Surfactant Protein D (SP‐D) and Systemic Scleroderma (SSc)

Maeda, Manabu; Ichiki, Yoshiro; Aoyama, Yumi; Kitajima, Yasuo

doi:10.1111/j.1346-8138.2001.tb00013.x

Cited by 16 publications

(8 citation statements)

References 17 publications

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“…Elevation of systemic levels of SP-D with smoking, COPD, or other lung injuries is believed to reflect ongoing damage associated with disruption of the alveolar epithelial integrity (16,18,37,38). In our cohort, plasma SP-D levels did not correlate with monocyte MMP-9 production ( Figure 5B) (r 5 0.08; P 5 0.52).…”

Section: Monocyte Mmp-9 Levels Do Not Correlate With Systemic Markersmentioning

confidence: 60%

“…Accordingly, we compared circulating monocyte MMP-9 production with the wholelung emphysema severity as determined by quantitative CT scan analysis and with two systemic markers of active lung injury (Clara cell secretory protein [CCSP] and surfactant protein-D [SP-D]) (16)(17)(18) that are altered in current smokers and subjects with COPD (19)(20)(21)(22)(23)(24). Some of the results of this manuscript have been previously published in the form of an abstract (25).…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

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The Role of Matrix Metalloproteinase-9 in Cigarette Smoke–induced Emphysema

Atkinson¹,

Lutey²,

Suzuki³

et al. 2011

Am J Respir Crit Care Med

115

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Rationale: Matrix metalloprotease (MMP)-9 is an elastolytic endopeptidase produced by activated macrophages that may be involved in the development of human pulmonary emphysema and could be inhibited with existing compounds. Mouse models have demonstrated that excess MMP-9 production can result in permanent alveolar destruction. Objectives: To determine if MMP-9 causes cigarette smoke-induced emphysema using MMP-9 knockout mice and human samples. Methods: Mouse lungs were analyzed for inflammation and airspace enlargement using a mainstream smoke-exposure model. Human macrophage mRNA was isolated from subjects with emphysema by laser capture microdissection. Human blood monocyte mRNA was isolated from subjects with greater than 30 pack-year smoking history. Human gene expression was determined by quantitative polymerase chain reaction and compared with emphysema severity determined by automated computed tomography analysis. Plasma Clara cell secretory protein and surfactant protein-D were quantified to measure ongoing lung injury. Measurements and Main Results: Mice deficient in MMP-9 develop the same degree of cigarette smoke-induced inflammation and airspace enlargement as strain-matched controls. Macrophages are the predominant source of MMP-9 production in human emphysema specimens and similar quantities of macrophage MMP-9 mRNA is present in areas of lung with and without emphysema. Circulating monocytes produce more MMP-9 in individuals with advanced emphysema severity despite no correlation of MMP-9 with markers of ongoing lung damage. Conclusions: These results suggest that MMP-9 in humans who smoke is similar to smoke-exposed mice, where MMP-9 is present in emphysematous lung but not correlated with the emphysema. To the degree that the mechanisms of emphysema in humans who smoke resemble the mouse model, these data suggest specific inhibition of MMP-9 is unlikely to be an effective therapy for cigarette smoke-induced emphysema. Clinical trial registered with www.clinicaltrials.gov (NCT 00757120).Keywords: pulmonary disease, chronic obstructive; laser capture microdissection; mice, knockout Several studies have implicated matrix metalloproteinase-9 (MMP-9, gelatinase B, type IV collagenase B), in emphysema and chronic obstructive pulmonary disease (COPD) pathogenesis (1-5). MMP-9 can be accurately measured and is an elastolytic protease that is produced in large quantities by inflammatory cells, thus making it suitable for investigation in emphysema (5-7). However, because the pathophysiology of emphysema follows such an indolent course, developing over decades in response to cigarette smoke, a link between MMP-9 activity and alveolar destruction is lacking.Mouse models have identified several MMPs that cause airspace enlargement by overexpression (8, 9), or that prevent airspace enlargement by gene deletion in smoking models (10). The recent discovery that mice transgenically altered to overexpress human MMP-9 in alveolar macrophages develop progressive airspace enlargement (8) adds importance to the e...

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Section: Monocyte Mmp-9 Levels Do Not Correlate With Systemic Markersmentioning

confidence: 60%

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

The Role of Matrix Metalloproteinase-9 in Cigarette Smoke–induced Emphysema

Atkinson¹,

Lutey²,

Suzuki³

et al. 2011

Am J Respir Crit Care Med

115

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show abstract

“…Previous studies evaluating the role of SP-D and KL-6 in SSc have demonstrated that these glycoproteins are positively, significantly correlated with the severity of radiographic fibrosis on chest imaging and inversely correlated with the % predicted FVC and DLCO on PFTs [7,11,12,20,21]. In a longitudinal analysis of 39 SSc patients with a mean follow-up of 2.9 years, Yanabe et al also found that increasing serial KL-6 measurements corresponded with lung function deterioration over time [8,10].…”

Section: Discussionmentioning

confidence: 99%

“…In a longitudinal analysis of 39 SSc patients with a mean follow-up of 2.9 years, Yanabe et al also found that increasing serial KL-6 measurements corresponded with lung function deterioration over time [8,10]. However, the majority of studies evaluating the role of these glycoproteins have involved SSc patients of Japanese ancestry and in particular in patients positive for Scl 70 [8,10,20,21]. Differences in ethnicity and prevalence of anti-Scl 70 in our cohort may explain the fact that we did not find an association between KL-6 and rapid decline in lung function.…”

Section: Discussionmentioning

confidence: 99%

Predicting Lung Function Decline with Serum Pneumoproteins: A Case Control Study

Mittoo¹,

Hudson²,

Lo³

et al. 2014

OJRA

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“…SP-D связывает поверхностные гликоконъюга-ты различных микроорганизмов и олигосахариды, ассо-циированные с поверхностью многих органических анти-генов [7,15,16]. Показано, что повышенная экспрессия SP-D может быть выявлена при ряде заболеваний легких у человека (муковисцидоз, острая интерстициальная пнев-мония, легочный альвеолярный протеиноз), а также в экспериментальных моделях повреждения легочной тка-ни (например, двуокисью кремния, избытком активных форм кислорода, инфекционными агентами) [17][18][19][20][21].…”

Section: контактная информацияunclassified