Mast Cell Function

Silva, Elaine Zayas Marcelino da; Jamur, Maria Célia; Oliver, Constance

doi:10.1369/0022155414545334

Cited by 495 publications

(304 citation statements)

References 598 publications

(645 reference statements)

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“…It is possible that by reducing the initial number of mast cells and macrophages, both the corticosteroids and Palovarotene may have interrupted a key mechanism by which local and distant host cells are geared into action, sense the presence of growth factor gradients (such that elicited by the rhBMP2-loaded Matrigel scaffold), and migrate toward and gather around the scaffold. The initial inflammation may be needed to set this cascade in motion, for example via de-granulation of recruited mast cells [70]. Release of tumor necrosis factor by mast cells was shown to promote migration of dendritic cells into lymph nodes [71].…”

Section: Discussionmentioning

confidence: 99%

“…Release of tumor necrosis factor by mast cells was shown to promote migration of dendritic cells into lymph nodes [71]. More generally, mast cells are well known for their roles in wound healing, tissue repair and angiogenesis by recruitment of progenitors at inflamed and damaged sites [70], and corticosteroids have been shown to reduce progenitor number at inflamed sites and tissues [72]. Clearly, the drugs may have hampered the release of cues that are needed by cells to migrate and navigate through matrix and tissues, and a decrease in mast cell number and activity could be an initial, important and comprehensive mechanism by which corticosteroids and Palovarotene inhibit HO.…”

Section: Discussionmentioning

confidence: 99%

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Effectiveness and mode of action of a combination therapy for heterotopic ossification with a retinoid agonist and an anti-inflammatory agent

Sinha

Uchibe

Usami

et al. 2016

Bone

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Heterotopic ossification (HO) consists of ectopic cartilage and bone formation following severe trauma or invasive surgeries, and a genetic form of it characterizes patients with Fibrodysplasia Ossificans Progressiva (FOP). Recent mouse studies showed that HO was significantly inhibited by systemic treatment with a corticosteroid or the retinoic acid receptor γ agonist Palovarotene. Because these drugs act differently, the data raised intriguing questions including whether the drugs affected HO via similar means, whether a combination therapy would be more effective or whether the drugs may hamper each other's action. To tackle these questions, we used an effective HO mouse model involving subcutaneous implantation of Matrigel plus rhBMP2, and compared the effectiveness of prednisone, dexamathaosone, Palovarotene or combination of. Each corticosteroid and Palovarotene reduced bone formation at max doses, and a combination therapy elicited similar outcomes without obvious interference. While Palovarotene had effectively prevented the initial cartilaginous phase of HO, the steroids appeared to act more on the bony phase. In reporter assays, dexamethasone and Palovarotene induced transcriptional activity of their respective GRE or RARE constructs and did not interfere with each other's pathway. Interestingly, both drugs inhibited the activity of a reporter construct for the inflammatory mediator NF-κB, particularly in combination. In good agreement, immunohistochemical analyses showed that both drugs markedly reduced the number of mast cells and macrophages near and within the ectopic Matrigel mass and reduced also the number of progenitor cells. In sum, corticosteroids and Palovarotene appear to block HO via common and distinct mechanisms. Most importantly, they directly or indirectly inhibit the recruitment of immune and inflammatory cells present at the affected site, thus alleviating the effects of key HO instigators.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effectiveness and mode of action of a combination therapy for heterotopic ossification with a retinoid agonist and an anti-inflammatory agent

Sinha

Uchibe

Usami

et al. 2016

Bone

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“…They are mainly located in the lamina propria and the submucosa but are also found in the intraepithelial, smooth muscle, and serosal layers of the intestine [43]. According to their granule contents, mast cells can be grouped as those containing tryptase but no chymase and those containing tryptase, chymase, and carboxypeptidase [13, 44, 45], each predominating in different locations [46]. The functions of intestinal mast cells include regulating permeability, secretion, peristalsis, nociception, innate and adaptive immunity, and angiogenesis and affecting many diverse GI diseases such as not only functional GI disorders but also organic diseases [47].…”

Section: Mast Cells In the Regulation Of Gi Physiology And Pathophmentioning

confidence: 99%

The Role of Mast Cells in Irritable Bowel Syndrome

Lee

2016

Gastroenterology Research and Practice

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Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, but its treatment is unsatisfactory as its pathophysiology is multifactorial. The putative factors of IBS pathophysiology are visceral hypersensitivity and intestinal dysmotility, also including psychological factors, dysregulated gut-brain axis, intestinal microbiota alterations, impaired intestinal permeability, and mucosal immune alterations. Recently, mucosal immune alterations have received much attention with the role of mast cells in IBS. Mast cells are abundant in the intestines and function as intestinal gatekeepers at the interface between the luminal environment in the intestine and the internal milieu under the intestinal epithelium. As a gatekeeper at the interface, mast cells communicate with the adjacent cells such as epithelial, neuronal, and other immune cells throughout the mediators released when they themselves are activated. Many studies have suggested that mast cells play a role in the pathophysiology of IBS. This review will focus on studies of the role of mast cell in IBS and the limitations of studies and will also consider future directions.

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“…Mast cells (MCs) are widely distributed throughout the extravascular area in the body where they play versatile roles dealing with innate immunity, IgEmediated allergy and inflammation. Indeed, they promote neutrophil phagocytosis, lymph node hyperplasia and can directly phagocytise and kill bacteria [86] . Data concerning NO/RNS generation by either rodent or human mast cells are still controversial.…”

Section: No Rns and Inflammationmentioning

confidence: 99%