Inflammatory lymphangiogenesis: cellular mediators and functional implications

Tan, Kui‐Thong; Chong, Shu Zhen; Angeli, Véronique

doi:10.1007/s10456-014-9419-4

Cited by 24 publications

(34 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Multiple types of leukocytes and macrophages contribute to proteolytic remodeling of the extracellular matrix (24,25). Angiogenesis and lymphangiogenesis facilitate additional recruitment of immune cells, resulting in enhancement of chronic inflammation (23,25,26). On the other hand, elevated levels of inflammatory cytokines such as TNFα, IL-1, and IL-6 induce a decrease in muscle mass and strength, called sarcopenia (27)(28)(29)(30).…”

Section: Chronic Inflammation By Sterile Continuous Micro-aspirationmentioning

confidence: 99%

Dysphagia, dystussia, and aspiration pneumonia in elderly people

Ebihara¹,

Sekiya²,

Miyagi³

et al. 2016

J. Thorac. Dis.

136

View full text Add to dashboard Cite

Despite the development and wide distribution of guidelines for pneumonia, death from pneumonia is increasing due to population aging. Conventionally, aspiration pneumonia was mainly thought to be one of the infectious diseases. However, we have proven that chronic repeated aspiration of a small amount of sterile material can cause the usual type of aspiration pneumonia in mouse lung. Moreover, chronic repeated aspiration of small amounts induced chronic inflammation in both frail elderly people and mouse lung. These observations suggest the need for a paradigm shift of the treatment for pneumonia in the elderly. Since aspiration pneumonia is fundamentally based on dysphagia, we should shift the therapy for aspiration pneumonia from pathogen-oriented therapy to function-oriented therapy. Function-oriented therapy in aspiration pneumonia means therapy focusing on slowing or reversing the functional decline that occurs as part of the aging process, such as "dementia → dysphagia → dystussia → atussia → silent aspiration". Atussia is ultimate dysfunction of cough physiology, and aspiration with atussia is called silent aspiration, which leads to the development of life-threatening aspiration pneumonia. Research pursuing effective strategies to restore function in the elderly is warranted in order to decrease pneumonia deaths in elderly people.

show abstract

Section: Chronic Inflammation By Sterile Continuous Micro-aspirationmentioning

confidence: 99%

Dysphagia, dystussia, and aspiration pneumonia in elderly people

Ebihara¹,

Sekiya²,

Miyagi³

et al. 2016

J. Thorac. Dis.

136

View full text Add to dashboard Cite

show abstract

“…Changes in the lymph node environment can include volume expansion from increased fluid burden, expansion of the LECstructured lymphatic sinuses, expansion of the fibroblastic reticular cell network, and proliferation of lymphocyte populations. 15 These changes are mechanically mediated and driven by vascular growth factors, cytokines, and CCL21-expressing T-cells entering with the afferent lymph as well as by lymph node reticular fibroblasts and B-cells (and later by neutrophils). 15 CCL21 is a noted LEC-secreted chemokine that guides leukocytes to lymphatic vessels for tissue egress; its levels are indicative in this review of both LEC numbers and activation.…”

Section: Inflammatory Lymph Node Remodelingmentioning

confidence: 99%

“…16 The mechanism by which lymphangiogenesis occurs, most notably the cell source of new LECs, has recently been described to be much more complex than the traditional vascular sprouting described in blood angiogenesis and is very much tissue specific. [16][17][18][19][20] Multiple cell types may participate or assist in lymphangiogenesis as a source of lymphatic growth factors that induce LEC proliferation 6,15 and equally many antiproliferative cells and cytokines have been described. 15,21 The predominant and consistently key signaling mechanism for lymphangiogenesis is VEGF receptor (VEGFR)-3 activation by its ligands VEGF-C and VEGF-D. 4,7 LEC VEGFR-3 signaling is requisite in developmental and adult models of lymphangiogenesis.…”

Section: Lymphangiogenesis Regulationmentioning

confidence: 99%

“…[16][17][18][19][20] Multiple cell types may participate or assist in lymphangiogenesis as a source of lymphatic growth factors that induce LEC proliferation 6,15 and equally many antiproliferative cells and cytokines have been described. 15,21 The predominant and consistently key signaling mechanism for lymphangiogenesis is VEGF receptor (VEGFR)-3 activation by its ligands VEGF-C and VEGF-D. 4,7 LEC VEGFR-3 signaling is requisite in developmental and adult models of lymphangiogenesis. 5,22 Serum levels of VEGF-C and VEGF-D are elevated in inflammatory disease further confirming a driving role in IAL.…”

Section: Lymphangiogenesis Regulationmentioning

confidence: 99%

“…Adult lymphangiogenesis is limited to acute and chronic conditions of inflammation and tissue remodeling. 15 Adult lymphatic vessels are otherwise quiescent explaining the lack of a lymphatic vascular phenotype upon genetic ablation of the predominant lymphatic growth factor, vascular endothelial growth factor (VEGF)-C in adult mice. 16 The mechanism by which lymphangiogenesis occurs, most notably the cell source of new LECs, has recently been described to be much more complex than the traditional vascular sprouting described in blood angiogenesis and is very much tissue specific.…”

Section: Lymphangiogenesis Regulationmentioning

confidence: 99%

See 2 more Smart Citations

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

Abouelkheir

Upchurch

Rutkowski

2017

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

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.

show abstract

Antigen archiving by lymph node stroma: A novel function for the lymphatic endothelium

Kedl

Tamburini

2015

Eur J Immunol

View full text Add to dashboard Cite

Secondary lymphoid stroma performs far more functions than simple structural support for lymphoid tissues, providing a host of soluble and membrane-bound cues to trafficking leukocytes during inflammation and homeostasis. More recently it has become clear that stromal cells can manipulate T cell responses, either through direct antigen-mediated stimulation of T cells or more indirectly through the retention and management of antigen after viral infection or vaccination. In light of recent data, this review provides an overview of stromal cell subsets and functions during the progression of an adaptive immune response with particular emphasis on antigen capture and retention by follicular dendritic cells (FDC) as well as the recently described “antigen archiving” function of lymphatic endothelial cells (LEC). Given its impact on the maintenance of protective immune memory, we conclude by discussing the most pressing questions pertaining to LEC antigen capture, archiving and exchange with hematopoetically derived antigen-presenting cells.

show abstract

Inflammatory lymphangiogenesis: cellular mediators and functional implications

Cited by 24 publications

References 81 publications

Dysphagia, dystussia, and aspiration pneumonia in elderly people

Dysphagia, dystussia, and aspiration pneumonia in elderly people

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

Antigen archiving by lymph node stroma: A novel function for the lymphatic endothelium

Contact Info

Product

Resources

About