Cytotoxic T lymphocyte antigen 4 immunoglobulin modified dendritic cells attenuate allergic airway inflammation and hyperresponsiveness by regulating the development of T helper type 1 (Th1)/Th2 and Th2/regulatory T cell subsets in a murine model of asthma

Ying, Le; Fu, Zhou; Luo, Jinyong; Zhou, Changqing; Chen, Y.; Wang, Longlun; Liu, E.

doi:10.1111/j.1365-2249.2011.04405.x

Cited by 18 publications

(37 citation statements)

References 28 publications

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“…Transforming growth factor β1 expressed by eosinophils in the airway is known to result in the remodeling response by promoting structural changes [26][27][28]. Moreover, lymphocytes play a significant role in airway inflammation [29]. We also found that the bronchial wall and smooth muscle thicknesses were increased in the asthma and IgG2a mAb groups.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 63%

“…This demonstrated that TSLP pathway inhibition could down-regulate TSLP, OX40L, a-SMA, Collagen I, IL-4, IL-5 and IL-13 levels, and up-regulate IFN-γ levels. a-SMA is expressed at higher levels in epithelial cells and periductular collagen fibers during biliary atresia-induced hepatic fibrosis [29], and its inhibition attenuates mouse lung fibrosis [30] Moreover, a hallmark of fibrosis is the accumulation of fibrillary collagens, especially collagen I. a-SMA and collagen I are widely used as indicators of fibrosis, including lung fibrosis [31]. Moreover, a hallmark of fibrosis is the accumulation of fibrillary collagens, especially collagen I. a-SMA and collagen I are widely used as indicators of fibrosis, including lung fibrosis [32].…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

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Thymic Stromal Lymphopoietin Signaling Pathway Inhibition Attenuates Airway Inflammation and Remodeling in Rats with Asthma

Cheng¹,

Xi²,

Dai³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Thymic stromal lymphopoietin (TSLP) is a cytokine that plays diverse roles in the regulation of immune responses. However, a detailed understanding of the TSLP signaling pathway in asthma remains elusive. In this study, we aimed to investigate the role of the TSLP signaling pathway in asthma and its effect on airway inflammation and remodeling. Methods: Forty Sprague Dawley (SD) rats were evenly classified into control, asthma, IgG2a mAb and anti-TSLP mAb groups. Ovalbumin (OVA)-induced asthma models were successfully established. Blood, bronchoalveolar lavage fluid (BALF) and lung tissue samples were prepared. Total BALF leukocytes were counted, and the proportions of different leukocyte types were determined. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry were performed to determine the mRNA and protein levels of TSLP, OX40L, α-smooth muscle actin (α-SMA, a marker of airway remodeling in asthma) and collagen I in the plasma. Enzyme-linked immunosorbent assay (ELISA) was carried out to measure the concentrations of TSLP, OX40L, and other inflammatory factors, such as interferon (IFN)-γ, interleukin (IL)-4, IL-5 and IL-13, in the plasma. Results: Compared with the control group, there were more leukocytes, increased EOS and LYM proportions, higher Underwood and PAS scores, increased WT_t, WT_m, WA_t/A₀, WA_m/WA_t, WT_t/R₀, WT_m/WT_t, TSLP, OX40L, a-SMA and collagen I mRNA and protein levels, and higher SLP, OX40L, IL-4, IL-5 and IL-13 levels, but lower MON proportions and IFN-γ levels in the asthma and IgG2a mAb groups. Compared with the asthma and IgG2a mAb groups, there were less leukocytes, decreased EOS and LYM proportions, lower Underwood and PAS scores, decreased WT_t, WT_m, WA_t/A₀, WA_m/WA_t, WT_t/R₀, WT_m/WT_t, TSLP, OX40L, a-SMA and Collagen I mRNA and protein levels, and lower levels of SLP, OX40L, IL-4, IL-5 and IL-13, but higher MON proportions and IFN-γ levels in the anti-TSLP mAb group. WT_m and WT_t were positively associated with the TSLP, OX40L, α-SMA and collagen-I levels in the rat lung tissues. Conclusion: The results indicate that TSLP may be an important contributor for asthma development as TSLP signaling blockade attenuates airway inflammation and remodeling in asthmatic rats.

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Section: Cellular Physiology and Biochemistrysupporting

confidence: 63%

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

Thymic Stromal Lymphopoietin Signaling Pathway Inhibition Attenuates Airway Inflammation and Remodeling in Rats with Asthma

Cheng¹,

Xi²,

Dai³

et al. 2018

Cell Physiol Biochem

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show abstract

“…Recently, the mechanism of Th1 and Th2 imbalance in asthma has attracted increasing attention. 33,34 As is well known, CD4 + T cells act as the dynamic player in the adaptive immune response including Th1 and Th2 cells. 34 Wherein Th2 cells guide B cells to synthesize IgE via secreting IL-4, up-regulate the OVA-IgG1 expression by producing IL-4 and IL-13, activate eosinophils via IL-5 secretion, enhance the proliferation of fibroblasts, collagen generation and mucus secretion through IL-13 generation, finally leading to airway inflammation and airway remodeling.…”

Section: Discussionmentioning

confidence: 99%

Influences of PON1 on airway inflammation and remodeling in bronchial asthma

Chen

Xie²,

Wang³

et al. 2017

J of Cellular Biochemistry

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This study aims to explore the influences of Paraoxonase-1 (PON1) involved in airway inflammation and remodeling in asthma. Mice were divided into control, asthma, asthma + PON1 and asthma + NC groups, and asthma models were established via aerosol inhalation of ovalbumin (OVA). HE, Masson, and PAS stains were used to observe airway inflammation and remodeling, Giemsa staining to assess inflammatory cells in bronchoalveolar lavage fluid (BALF), qRT-PCR and Western blot to detect PON1 expression, lipid peroxidation and glutathione assays to quantify malondialdehyde (MDA) activity and glutathione peroxidase (GSH) levels, ELISA to determine inflammatory cytokines and immunoglobulin, and colorimetry to detect PON1 activities. Additionally, mice lung macrophages and fibroblasts were transfected with PON1 plasmid in vitro; ELISA and qRT-PCR were performed to understand the effects of PON1 on inflammatory cytokines secreted by lung macrophages, MTT assay for lung fibroblasts proliferation and qRT-PCR and Western blot for the expressions of PON1, COL1A1, and fibronectin. After overexpression of PON1, the asthma mice had decreased inflammatory cell infiltration, fibrosis degree, and airway wall thickness; inflammatory cells and inflammatory cytokines in BALF were also reduced, expressions of OVA-IgE and IgG1, and MDA activity were decreased, but the expressions of OVA-IgG2a and INF-γ and GSH levels were increased. Besides, PON1 significantly inhibited microphage expression of LPS-induced inflammatory cytokines, lung fibroblast proliferation, and COL1A1 and fibronectin expression.Thus, PON1 could relieve airway inflammation and airway remodeling in asthmatic mice and inhibit the secretion of LPS-induced macrophage inflammatory cytokines and the proliferation of lung fibroblasts. K E Y W O R D Sairway inflammation, airway remodeling, asthma, paraoxonase-1

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“…Stem cell therapy influences the systemic immunologic response, triggering an increase in antiinflammatory cytokine and the production of regulatory T-cells, with decreased production of cytotoxic T-cells (Ying et al, 2011). Recently, a study in a rat model of stroke showed that, following stroke, spleen size was reduced concomitantly with CD8+ T-cell counts.…”

Section: Modulation Of the Systemic Immunologic Responsementioning

confidence: 99%

Stem Cells in Traumatic Brain Injury

Dobrowolski

Lepski

2013

American Journal of Neuroscience

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Traumatic Brain Injury (TBI) is a devastating clinical condition that often causes permanent incapacity, especially in the younger population. The clinical relevant of TBI justifies the scientific interest in the pathophysiology of TBI, as well as in protective effects and development of treatment options. Stem cells have the ability to induce neuroprotection and neural repair inflammatory suppression, causing tissue reconstruction completely or partially damaged cells to preventing cell death to evolve. However the neurological improvement observed in preclinical studies and clinical tests based on neurological and behavioral disorders and the mechanism of action of stem cells remains unknown. In this study the authors discuss the current status of using stem cells to treat TBI, including the basic cell types and potential mechanisms of action, preclinical data and points out lack of studies and hurdles for clinical application. The authors also focusing on the recent demonstration that neurogenesis occurs in all mammals throughout adult life, although at a low rate, is possible to induce neurogenesis de novo in the adult mammalian brain, particularly in the neocortex where it does not normally occur and that it may become possible to manipulate endogenous multipotent precursors in situ to replace lost or damaged neurons. Elucidation of the relevant molecular controls may both allow control over transplanted precursor cells and potentially allow the development of neuronal replacement therapies for neurodegenerative disease and other central nervous system injuries that do not require transplantation of exogenous cells. Discuss strategies of enhance the neurogenesis (for example by exogenous tropics factor administration) and the transplantation of different types of neural progenitor cells after TBI. Each strategy is discussed with an emphasis on highlighting the progress and limiting factors relevant to the development of clinical trials of cellular replacement therapy for severe TBI in humans.

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Cytotoxic T lymphocyte antigen 4 immunoglobulin modified dendritic cells attenuate allergic airway inflammation and hyperresponsiveness by regulating the development of T helper type 1 (Th1)/Th2 and Th2/regulatory T cell subsets in a murine model of asthma

Cited by 18 publications

References 28 publications

Thymic Stromal Lymphopoietin Signaling Pathway Inhibition Attenuates Airway Inflammation and Remodeling in Rats with Asthma

Thymic Stromal Lymphopoietin Signaling Pathway Inhibition Attenuates Airway Inflammation and Remodeling in Rats with Asthma

Influences of PON1 on airway inflammation and remodeling in bronchial asthma

Stem Cells in Traumatic Brain Injury

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