Human rhinovirus infection of human bronchial epithelial cells results in migration of human airway smooth muscle cells

Shariff, Sami; Nikitenko, Sergei; Qureshi, Abid; Arnason, Jason; Shelfoon, Chris; Traves, Suzanne L.; Leigh, Richard

doi:10.1186/1710-1492-10-s1-a69

Cited by 1 publication

(1 citation statement)

References 4 publications

(4 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Qureshi et al, demonstrated that serum collected from primary human bronchial epithelial (HBE) cells infected with HRV-16, promoted significant ASMC migration, suggesting that HRV acts as a chemotactic agent for ASMCs [ 83 ]. Shariff et al, further showed that HRV-16 infected HBE cells cultured with ASMCs promoted greater ASMC directional migration compared to supernatants from HBE cells exposed to medium, which became maximal at 4 h. Pre-treatment with dexamethasone abolished ASMC chemotaxis [ 84 ]. They further showed that HRV-16 induced ASMC migration was most likely due to promotion of CCL5, CXCL7, and CXCL10 secretion from HBE cells, which in turn induced p38, ERK1/2, and JNK pathway activation of ASMCs [ 85 ].…”

Section: Promoters Of Airway Smooth Muscle Cell Migrationmentioning

confidence: 99%

Regulation of human airway smooth muscle cell migration and relevance to asthma

et al. 2017

View full text Add to dashboard Cite

Airway remodelling is an important feature of asthma pathogenesis. A key structural change inherent in airway remodelling is increased airway smooth muscle mass. There is emerging evidence to suggest that the migration of airway smooth muscle cells may contribute to cellular hyperplasia, and thus increased airway smooth muscle mass. The precise source of these cells remains unknown. Increased airway smooth muscle mass may be collectively due to airway infiltration of myofibroblasts, neighbouring airway smooth muscle cells in the bundle, or circulating hemopoietic progenitor cells. However, the relative contribution of each cell type is not well understood. In addition, although many studies have identified pro and anti-migratory agents of airway smooth muscle cells, whether these agents can impact airway remodelling in the context of human asthma, remains to be elucidated. As such, further research is required to determine the exact mechanism behind airway smooth muscle cell migration within the airways, how much this contributes to airway smooth muscle mass in asthma, and whether attenuating this migration may provide a therapeutic avenue for asthma. In this review article, we will discuss the current evidence with respect to the regulation of airway smooth muscle cell migration in asthma.

show abstract

Section: Promoters Of Airway Smooth Muscle Cell Migrationmentioning

confidence: 99%