Cytokine Production by Cell Cultures From Bronchial Subepithelial Myofibroblasts

Zhang, S.; Howarth, PH; Roche, William R.

doi:10.1002/(sici)1096-9896(199609)180:1<95::aid-path614>3.0.co;2-b

Cited by 53 publications

(14 citation statements)

References 26 publications

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“…It has been reported that HC has inhibitory effects on anaphylactic reaction and mast cell activation (Li et al, 2005). SCF is a growth factor in both hematopoietic cells and germ cells, and it is produced in two forms, the soluble form, and the membrane-bound form by a variety of cells such as fibroblasts and epithelial cells (Wen et al, 1996;Zhang et al, 1996;Linnekin, 1999). It is also essential for the activation and chemotaxis of MCs, which is a critical step in an inflammatory response such as allergic inflammation (Nilsson et al, 1994;Schwartz, 1994).…”

Section: Discussionmentioning

confidence: 99%

The inhibitory effect of Houttuynia cordata extract on stem cell factor-induced HMC-1 cell migration

Kim

et al. 2007

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

The inhibitory effect of Houttuynia cordata extract on stem cell factor-induced HMC-1 cell migration

Kim

et al. 2007

Journal of Ethnopharmacology

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“…Another example of gene-gene interaction may occur in the leukotriene pathway. The cysteinyl leukotrienes LTC 4 , LTD 4 , and LTE 4 are critical mediators of airway narrowing, microvascular leakage, mucus secretion, and eosinophilia in bronchial asthma. 40,41 The terminal enzyme for cysteinyl leukotriene (Cyst-LT) synthesis is LTC 4 synthase encoded on chromosome 5q35.…”

Section: Candidate Genesmentioning

confidence: 99%

Genetic and environmental interaction in allergy and asthma☆☆☆

Holgate

1999

Journal of Allergy and Clinical Immunology

159

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Asthma is an inflammatory disorder of the airways involving coordinate up-regulation of T(H)2-type cytokines encoded in a cluster on chromosome 5q(31-33) on T cells and inflammatory cells. There is also a requirement for local airway susceptibility factors that, together with T(H)2 polarization, results in hyperresponsiveness, variable airflow obstruction, and, over time, remodeling of the airway wall. Asthma has strong genetic and environmental components that interact both in the induction and subsequent expression of the disease phenotypes. Multiple genes are involved and probably interact. Whole genome screens are beginning to identify gene-rich regions of special relevance to asthma and atopy, although a novel disease-related gene has yet to be discovered from these. By contrast, there are a plethora of candidate genes whose function in relation to disease pathophysiologic mechanisms and response to treatment are known. Two examples are polymorphisms involving IL-4 receptors and the enzymes controlling cysteinyl leukotriene production. Abnormal signaling between the epithelium, which is in contact with the environment, and the underlying (myo)fibroblasts and dendritic cells indicating reactivation of the epithelial mesenchymal trophic unit, which is involved in fetal lung development and branching, provide a basis for asthma that encapsulates both T(H)2 polarization and airway wall remodeling.

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“…Numerous studies have identified the ␣-isoform of smooth muscle actin as a more specific marker for smooth muscle cells or myofibroblasts, and hence the presence or absence of this has historically been used to confirm the presence of smooth muscle cell populations and/or tissues (16,46,50,55). In primary cultures of mesenchyme-derived human airway cells, we could not identify the level of expression of this protein to be a differentiating feature.…”

Section: Discussionmentioning

confidence: 78%

Can lineage-specific markers be identified to characterize mesenchyme-derived cell populations in the human airways?

Singh

Billington

Sayers

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Mesenchyme-derived cells in the airway wall including airway smooth muscle cells, fibroblasts, and myofibroblasts are known to play important roles in airway remodeling. The lack of specific phenotypical markers makes it difficult to define these cell populations in primary cultures. Most relevant studies to date have used animal airway tissues, vascular tissues, or transformed cell lines with only limited studies attempting to phenotypically characterize human airway mesenchymal cells. The objectives of this study were to evaluate reported markers and identify novel markers to define these cell types. We could not identify any specific marker to define these cell populations in vitro that permitted unequivocal identification using immunocytochemistry. However, characteristic filamentous alpha-smooth muscle actin distribution was observed in a significant ( approximately 25%) proportion of human airway smooth muscle cells, whereas this was not observed in airway fibroblasts. A significantly higher proportion of airway fibroblasts expressed alpha(1)- and alpha(2)-integrin receptors compared with human airway smooth muscle cells as assessed by fluorescence activated cell sorting. Global gene expression profiling identified aldo-keto reductase 1C3 (AKR1C3) and cathepsin K as being novel markers to define airway smooth muscle cells, whereas integrin-alpha(8) (ITGA8) and thromboxane synthase 1 (TBXAS1) were identified as novel airway fibroblast-specific markers, and these findings were validated by RT-PCR. Ex vivo studies in human airway tissue sections identified high-molecular weight caldesmon and alpha-smooth muscle actin as being expressed in smooth muscle bundles, whereas ITGA8 and TBXAS1 were absent from these.

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Cytokine Production by Cell Cultures From Bronchial Subepithelial Myofibroblasts

Cited by 53 publications

References 26 publications

The inhibitory effect of Houttuynia cordata extract on stem cell factor-induced HMC-1 cell migration

The inhibitory effect of Houttuynia cordata extract on stem cell factor-induced HMC-1 cell migration

Genetic and environmental interaction in allergy and asthma☆☆☆

Can lineage-specific markers be identified to characterize mesenchyme-derived cell populations in the human airways?

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