Interplay of extracellular matrix and leukocytes in lung inflammation

Abstract

During inflammation, leukocytes influx into lung compartments and interact with extracellular matrix (ECM). Two ECM components, versican and hyaluronan, increase in a range of lung diseases. The interaction of leukocytes with these ECM components controls leukocyte retention and accumulation, proliferation, migration, differentiation, and activation as part of the inflammatory phase of lung disease. In addition, bronchial epithelial cells from asthmatic children co-cultured with human lung fibroblasts generate an ECM that is adherent for monocytes/macrophages. Macrophages are present in both early and late lung inflammation. Matrix metalloproteinase 10 (MMP10) is induced in alveolar macrophages with injury and infection and modulates macrophage phenotype and their ability to degrade collagenous ECM components. Collectively, studies outlined in this review highlight the importance of specific ECM components in the regulation inflammatory events in lung disease. The widespread involvement of these ECM components in the pathogenesis of lung inflammation make them attractive candidates for therapeutic intervention.

LncRNA‐RP11‐714G18.1 suppresses vascular cell migration via directly targeting LRP2BP

“…In present study, we demonstrated that both RP11‐714G18.1 and LRP2BP could suppress vascular cell migration through downregulation of MMP1 expression. MMP1, also known as interstitial collagenase, is a major member of the MMP family that can facilitate vascular cell migration via degrading extracellular matrix components . It is believed to be closely associated with the vulnerability of atherosclerotic plaques as well as the risk of acute coronary syndromes .…”

“…MMP1, also known as interstitial collagenase, 31 is a major member of the MMP family that can facilitate vascular cell migration via degrading extracellular matrix components. [32][33][34] It is believed to be closely associated with the vulnerability of atherosclerotic plaques as well as the risk of acute coronary syndromes. 35,36 Moreover, overexpression of MMP1 was detected in the shoulder region of the plaque, which seemed to be the area prone to rupture.…”

Treatment of Dystrophic mdx Mice with an ADAMTS-5 Specific Monoclonal Antibody Increases the Ex Vivo Strength of Isolated Fast Twitch Hindlimb Muscles

“…Also relevant to the pathology of muscular dystrophy, is that versican and ADAMTS versicanases have been implicated in regulating inflammation in various disease models [28][29][30]. A carefully regulated inflammatory response is necessary for effective regenerative myogenesis.…”

Contribution of airway eosinophils in airway wall remodeling in asthma: Role of MMP‐10 and MET

“…MMP10 gene expression is upregulated in airway epithelial cells infected with rhinovirus and respiratory syncytial virus . MMP10 may drive the conversion of pro‐inflammatory M1‐biased macrophages toward immunosuppressive M2‐biased cells, and, in the context of airway remodeling, MMP‐10 also controls the activation of ECM‐degrading activity in M2 macrophages …”