Literature DB >> 20395563

T Cells localize with proliferating smooth muscle alpha-actin+ cell compartments in asthma.

David Ramos-Barbón1, Rebeca Fraga-Iriso, Nadia S Brienza, Carmen Montero-Martínez, Héctor Verea-Hernando, Ron Olivenstein, Catherine Lemiere, Pierre Ernst, Qutayba A Hamid, James G Martin.   

Abstract

RATIONALE: Airway remodeling in asthma comprises increased airway smooth muscle (ASM), an alteration linked to airway hyperresponsiveness and disease severity. Experimental studies showed that T cells adhere to ASM through vascular cell adhesion molecule-1 (VCAM-1) and drive ASM growth through direct contact between the T cells and smooth muscle alpha-actin (alpha-SMA)(+) cells.
OBJECTIVES: To support the hypothesis of a T-cell/alpha-SMA(+) cell contact mechanism of ASM remodeling in asthma, using bronchial biopsies.
METHODS: We performed quantitative morphology on T cells, proliferating cell nuclear antigen (PCNA), alpha-SMA, and VCAM-1 on biopsies from subjects with moderate and severe asthma and healthy control subjects.
MEASUREMENTS AND MAIN RESULTS: We demonstrate ASM cell proliferation and infiltration by T cells in proportion to severity in the subjects with asthma. T cells localized with alpha-SMA(+)PCNA(+) cells, suggesting direct intercellular contact and a relationship with alpha-SMA(+) cell proliferation. Furthermore, the subjects with asthma developed a proliferating compartment of subepithelial alpha-SMA(+), nonorganized airway contractile elements (NOACE), suggesting a phenotype gradient from undifferentiated cells to smooth muscle-like cells. T-cell juxtaposition events were also observed in this compartment and correlated to its mass. The subjects with asthma showed VCAM-1 expression in postcapillary venules and clusters of VCAM-1 immunoreactivity in ASM and NOACE, consistent with a role of VCAM-1 in T-cell/alpha-SMA(+) cell interaction.
CONCLUSIONS: T cells may induce alpha-SMA(+) cell proliferation through direct intercellular contact. NOACE may in part contribute to ASM growth through differentiation and translocation of alpha-SMA(+) cells. The findings support the role of the T cell in ASM remodeling in asthma.

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Year:  2010        PMID: 20395563     DOI: 10.1164/rccm.200905-0745OC

Source DB:  PubMed          Journal:  Am J Respir Crit Care Med        ISSN: 1073-449X            Impact factor:   21.405


  36 in total

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9.  Differential roles of CXCL2 and CXCL3 and their receptors in regulating normal and asthmatic airway smooth muscle cell migration.

Authors:  Laila A Al-Alwan; Ying Chang; Andrea Mogas; Andrew J Halayko; Carolyn J Baglole; James G Martin; Simon Rousseau; David H Eidelman; Qutayba Hamid
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10.  Ca(2+)-activated K(+) channel-3.1 blocker TRAM-34 attenuates airway remodeling and eosinophilia in a murine asthma model.

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Journal:  Am J Respir Cell Mol Biol       Date:  2012-11-29       Impact factor: 6.914

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