Airway Basophil and Mast Cell Density in Patients with Bronchial Asthma: Relationship to Bronchial Hyperresponsiveness

Abstract

We investigated the role of basophils and mast cells in the pathogenesis of bronchial asthma. Eight asthmatics (6 atopic, 2 nonatopic) and 6 control subjects were enrolled in this study. Bronchial responsiveness to acetylcholine (PC20ACh) was measured in asthmatics and endobronchial biopsy from right upper lobe bronchus was performed on the same day. Basophils and mast cells in the airways were identified by immunohistochemistry using a monoclonal antibody against tryptase and anti-IgE. The number of basophils of asthmatics was 52.2 +/- 12.5/mm(2). In contrast, no basophils were found in the airways of control subjects. There was a significant increase of number of mast cells in the asthma group compared to the control group (168.6 +/- 32.6 vs. 22.3 +/- 6.1, p<0.01). There was an inverse correlation between airway basophil and mast cell numbers and PC20ACh (r=-0.82, r=0.72, p<0.05). These findings suggest a possible role for basophils and mast cells in the pathophysiology of asthma.

Regulation of stem cell factor expression in inflammation and asthma

“…These findings of the mast cell signature confirmed previous data from the literature in glucocorticoid-treated asthmatics (Bradding et al 1994, Koshino et al 1996, Djukanovic et al 1997, Olivieri et al 1997.…”

“…In vitro it increases the antigen-induced degranulation of human pulmonary mast cells (Bischoff & Dahinden 1992, Okayama et al 1994) and it-self induces mast cell degranulation both in vitro (Columbo et al 1992, Takaishi et al 1994, Taylor et al 1996a) and in vivo (Wershil et al 1992, Costa et al 1996. Mast cell number and activation are locally increased in chronic inflammatory diseases such as asthma (Lozewicz et al 1988, Beasley et al 1989, Djukanovic et al 1990, Bradley et al 1991, Ollerenshaw & Woolcock 1992, Saetta et al 1992, Pesci et al 1993, Laitinen et al 1993, Bradding et al 1994, Koshino et al 1996. Since SCF is the principal growth factor for mast cells, it might be expressed in human bronchi and regulated in airway structural cells in pro-and anti-inflammatory conditions.…”

Lack of neurokinin-1 receptor expression affects tissue mast cell numbers but not their spatial relationship with nerves

“…These findings suggest that these tissues have the ability to accommodate increased numbers of mast cells if additional precursor cells or immature mast cells are provided. This is not surprising because the number of mast cells in tissues is frequently increased in various chronic inflammatory conditions (16,19,20,25,(51)(52)(53). However, our findings would indicate that tissue mast cell numbers are expandable even under normal physiological conditions.…”

“…An increase in the local density of mast cells within inflamed tissue has been reported in asthma (25), rheumatoid arthritis (19), interstitial cystitis (51-53), and other chronic inflammatory conditions. Mast cell-nerve communication seems to be increased in cystitis (13,35), suggesting that inflammation results in the production of mediators that modulate this connection, either by enhanced recruitment of mast cell precursors from the circulation or by the local proliferation and/or migration of resident mast cells (56).…”

Human Mast Cells Transmigrate Through Human Umbilical Vein Endothelial Monolayers and Selectively Produce IL-8 in Response to Stromal Cell-Derived Factor-1α

“…After partial differentiation in this site, they enter the circulation and complete differentiation in peripheral tissues (1). In humans, significant increases in mast cell density in the local tissue have been described in a number of diseases, such as asthma (2), allergic alveolitis (3), solid tumors (4), rheumatoid arthritis (5), and inflammatory bowel diseases (6). In rodents, pathogen-induced increases in tissue mast cell number are associated with increases in blood mast cell precursors (7).…”