Murine T Cell-Derived Contractile Activity for Bronchial Smooth Muscle Cells

Abe, Akemi; Koyama, Satoshi; Ohtomo, Takayuki; Kitamura, Noriko; Kaminuma, Osamu; Mori, Akio

doi:10.1159/000337743

Cited by 4 publications

(2 citation statements)

References 39 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was shown that IL-2 activated T lymphocytes induced proliferation and migration of muscle precursor cells. An additional recent study reported that supernatants of cultured anti-CD3 activated murine TH (T helper) lymphocytes induced the contraction of human bronchial smooth muscle cells [16]. …”

Section: Introductionmentioning

confidence: 99%

Activated Lymphocytes Secretome Inhibits Differentiation and Induces Proliferation of C2C12 Myoblasts

Al-Shanti

Durcan²,

Al-Dabbagh³

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: ageing is associated with a marked decline in immune function which may contribute to the local environment that can influence the regenerative process of skeletal muscle cells. Methods: Herein, we focused on determining the effect of an activated immune system secretome on myoblast differentiation and proliferation as possible means to attenuate adverse effects of muscle aging. C2C12 myoblasts were used as model to assess the impact of lymphocyte conditioned media (CM) following anti-CD3/IL-2 activation. Results: Myoblasts cultured with activated lymphocytes CM exhibited reduced morphological and biochemical differentiation (98±20, p<0.005) and increased entry to the S Phase of the cell cycle (61%±7, p<0.001), when compared with myoblasts cultured with non-activated lymphocytes CM. Associated with increased proliferation and reduced differentiation, muscle specific transcription factors MyoD and myogenin were significantly reduced in C2C12 treated with activated lymphocytes CM vs control CM, respectively (myoD: 0.5±0.12 fold reduction P<0.005); myogenin: 0.38±0.08 fold reduction; p<0.005). Moreover, key protein of proliferation pERK1/2 increased (46±11U/ml, p<0.05) whereas mediator of differentiation pAkt decreased (21±12U/ml, p<0.05) in C2C12 treated with activated vs. non-activated CM. Conclusion: our data demonstrate that, following activation, secretome of the immune system cells elicit marked regulatory effects on skeletal muscle growth and differentiation; enhancing the former with the loss of the latter.

show abstract

Section: Introductionmentioning

confidence: 99%

Activated Lymphocytes Secretome Inhibits Differentiation and Induces Proliferation of C2C12 Myoblasts

Al-Shanti

Durcan²,

Al-Dabbagh³

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…T cells are capable of producing bronchoactive mediators, including acetylcholine [135]. Moreover, we identified a higher-molecular-weight substance produced by murine T cells that induces the contraction of bronchial smooth muscle cells [136]. Allergen-induced late-phase airway obstruction was observed in mice transferred with OVA-reactive T cell clones [137].…”

Section: Th9 Cells Induce Bhr Accompanied By But Not Dependent On mentioning

confidence: 99%

Potential Mechanisms of T Cell-Mediated and Eosinophil-Independent Bronchial Hyperresponsiveness

Saeki

Nishimura

Kitamura

et al. 2019

IJMS

Self Cite

View full text Add to dashboard Cite

Bronchial asthma is a chronic disease characterized by reversible airway obstruction, mucus production, and bronchial hyperresponsiveness (BHR). Although Th2 cell-mediated eosinophilic inflammation is an important disease mechanism in the majority of patients with bronchial asthma, recent studies suggest the possible development of Th2-independent airway inflammation and BHR. These non-Th2 endotype patients seem to consist of multiple subgroups, and often do not respond to inhaled corticosteroids. Therefore, to understand the pathogenesis of asthma, it is important to characterize these non-Th2 subgroups. Recently, we demonstrated that Th9 cells induce eosinophil infiltration and eosinophil-independent BHR, and Th9 cells-mediated BHR may be resistant to glucocorticoid. In this review, we summarize the contribution of several T cell subsets in the development of bronchial asthma and introduce our recent study demonstrating Th9 cell-mediated and eosinophil-independent BHR.

show abstract

A Contraction Assay System Using Primary Cultured Mouse Bronchial Smooth Muscle Cells

Kouyama¹,

Otomo-Abe²,

Kitamura³

et al. 2013

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

Background: Contraction of bronchial smooth muscle is the main mechanism of asthmatic responses. Inflammatory cells such as eosinophils and mast cells produce chemical mediators that induce smooth muscle contraction. To investigate the mechanisms of IgE-independent asthmatic response in murine asthma models, a novel in vitro assay system using primary cultured mouse bronchial smooth muscle cells (BSMC) was explored. Method: Trachea and bronchi were taken from young mice and underwent primary culture. BSMC were expanded in culture and then embedded in a collagen gel. The well-known constrictors leukotriene D₄ (LTD₄), methacholine and histamine were applied to the BSMC gels. The gel images were captured by an image analyzer and contractile responses were evaluated. Results: LTD₄ and methacholine significantly induced the gel contraction in a dose-dependent manner, but histamine did not. Montelukast, a CysLT type ΙΙ receptor antagonist, and atropine, a muscarinic acetylcholine receptor antagonist, inhibited the contractile responses in an agonist-specific manner. Conclusion: A contraction assay system using cultured mouse BSMC was successfully established for the first time. It may go a long way toward identifying bronchoconstricting mediators involved in murine asthma models.

show abstract

Murine T Cell-Derived Contractile Activity for Bronchial Smooth Muscle Cells

Cited by 4 publications

References 39 publications

Activated Lymphocytes Secretome Inhibits Differentiation and Induces Proliferation of C2C12 Myoblasts

Activated Lymphocytes Secretome Inhibits Differentiation and Induces Proliferation of C2C12 Myoblasts

Potential Mechanisms of T Cell-Mediated and Eosinophil-Independent Bronchial Hyperresponsiveness

A Contraction Assay System Using Primary Cultured Mouse Bronchial Smooth Muscle Cells

Contact Info

Product

Resources

About