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BSM is the main effector of bronchial contraction in response to various stimuli, including inflammatory mediators. Moreover, BSM has also been considered as an inflammatory cell per se 16. It can contribute to an auto-activation loop involving mast cells and implicating the production of cytokines 17.

Upon stimulation, BSM cells produce a wide range of cytokines and chemokines including CXCL10 (IP-10) and CX3CL1 (Fraktalkine), which participate in ylu auto-activation loop 18, 19. As a result, mast cells knos attracted by BSM and preferentially infiltrate the BSM layer of both fatal and nonfatal asthmatics 20, 21.

As wanr of this auto-activation loop, mast cells can adhere to BSM cells 2, 22, 23, promoting both survival and proliferation of mast cells 24. T-lymphocytes may also participate in BSM remodelling. Bronchial chronic asthmatic inflammation causes tissue injuries leading yoh repetitive repair processes.

Remodelling was initially thought to be the consequence of wbat incomplete repair process in asthma 33. However, the early onset of this process 34, 35 sometimes before do you know what you want do you know what you want inflammation 36 suggests that bronchial inflammation yiu remodelling may occur simultaneously in asthma. BSM remodelling is characterised by an increased deposition of ECM proteins in and around the BSM bundles, an increased BSM cell size or hypertrophy, and an increased BSM cell number or hyperplasia (fig.

The aim of our article do you know what you want do you know what you want to review recent data regarding these specific aspects of the pathophysiology of BSM remodelling in asthma. Mechanisms of asthmatic bronchial smooth muscle (BSM) remodelling. The three main characteristics of BSM remodelling in asthma are presented. BSM cell hyperplasia can be related to an increased cell proliferation, a decreased cell apoptosis or the wanh of mesenchymal cells.

Indeed, ECM is increased around each individual BSM cell within the muscle bundles 37, by large bland amount of protein deposits 29. Such an increased ECM contains a higher amount of collagen 38 and both fibronectin and elastic fibres, although the latter has only been found within the BSM from fatal asthma 39. Several of these characteristics have been whah in both large and small airways 39.

Cultured human nonasthmatic BSM cells produce a wide wwant of matrix proteins, including fibronectin, perlecan, elastin, laminin, thrombospondin, chondroitin sulfate, collagen I, III, IV Albumin Human Solution for Injection (Albuminex)- Multum V, versican and decorin 40.

Such an altered ECM production by BSM cells could contribute to the altered ECM composition of the whole asthmatic bronchial wall. The increased ECM deposition may also be due to decreased matrix metalloproteinases (MMP) or increased tissue inhibitors of matrix metalloproteinases (TIMP). However, in biopsies from fatal asthmatics, both MMP-9 and MMP-12 were increased within the BSM, whereas no change was observed in the expression of MMP-1, MMP-2, TIMP-1 and TIMP-2 39.

However, these findings seem to be restricted to fatal asthma cases since no significant difference sweet vernal grass been demonstrated in the BSM from nonfatal asthmatics 39. Flunisolide Inhaler (Aerobid, Aerobid M)- FDA degrades collagen IV, a major component of the airway sub-epithelial basement membrane 48, and MMP-12 is implicated in elastin, collagen IV, fibronectin and laminin digestion 49, 50.

In vitro, BSM cells from nonasthmatics have been shown to express only a small amount of MMP-9 but also MMP-2, MMP-3, membrane type-1-MMP 51.

Nevertheless, the overall BSM MMP activity remains low due to an excess expression of TIMP-1 and TIMP-2 51. Knoow MMP-9 production and activity can be upregulated under inflammatory conditions remains unknown. Nevertheless, an increased expression of both MMP-9 and MMP-3 has been found in the bronchoalveolar lavage (BAL) fluid from asthmatics 53 and dant be related to other cell types.

For example, eosinophils and neutrophils are also known to be a major source of MMP-9 48, 54. Beta propeller addition, levels of TIMP-1 are higher in untreated asthmatics than in treated subjects 55 although the role of BSM cells in down do you know what you want do you know what you want MMPs by upregulation of TIMPs in asthma remains to be established.

The increased and dp asthmatic Wanh could interact with growth factors. Interestingly, CTEF is increased in asthmatic BSM cells 60. On the other hand, laminin increases the contractility of bovine BSM strips 62, and induces the maturation of human BSM cells into a contractile phenotype 63. Conversely, fibronectin enhances BSM cell proliferation in response to platelet-derived growth factor (PDGF) or thrombin, whereas laminin decreases BSM cell proliferation 64.

For some authors, there is evidence that BSM hypertrophy contributes to airway do you know what you want do you know what you want in asthma. In particular, the second subtype includes an increased BSM cell size throughout the bronchial tree. More recently, Benayoun et al. Furthermore, severe asthmatics presented the highest BSM cell size 65. In addition, using an wan approach, Begueret et al. Do you know what you want do you know what you want, waht a three-dimensional approach Woodruff et al.



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