Immunohistochemical analysis of substance P containing nerve fibres and their contacts with mast cells in the diabetic rat's tongue

Batbayar, Bayarchimeg; Somogyi, J.; Zelles, T; Fehér, Erzsébet

doi:10.1556/abiol.54.2003.3-4.6

Cited by 18 publications

(20 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was demonstrated that calcitonin gene-related peptide (CGRP) and substance P (SP) nerve fibers innervate the mucosal and submucosal vessels of the upper gastrointestinal tract [7,8]. SP and CGRP are thought to be the mediators of neurogenic inflammation [9][10][11]. Peptides synthesized in primary sensory neurons are released through the axon reflex from small-diameter fibers in the peripheral tissues near blood vessels and they may act as neurogenic mediators of inflammation and pain.…”

Section: Introductionmentioning

confidence: 99%

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

et al. 2006

View full text Add to dashboard Cite

It is suggested that different neuropeptides regulate gastric mucosal integrity and participate in the development of chronic gastritis. The aim of this study was to examine the roles and changes of immunoreactive (IR) nerves and immunocompetent cells in human gastritis. Immunohistochemical, immunocytochemical, and confocal laser microscopic methods were used. All investigated nerve fibers were found in different quantities in the mucosa of both control and gastritis samples. The number of SP, NPY, and VIP IR nerve fibers increased significantly (P < 0.05) in gastritis. No IR immunocompetent cells (lymphocytes, plasma cells, mast cells) were found in the control, however, some showed NPY (16.8%) and SP (9.4%) immunoreactivity in chronic gastritis. The distance between nerve fibers and immunocompetent cells was 200 nm to 1 microm. In conclusion, the increased number of SP, NPY, and VIP IR nerves and IR immunocytes suggests that they participate in development of neurogenic inflammation, repairing processes of chronic gastritis.

show abstract

Section: Introductionmentioning

confidence: 99%

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Alterations in the number of SP-reactive fibers and mast cell-nerve contacts have been reported as parts of the pathology of several diseases (3,19,45). SP can activate mast cells both through binding of the neurokinin-1 receptor present on these cells (8) and through receptor-independent mechanisms (10).…”

mentioning

confidence: 99%

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Karlsen¹,

Bletsa²,

Gjerde³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Neurogenic inflammation is known to induce lowering of interstitial fluid pressure (P if) in mouse skin. This study examined the possible role of mast cell activation secondary to neuropeptide release in lowering of P if by using , and neurokinin A, from the capsaicin-sensitive nerve endings. Capsaicin releases neuropeptides through binding to the vanilloid receptor subtype 1 (VR1) (9), which in turn induces an inflammatory response in various tissues of both rodents and humans (2, 21). This response is characterized by increased arteriolar vasodilatation and protein extravasation due to increased permeability of the postcapillary venules resulting in fluid accumulation in the tissue. Previous reports from our research group have shown that the response in the initial phase of neurogenic inflammation involves lowering of interstitial fluid pressure (P if ) as observed both in rat trachea (16) and mouse skin (25). P if is important in tissue fluid homeostasis both in the regulation of fluid filtration across the capillary and as the filling pressure for the lymphatics (1). In contrast to the classic view of P if serving as an edema-preventing mechanism, P if has been shown to play an active part in the initial phase of edema in a number of inflammatory models with a lowering of P if to more negative values (16,31,34,35). According to Starling's hypothesis, this lowering of P if will increase net filtration pressure across the capillary and hence contribute to fluid accumulation in the interstitial space.Mast cells have been thought of as possible participants in the neurogenic inflammatory response because they contain numerous inflammatory mediators and are localized in close proximity to the capsaicin-sensitive nerve endings (37,39). Alterations in the number of SP-reactive fibers and mast cell-nerve contacts have been reported as parts of the pathology of several diseases (3,19,45). SP can activate mast cells both through binding of the neurokinin-1 receptor present on these cells (8) and through receptor-independent mechanisms (10). The significance of mast cell activation as a part of neurogenic inflammation has been questioned in a number of studies, and the results are yet not conclusive. Supporting the involvement of mast cells are the findings that stimulation of the rat saphenous nerve induces mast cell degranulation (27) and that SP in high concentrations (40) as well as topical application of capsaicin (7) induce cutaneous mast cell degranulation in human forearm. In contrast, Petersen et al. (32) detected no release of SP and histamine after capsaicin injection in the same area.In light of the knowledge that capsaicin-sensitive nerve endings are localized close to connective tissue mast cells (CTMCs) in mouse skin (6) and that mast cell activation by compound 48/80 (C48/80) induces a lowering of P if in skin of both rats and mice (20,25,36), the question arises as to whether mast cells are involved in the events leading to lowering of P if in neurogenic inflammation. In a recent study (25) we exami...

show abstract

“…Streptozotocin-induced diabetic rats showed significant increases in mesenteric artery weight, wall-to-lumen ratio, arterial wall ECM deposition, and gene expression of epidermal growth factor (EGF) and TGF-β1 [97]. In those rats, diabetes also associated with an increase of mast cell numbers to the tongues [98] and in mesenteric vessels [97] — often associated with fibrosis, a common feature of diabetic microvascular complications [35]. In those experimental diabetic rats, treatment with the mast cell degranulation inhibitor tranilast (N-[3,4-demethoxycinnamoyl]-anthranilic acid) reduced mesenteric vessel fibrosis, artery weight, wall-to-lumen ratio, and matrix deposition, although it did not influence tryptase-positive mast cell infiltration, plasma glucose level, or systolic blood pressure [35, 99].…”

Section: Mast Cell Chymases and Tryptases In Metabolic Diseasesmentioning

confidence: 99%

Mast Cell Chymase and Tryptase as Targets for Cardiovascular and Metabolic Diseases

He¹,

Shi²

2012

CPD

View full text Add to dashboard Cite

Mast cells are critical effectors in inflammatory diseases, including cardiovascular and metabolic diseases and their associated complications. These cells exert their physiological and pathological activities by releasing granules containing histamine, cytokines, chemokines, and proteases, including mast cell-specific chymases and tryptases. Several recent human and animal studies have shown direct or indirect participation of mast cell-specific proteases in atherosclerosis, abdominal aortic aneurysms, obesity, diabetes, and their complications. Animal studies have demonstrated the beneficial effects of highly selective and potent chymase and tryptase inhibitors in several experimental cardiovascular and metabolic diseases. In this review, we summarize recent discoveries from in vitro cell-based studies to experimental animal disease models, from protease knockout mice to treatments with recently developed selective and potent protease inhibitors, and from patients with preclinical disorders to those affected by complications. We hypothesize that inhibition of chymases and tryptases would benefit patients suffering from cardiovascular and metabolic diseases.

show abstract

Immunohistochemical analysis of substance P containing nerve fibres and their contacts with mast cells in the diabetic rat's tongue

Cited by 18 publications

References 21 publications

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Mast Cell Chymase and Tryptase as Targets for Cardiovascular and Metabolic Diseases

Contact Info

Product

Resources

About