related pathology. There are still several "missing pieces of such a big puzzle" of lymphangiogenesis and inflammation, with a direct impact on the ineffectiveness of the anti-inflammatory therapy as lymphangiogenesis inhibitors. The present paper will focus on the controversial issues of lymphangiogenesis and inflammation.

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Section: Lymphangiogenesis: Step By Step From Friendship To Hostilitymentioning

confidence: 99%

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Cimpean

Raica

2015

Arch. Immunol. Ther. Exp.

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“…Obstructed intestinal lymphatics are an established histological hallmark of CD, which stands somewhat in contrast to the lymphatic expansion observed in the mucosa of patients with IBDs (9-13), because it remains unclear whether lymphatic insufficiency due to obstruction is the cause of IBD or whether excessive lymphatic growth results from lymphatic insufficiency. In postoperative CD patients, a low density of lymphatic vessels has been attributed to recurrence of the disease (14), and an inability of lymphatic vessels to function has been associated with lymphedema of the intestinal walls in IBD patients (15). In animal models, VEGF-C administration was shown to stimulate lymphatic function and abrogate experimental colitis (16,17).…”

Section: Introductionmentioning

confidence: 99%

Lymphatic deletion of calcitonin receptor–like receptor exacerbates intestinal inflammation

Davis¹,

Kechele²,

Blakeney³

et al. 2017

JCI Insight

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“…However, this has not been shown to occur during intestinal inflammation, where VEGF-C/D is upregulated. 15,47 We first investigated whether MΦ could be a source of VEGF-C/D in murine experimental colitis. Colonic cross sections from 2% DSS-treated WT mice were stained for VEGF-C, VEGF-D, and the MΦ marker Mac-2.…”

Section: Resultsmentioning

confidence: 99%

A Critical Role for Monocytes/Macrophages During Intestinal Inflammation-associated Lymphangiogenesis

Becker

Kurmaeva

Gavins

et al. 2016

Inflammatory Bowel Diseases

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Background Inflammation-associated lymphangiogenesis (IAL) is frequently observed in inflammatory bowel diseases. IAL is believed to limit inflammation by enhancing fluid and immune cell clearance. Although monocytes/macrophages (MΦ) are known to contribute to intestinal pathology in inflammatory bowel disease, their role in intestinal IAL has never been studied mechanistically. We investigated contributions of monocytes/MΦ to the development of intestinal inflammation and IAL. Methods Because inflammatory monocytes express CC chemokine receptor 2 (CCR2), we used CCR2 diphtheria toxin receptor transgenic (CCR2.DTR) mice, in which monocytes can be depleted by diphtheria toxin injection, and CCR2−/− mice, which have reduced circulating monocytes. Acute or chronic colitis was induced by dextran sodium sulfate or adoptive transfer of CD4+CD45RBhigh T cells, respectively. Intestinal inflammation was assessed by flow cytometry, immunofluorescence, disease activity, and histopathology, whereas IAL was assessed by lymphatic vessel morphology and density. Results We demonstrated that intestinal MΦ expressed vascular endothelial growth factor-C/D. In acute colitis, monocyte-depleted mice were protected from intestinal injury and showed reduced IAL, which was reversed after transfer of wild-type monocytes into CCR2−/− mice. In chronic colitis, CCR2 deficiency did not attenuate inflammation but reduced IAL. Conclusions We propose a dual role of MΦ in (1) promoting acute inflammation and (2) contributing to IAL. Our data suggest that intestinal inflammation and IAL could occur independently, because IAL was reduced in the absence of monocytes/MΦ, even when inflammation was present. Future inflammatory bowel disease therapies might exploit promotion of IAL and suppression of MΦ independently, to restore lymphatic clearance and reduce inflammation.

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Relationship between levels of angiogenic and lymphangiogenic factors and the endoscopic, histological and clinical activity, and acute-phase reactants in patients with inflammatory bowel disease

Abstract: MCS determination suggests a local increase in ALFs that correlates with IBD activity. Although the correlation between ALFs in serum and MCS was not good, the study of some of these factors as possible targets of new drugs for IBD constitutes a key new line of research.

Cited by 28 publications

References 43 publications

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Lymphatic deletion of calcitonin receptor–like receptor exacerbates intestinal inflammation

A Critical Role for Monocytes/Macrophages During Intestinal Inflammation-associated Lymphangiogenesis

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