Review article: lymphatic system and associated adipose tissue in the development of inflammatory bowel disease

Weid, Pierre‐Yves von der; Rainey, Kelly J

doi:10.1111/j.1365-2036.2010.04407.x

Cited by 62 publications

(48 citation statements)

References 159 publications

(181 reference statements)

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“…Adipose tissue acts as a secretory organ that generates signals that have a negative impact on lymphatic vasculature tone and permeability. In this scenario, lymphatic dysfunction could lead to further adiposity, thus worsening the condition in a vicious cycle [30,31]. Plant fractions enriched in rutin (i.e.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of AdipoDren® in Reducing Interleukin-1-Induced Lymphatic Endothelial Hyperpermeability

et al. 2016

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Lymphatic leakage can be seen as a detrimental phenomenon associated with fluid retention and deposition as well as gain of weight. Moreover, lymphatic dysfunction is associated with an inflammatory environment and can be a substrate for other health conditions. A number of treatments can ameliorate lymphatic vasculature: natural substances have been used as treatment options particularly suitable for their consolidated effectiveness and safety profile. Here we report the protective effect of AdipoDren®, an association of a series of plant-derived natural complexes, on lymphatic endothelium permeability promoted by interleukin-1 beta (IL-1β) and the associated molecular mechanisms. AdipoDren® demonstrated a protective effect on dermal lymphatic endothelial cell permeability increased by IL-1β. Reduced permeability was due to the maintenance of tight junctions and cell-cell localisation of occludin and zonula occludens-1 (ZO-1). Moreover, AdipoDren® reduced the expression of the inflammatory key element cyclooxygenase-2 (COX-2), while not altering the levels of endothelial and inducible nitric oxide synthases (eNOS and iNOS). The upregulation of antioxidant enzymatic systems (catalase and superoxide dismutase-1, SOD-1) and the downregulation of pro-oxidant markers (p22 phox subunit of NADPH oxidase) were also evident. In conclusion, AdipoDren® would be useful to ameliorate conditions of altered lymphatic vasculature and to support the physiological functionality of the lymphatic endothelium.

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Section: Discussionmentioning

confidence: 99%

Efficacy of AdipoDren® in Reducing Interleukin-1-Induced Lymphatic Endothelial Hyperpermeability

et al. 2016

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“…Poor lymphatic function, accompanied by leaking mesenteric lymph and coupled with increased cytokine accumulation from the surrounding inflamed tissue, creates an adipogenic environment similar to that in well-characterized peripheral lymphedema models. 73,81,82 Conversely, mouse models with congenital intestinal lymphatic dysplasia or targeted deletion of LECs both exhibit increased intestinal inflammation. 21 Blockade of IAL using an antibody against VEGFR-3 has also led to increased leukocyte accumulation and edema in a spontaneous mouse irritable bowel disease model.…”

Section: Lymphangiogenesis In Intestinal Inflammationmentioning

confidence: 99%

“…Inflammation models have also demonstrated local and lymph node adiposity with IAL. 73 Adipose-lymphatic interactions are not all malicious, however, as perinodal adipose tissue and adipose-resident monocytes along collecting lymphatic vessels play an important role in maintaining lymph node and immune surveillance functions, respectively. 73,75 Measurements of lymph flow in generalized obesity demonstrate reduced lymphatic function, and its improvement with weight loss and exercise in the same animals.…”

Section: Lymphangiogenesis and Renal Diseasementioning

confidence: 99%

Lymphangiogenesis: fuel, smoke, or extinguisher of inflammation’s fire?

Abouelkheir

Upchurch

Rutkowski

2017

Exp Biol Med (Maywood)

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Lymphangiogenesis is a recognized hallmark of inflammatory processes in tissues and organs as diverse as the skin, heart, bowel, and airways. In clinical and animal models wherein the signaling processes of lymphangiogenesis are manipulated, most studies demonstrate that an expanded lymphatic vasculature is necessary for the resolution of inflammation. The fundamental roles that lymphatics play in fluid clearance and immune cell trafficking from the periphery make these results seemingly obvious as a mechanism of alleviating locally inflamed environments: the lymphatics are simply providing a drain. Depending on the tissue site, lymphangiogenic mechanism, or induction timeframe, however, evidence shows that inflammation-associated lymphangiogenesis (IAL) may worsen the pathology. Recent studies have identified lymphatic endothelial cells themselves to be local regulators of immune cell activity and its consequential phenotypes – a more active role in inflammation regulation than previously thought. Indeed, results focusing on the immunocentric roles of peripheral lymphatic function have revealed that the basic drainage task of lymphatic vessels is a complex balance of locally processed and transported antigens as well as interstitial cytokine and immune cell signaling: an interplay that likely defines the function of IAL. This review will summarize the latest findings on how IAL impacts a series of disease states in various tissues in both preclinical models and clinical studies. This discussion will serve to highlight some emerging areas of lymphatic research in an attempt to answer the question relevant to an array of scientists and clinicians of whether IAL helps to fuel or extinguish inflammation. Impact statement Inflammatory progression is present in acute and chronic tissue pathologies throughout the body. Lymphatic vessels play physiological roles relevant to all medical fields as important regulators of fluid balance, immune cell trafficking, and immune identity. Lymphangiogenesis is often concurrent with inflammation and can potentially aide or worsen disease progression. How new lymphatic vessels impact inflammation and by which mechanism is an important consideration in current and future clinical therapies targeting inflammation and/or vasculogenesis. This review identifies, across a range of tissue-specific pathologies, the current understanding of inflammation-associated lymphangiogenesis in the progression or resolution of inflammation.

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“…In addition to lymphangiogenesis, collecting lymphatic contraction is found to be reduced in models of inflammatory bowel disease. 92 Factors such as macrophages, mast cells, iNOS, and prostaglandins contribute to this suppression of lymphatic contraction. 92 Other inflammatory cytokines and growth factors produced during inflammation may also affect collecting lymphatic function.…”

mentioning

confidence: 99%

“…92 Factors such as macrophages, mast cells, iNOS, and prostaglandins contribute to this suppression of lymphatic contraction. 92 Other inflammatory cytokines and growth factors produced during inflammation may also affect collecting lymphatic function. The role of cytokines, chemokines, and growth factors in lymphatic contraction remains an area of research focus.…”

mentioning

confidence: 99%