Quantitation of Types I and III Collagen in Biopsy Lung Samples from Patients with Cryptogenic Fibrosing Alveolitis

Kirk, J.M.E.; Heard, Brian E.; Kerr, I.H.; Turner-Warwick, M; Laurent, Geoffrey J.

doi:10.1016/s0174-173x(84)80039-4

Cited by 66 publications

(26 citation statements)

References 20 publications

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“…On the contrary, this isotype of collagen was significantly reduced in the lungs of patients who had died of fibrosing alveolitis Reprint requests to: Professor A CavalIeri, Cattedra di Medicina del Lavoro, Universita' di Modena, v Campi 287, 1-41100 Modena, Italy. (7). A similar phenomenon was evidenced in the lungs of rats exposed to silica (8), in skin scars (9), and in alcoholic liver fibrosis (10).…”

supporting

confidence: 56%

“…lncreased levels of PIIINP have been found in BAL fluids during the early active stage of fibrosing alveolitis (13) and in sarcoidosis (14) and asbestos alveolitis, in the latter case in both animals and exposed workers (15). Furthermore an increased level of PIlINP was observed in the serum of a patient with cryptogenic fibrosing alveolitis (7). Nevertheless a recent study failed to demonstrate a significantly higher level of serum PIIINP in workers with asbestosis than in a group of asbestos-exposed workers without radiological signs of fibrosis (16).…”

mentioning

confidence: 99%

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Evaluation of serum aminoterminal propeptide of type III procollagen as an early marker of the active fibrotic process in asbestos-exposed workers.

Cavalleri¹,

Gobba²,

Bacchella³

et al. 1991

Scand J Work Environ Health

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supporting

confidence: 56%

mentioning

confidence: 99%

Evaluation of serum aminoterminal propeptide of type III procollagen as an early marker of the active fibrotic process in asbestos-exposed workers.

Cavalleri¹,

Gobba²,

Bacchella³

et al. 1991

Scand J Work Environ Health

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“…6) and for lung homogenates of humans with idiopathic pulmonary fibrosis (30). Both conditions show early transcripts for type III collagen (43,44) and an increased ratio of type III to type I collagen protein (45). We have shown the bleomycin-induced fibrotic change by staining the deposition of reticular fibers, whose major component is type III collagen (46,47).…”

Section: Discussionmentioning

confidence: 99%

Cysteinyl leukotriene 1 receptor controls the severity of chronic pulmonary inflammation and fibrosis

Beller

Friend

Maekawa

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

131

102

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The cysteinyl leukotrienes (cys-LTs), leukotriene (LT) C4, LTD4, and LTE 4 , are smooth muscle constrictors that signal via the CysLT 1 receptor. Here we report that the cys-LTs play an important role in chronic pulmonary inflammation with fibrosis induced by bleomycin in mice. Targeted disruption of LTC 4 synthase, the pivotal enzyme for cys-LT biosynthesis, protected significantly against alveolar septal thickening by macrophages and fibroblasts and collagen deposition. In contrast, targeted disruption of the CysLT 1 receptor significantly increased both the concentration of cys-LTs in the bronchoalveolar lavage fluid and the magnitude of septal thickening as defined by morphology, digital image analysis, and deposition of reticular fibers. These findings change our understanding of the pathobiology mediated by the cys-LTs by revealing their role in chronic inflammation with fibrosis, likely via the CysLT 2 receptor, and by uncovering a dual role for the CysLT1 receptor, namely proinflammatory acute constriction of smooth muscle and antiinflammatory counteraction of chronic injury.T he cysteinyl leukotrienes (cys-LTs), originally termed slow reacting substance (SRS) because of the gradual progression of their contractile response in smooth muscle relative to the brisk action elicited by histamine (1-3), were viewed only as smooth muscle agonists after their structural definition (4) and chemical synthesis (5). When inhaled, cys-LTs constrict human normal or asthmatic airways with a thousand times the potency of histamine (6-8). They also are more active in eliciting an intradermal wheal and flare response (9). Their role in the pathobiology of bronchial asthma was established by the therapeutic efficacy of agents that block their biosynthesis or their action at a receptor defined by transmission of a smooth muscle response (10, 11).The cys-LTs are generated after arachidonic acid is released from the outer nuclear membrane of cells by cytosolic phospholipase A 2 and converted to the epoxide leukotriene (LT) A 4 by 5-lipoxygenase (5-LO) in the presence of the 5-LO activating protein (12). An integral perinuclear membrane protein, LTC 4 synthase (LTC 4 S), conjugates reduced glutathione to LTA 4 to form LTC 4 (13, 14). After carrier-mediated export (15), LTC 4 is converted to additional receptor-active metabolites, LTD 4 and LTE 4 , by the sequential cleavage from the tripeptide adduct of glutamate (16, 17) and glycine. Alternatively, LTA 4 can be converted by LTA 4 hydrolase to a dihydroxy LT, LTB 4 . Two receptors for the cys-LTs, CysLT 1 receptor and CysLT 2 receptor, have been cloned for the human (18-22) and the mouse (23-25).The therapeutic agents developed for the management of bronchial asthma at the receptor level block the agonist activity of the cys-LTs at the CysLT 1 receptor and not at the CysLT 2 receptor. Targeted disruption of either LTC 4 S or the CysLT 1 receptor elicits marked and comparable attenuation of IgEdependent, mast cell-mediated passive cutaneous anaphylaxis and of zymosan-elicited i...

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“…In bone marrow disease, the term reticulin fibrosis or collagen fibrosis is used [27], and a variable response of reticulin fibrosis to corticosteroids has been reported [27]. Even in patients with CFA, variable amounts of both type I and III collagen are present, and patients with a larger proportion of type III collagen show a better response to steroid therapy [28]. This is consistent with evidence that long-term steroid therapy can result in a reduction in RBM thickness in asthma [29].…”

Section: Discussionmentioning

confidence: 99%

Ultrastructure of the reticular basement membrane in asthmatic adults, children and infants

Saglani

Molyneux²,

Gong³

et al. 2006

European Respiratory Journal

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Reticular basement membrane (RBM) thickening in asthma is considered to be the result of subepithelial fibrosis. Thus, the RBM in asthma should contain an excess of fibrils identified as interstitial collagen and the ratio of fibril to matrix should be increased above normal levels.Electron micrographs of the RBM were compared with those of interstitial collagen deeper in the bronchial wall using endobronchial biopsy specimens from adult asthmatics (aged 18-41 yrs (n510)), children with difficult asthma (aged 6-16 yrs (n510)), wheezy infants with reversible airflow limitation (aged 0.3-2 yrs (n510)) and age-matched nonasthmatic controls: 10 adults, nine children and nine symptomatic infants with normal lung function.Fibrils in the RBM were significantly thinner (median (range) width 39 (30-52) nm versus 59 (48-73) nm), and fewer fibrils were banded than in the interstitial collagen (ratio of banded to nonbanded fibrils 0.08 (0-0.17) versus 0.22 (0-1.3)). The ratio of fibrils to matrix in the thickened RBM of asthmatics did not differ from that of their respective controls (1.34 (0.63-2.49) versus 1.18 (0.31-2.6)).The ratio of fibril to matrix in the thickened reticular basement membrane of asthmatics is normal, and, contrary to what is expected in fibrosis, the fibrils do not resemble those of interstitial collagen.

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Quantitation of Types I and III Collagen in Biopsy Lung Samples from Patients with Cryptogenic Fibrosing Alveolitis

Cited by 66 publications

References 20 publications

Evaluation of serum aminoterminal propeptide of type III procollagen as an early marker of the active fibrotic process in asbestos-exposed workers.

Evaluation of serum aminoterminal propeptide of type III procollagen as an early marker of the active fibrotic process in asbestos-exposed workers.

Cysteinyl leukotriene 1 receptor controls the severity of chronic pulmonary inflammation and fibrosis

Ultrastructure of the reticular basement membrane in asthmatic adults, children and infants

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