Studies on the Function of Mast Cells Infiltrating in Nasal Polyps

Seki, Harumi; Otsuka, Hirokuni; Pawankar, Ruby

doi:10.3950/jibiinkoka.95.1012

Cited by 5 publications

(8 citation statements)

References 14 publications

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“…This may be explained in that IL-4 promotes FcεRI alpha-chain gene transcription and thus increases alpha-chain protein synthesis in the cells, whereas the binding of IgE may anchor the Fcε RI on the cell surface, resulting in suppressing the internalization of FcεRI. These findings may explain our earlier observations that mast cells from allergic nasal polyps released significantly higher amounts of histamine when stimulated with anti-IgE, as against those from non-allergic nasal polyps [70].…”

Section: Mast Cells and The Fcε ε ε εRimentioning

confidence: 72%

Mast Cell-IgE-and Mast Cell-Structural Cell Interactions in Allergic Airway Disease

Pawankar

Yamagishi²,

Takizawa³

et al. 2003

CDTIA

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Allergic diseases like atopic rhinitis, bronchial asthma, and urticaria are prevalent and on the rise. Mast cells are known to play a central role in the immediate phase reaction of allergic diseases through the IgE-mediated release of a variety of chemical mediators like histamine, leukotrienes, and prostaglandins. On the other hand, T lymphocytes, basophils and eosinophils are thought to be responsible in inducing the late phase response. Yet, recent studies show that the mast cell cannot be simplistically assigned a role in the immediate phase allergic response, and that this cell plays a crucial role in ongoing allergic inflammation, including the development of hyper-responsiveness. In the present article, the author will try to discuss the integrated roles of mast cells in IgE-mediated allergic inflammation with specific emphasis on the roles of mast cell-IgE networking and mast cell-structural cell interactions in the late phase allergic response and chronic allergic inflammation.

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Section: Mast Cells and The Fcε ε ε εRimentioning

confidence: 72%

Mast Cell-IgE-and Mast Cell-Structural Cell Interactions in Allergic Airway Disease

Pawankar

Yamagishi²,

Takizawa³

et al. 2003

CDTIA

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“…In humans, the underlying disease (e.g. atopic or nonatopic) [2,27,32,33] might also be important. The findings of Takeda et al [34] indicate that the neuro peptide-induced histamine release occurs only in the sensi tized nasal mucosa of guinea pigs (after exposure to the al lergen toluene diisocyanate) and is due to subsequent anti- …”

Section: Discussionmentioning

confidence: 99%

“…Intravenous injec tions of SP increased vascular permeability in the tracheal mucosa of guinea pigs, a factor for the development of air way hyperresponsiveness in bronchial asthma [22], However, there is still controversy in this discussion, since there are a number of studies which were not able to demonstrate mediator release after SP administration in hu man and bovine mucosal mast cells [23][24][25][26][27], whereas ro dent intestinal mucosal [28], rat lung [29] and human skin mast cells [24] did release histamine in response to SP. This could be due to the material used, since mast cells show a broad heterogeneity, and cells of different species behave differently [23][24][25][26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

“…SP has also been reported to evoke anion secretion by activating cholinergic and noncholinergic neurons followed by histamine release in ro dents [35] -but sparsely in humans. Most of the in vitro investigations concerning the effect of SP on human muco sal mast cells failed to release histamine after SP stimula tion, but most of them have been conducted using collagenase-dispersed cell cultures [24,27] and this probably re flects only a partial picture of the inflammatory response. We believe that it may be essential for human nasal mucosal mast cells to be in the organ microenvironment to liberate histamine in response to SP.…”

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confidence: 99%

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Substance-P-lnduced Histamine Release from Human Nasal Mucosa in vitro

Schierhorn

Brunnée

Schultz

et al. 1995

Int Arch Allergy Immunol

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There is growing evidence that substance P (SP) is one of the main neuropeptides involved in neurogenic inflammation of the airways. However, a number of studies were not able to demonstrate histamine release from human mucosal mast cells after SP administration. Since cultures of isolated cell systems provide only a partial picture of the inflammatory processes in vivo, organ culture models promise to offer physiologically relevant assay systems for studying tissue interactions. Thus, we examined the influence of SP on histamine release and its morphological effects on human nasal mucosa using a previously described histoculture technique. Compared to controls, the histamine content in the culture bath was significantly elevated after SP stimulation (p < 0.05). Histomorphometry showed a decreased density of mast cells and an increased percentage of degranulated mast cells. These findings were dose and time dependent and support the hypothesis of a close interaction between C-sensory nerves and mast cells implying that these interactions are of pathogenetic importance in nasal mucosa inflammation.

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“…Plasma cells are increased in comparison with the normal nasal mucosa. 183 By means of immunohistochemical staining, the numbers of macrophages, neutrophils, and CD8 ϩ T lymphocytes are normal. However, in one study of cells isolated from digested nasal polyp tissue, CD8 ϩ T lymphocytes predominated over CD4 ϩ T lymphocytes.…”

Section: Summary Statementsmentioning

confidence: 99%

Otolaryngology‐Head and Neck Surgery

Meltzer

Hamilos

Hadley

et al. 2004

Otolaryngol.--head neck surg.

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BACKGROUND: There is a need for more research on all forms of rhinosinusitis. Progress in this area has been hampered by a lack of consensus definitions and the limited number of published clinical trials.OBJECTIVES: To develop consensus definitions for rhinosinusitis and outline strategies useful in clinical trials.STUDY DESIGN: Five national societies, The can Rhinologic Society formed an expert panel from multiple disciplines. Over two days, the panel developed definitions for rhinosinusitis and outlined strategies for design of clinical trials.RESULTS: Committee members agreed to adopt the term "rhinosinusitis" and reached consensus on definitions and strategies for clinical research on acute presumed bacterial rhinosinusitis, chronic rhinosinusitis without polyposis, chronic rhinosinusitis with polyposis, and classic allergic fungal rhinosinusitis. Symptom and objective criteria, measures for monitoring research progress, and use of symptom scoring tools, quality-of-life instruments, radiologic studies, and rhinoscopic assessment were outlined for each condition.CONCLUSIONS: The recommendations from this conference should improve accuracy of clinical diagnosis and serve as a starting point for design of rhinosinusitis clinical trials. (Otolaryngol Head Neck Surg 2004;131:S1-S62.) I. PREFACERecognizing a need for evidence-based rhinosinusitis guidelines, 5 national societies, The American

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Studies on the Function of Mast Cells Infiltrating in Nasal Polyps

Cited by 5 publications

References 14 publications

Mast Cell-IgE-and Mast Cell-Structural Cell Interactions in Allergic Airway Disease

Mast Cell-IgE-and Mast Cell-Structural Cell Interactions in Allergic Airway Disease

Substance-P-lnduced Histamine Release from Human Nasal Mucosa in vitro

Otolaryngology‐Head and Neck Surgery

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