scholarly journals Anisakis pegreffii Extract Induces Airway Inflammation with Airway Remodeling in a Murine Model System

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jun Ho Choi ◽  
Ju Yeong Kim ◽  
Myung-hee Yi ◽  
Myungjun Kim ◽  
Tai-Soon Yong
Keyword(s):  
T Cells ◽  
Inflammatory Response ◽  
Airway Inflammation ◽  
Lung Tissue ◽  
Respiratory System ◽  
Murine Model ◽  
Lung Inflammation ◽  
Airway Remodeling ◽  
Collagen Deposition ◽  
Anisakis Pegreffii

Exposure of the respiratory system to the Anisakis pegreffii L3 crude extract (AE) induces airway inflammation; however, the mechanism underlying this inflammatory response remains unknown. AE contains allergens that promote allergic inflammation; exposure to AE may potentially lead to asthma. In this study, we aimed to establish a murine model to assess the effects of AE on characteristic features of chronic asthma, including airway hypersensitivity (AHR), airway inflammation, and airway remodeling. Mice were sensitized for five consecutive days each week for 4 weeks. AHR, lung inflammation, and airway remodeling were evaluated 24 h after the last exposure. Lung inflammation and airway remodeling were assessed from the bronchoalveolar lavage fluid (BALF). To confirm the immune response in the lungs, changes in gene expression in the lung tissue were assessed with reverse transcription-quantitative PCR. The levels of IgE, IgG1, and IgG2a in blood and cytokine levels in the BALF, splenocyte, and lung lymph node (LLN) culture supernatant were measured with ELISA. An increase in AHR was prominently observed in AE-exposed mice. Epithelial proliferation and infiltration of inflammatory cells were observed in the BALF and lung tissue sections. Collagen deposition was detected in lung tissues. AE exposure increased IL-4, IL-5, and IL-13 expression in the lung, as well as the levels of antibodies specific to AE. IL-4, IL-5, and IL-13 were upregulated only in LLN. These findings indicate that an increase in IL-4+ CD4+ T cells in the LLN and splenocyte resulted in increased Th2 response to AE exposure. Exposure of the respiratory system to AE resulted in an increased allergen-induced Th2 inflammatory response and AHR through accumulation of inflammatory and IL-4+ CD4+ T cells and collagen deposition. It was confirmed that A. pegreffii plays an essential role in causing asthma in mouse models and has the potential to cause similar effects in humans.

Mycoplasma pneumoniaeinfection increases airway collagen deposition in a murine model of allergic airway inflammation

2005 ◽  
Vol 289 (1) ◽  
pp. L125-L133 ◽  
Author(s):  
Hong Wei Chu ◽  
John G. Rino ◽  
Rachel B. Wexler ◽  
Krista Campbell ◽  
Ronald J. Harbeck ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Lung Tissue ◽  
Murine Model ◽  
Allergic Airway Inflammation ◽  
Saline Control ◽  
Mrna Levels ◽  
Chronic Asthma ◽  
Collagen Deposition ◽  
Airway Wall ◽  
Tgf Β1

Mycoplasma pneumoniae (Mp) has been linked to chronic asthma. Airway remodeling (e.g., airway collagen deposition or fibrosis) is one of the pathological features of chronic asthma. However, the effects of respiratory Mp infection on airway fibrosis in asthma remain unclear. In the present study, we hypothesized that respiratory Mp infection may increase the airway collagen deposition in a murine model of allergic airway inflammation in part through upregulation of transforming growth factor (TGF)-β1. Double (2 wk apart) inoculations of Mp or saline (control) were given to mice with or without previous allergen (ovalbumin) challenges. On days 14 and 42 after the last Mp or saline, lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analyses of collagen and TGF-β1 at protein and mRNA levels. In allergen-naïve mice, Mp did not alter airway wall collagen. In allergen-challenged mice, Mp infections did not change airway wall collagen deposition on day 14 but increased the airway collagen on day 42; this increase was accompanied by increased TGF-β1 protein in the airway wall and reduced TGF-β1 protein release from the lung tissue into BAL fluid. Our results suggest that Mp infections could modulate airway collagen deposition in a murine model of allergic airway inflammation with TGF-β1 involved in the collagen deposition process.

scholarly journals PRMT5 in T cells drives Th17 responses, mixed granulocytic inflammation and severe allergic airway inflammation

2021 ◽  
Author(s):  
Brandon W Lewis ◽  
Stephanie A Amici ◽  
Hye-Young Kim ◽  
Emily Shalosky ◽  
Aiman Khan ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Airway Inflammation ◽  
Severe Asthma ◽  
Lung Inflammation ◽  
Airway Remodeling ◽  
Symptom Control ◽  
Hospital Costs ◽  
Allergic Airway Inflammation ◽  
Arginine Methylation

Severe asthma is characterized by steroid insensitivity and poor symptom control, and is responsible for the majority of asthma-related hospital costs. Therapeutic options remain limited, in part due to a lack of mechanisms driving severe asthma phenotypes. Increased arginine methylation, catalyzed by protein arginine methyltransferases (PRMTs), is increased in asthmatic lungs. Here, we show that PRMT5 drives allergic airway inflammation in a mouse model reproducing multiple aspects of human severe asthma. We find that PRMT5 is required in CD4+ T cells for chronic steroid-insensitive severe lung inflammation, with selective T cell deletion of PRMT5 robustly suppressing eosinophilic and granulocytic lung inflammation, pathology, airway remodeling and hyperresponsiveness. Mechanistically, we observed high pulmonary sterol metabolic activity, ROR-γt and Th17 responses, with PRMT5-dependent increases in ROR-γt agonist desmosterol. Our work demonstrates that T cell PRMT5 drives severe allergic lung inflammation and has potential implications for the pathogenesis and therapeutic targeting of severe asthma.

Enhanced Infiltration of Central Memory T Cells to the Lung Tissue during Allergic Lung Inflammation

2021 ◽  
pp. 1-15
Author(s):  
Mashael Alabed ◽  
Asma Sultana Shaik ◽  
Narjes Saheb Sharif-Askari ◽  
Fatemeh Saheb Sharif-Askari ◽  
Shirin Hafezi ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Lung Tissue ◽  
Lung Inflammation ◽  
Inflammatory Responses ◽  
Memory T Cells ◽  
Central Memory ◽  
Effector Memory ◽  
Differential Distribution ◽  
Allergic Lung Inflammation

Memory T cells play a central role in regulating inflammatory responses during asthma. However, tissue distribution of effector memory (T<sub>EM</sub>) and central memory (T<sub>CM</sub>) T-cell subtypes, their differentiation, and their contribution to the persistence of lung tissue inflammation during asthma are not well understood. Interestingly, an increase in survival and persistence of memory T cells was reported in asthmatic lungs, which may suggest a shift toward the more persistent T<sub>CM</sub> phenotype. In this report, we investigated the differential distribution of memory T-cell subtypes during allergic lung inflammation and the mechanism regulating that. Using an OVA-sensitized asthma mouse model, we observed a significant increase in the frequency of T<sub>CM</sub> cells in inflamed lungs compared to healthy controls. Interestingly, adoptive transfer techniques confirmed substantial infiltration of T<sub>CM</sub> cells to lung tissues during allergic airway inflammation. Expression levels of T<sub>CM</sub> homing receptors, CD34 and GlyCAM-1, were also significantly upregulated in the lung tissues of OVA-sensitized mice, which may facilitate the increased T<sub>CM</sub> infiltration into inflamed lungs. Moreover, a substantial increase in the relative expression of T<sub>CM</sub> profile-associated genes (EOMES, BCL-6, ID3, TCF-7, BCL-2, BIM, and BMI-1) was noted for T<sub>EM</sub> cells during lung inflammation, suggesting a shift for T<sub>EM</sub> into the T<sub>CM</sub> state. To our knowledge, this is the first study to report an increased infiltration of T<sub>CM</sub> cells into inflamed lung tissues and to suggest differentiation of T<sub>EM</sub> to T<sub>CM</sub> cells in these tissues. Therapeutic interference at T<sub>CM</sub> infiltration or differentiations could constitute an alternative treatment approach for lung inflammation.

scholarly journals CD4+ cells are required for chronic eosinophilic lung inflammation but not airway remodeling

2009 ◽  
Vol 296 (2) ◽  
pp. L229-L235 ◽  
Author(s):  
Taylor A. Doherty ◽  
Pejman Soroosh ◽  
David H. Broide ◽  
Michael Croft
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Lung Inflammation ◽  
Chronic Exposure ◽  
Acute Inflammation ◽  
Airway Remodeling ◽  
Allergen Challenge ◽  
Cd4 Cells ◽  
Inkt Cells ◽  
Subepithelial Fibrosis

The contribution of CD4 T cells and other CD4+ cells to lung inflammation and airway remodeling remains unclear during bouts of chronic exposure to airborne allergen. Previously, murine models have shown that CD4 T cells are required for initiation of acute inflammation and the remodeling process. However, it is unknown whether CD4 T cells or other CD4+ cells continue to be required for remodeling during ongoing allergen challenges after the development of acute eosinophilic lung inflammation. To test this, mice were sensitized and challenged with ovalbumin (OVA). After acute airway inflammation was established, a CD4 depleting antibody was administered for 4 wk during a period of chronic exposure to intranasal OVA, resulting in effective depletion of CD4+ cells from all organs, including the lung, lung-draining lymph nodes, and spleen. In these mice, levels of peribronchial inflammation, bronchoalveolar (BAL) eosinophils, and lung CD11c+, CD8+, and Siglec-F+CD11c- cells were significantly reduced. However, mucus metaplasia, peribronchial subepithelial fibrosis, and smooth muscle mass were not affected. Additionally, depletion of CD4+ cells before the last week of chronic allergen challenges also led to significant reductions in BAL eosinophils, peribronchial inflammation, and lung CD11c+, CD8+, and Siglec-F+CD11c- cells. These results show that CD4 T cells, and other CD4+ cells including subsets of dendritic cells, iNKT cells, and LTi cells, play a role in ongoing eosinophilic lung inflammation during periods of chronic allergen challenge, but are not required for progressive airway remodeling that develops after initial acute inflammation.

Low-level laser therapy attenuates lung inflammation and airway remodeling in a murine model of idiopathic pulmonary fibrosis: Relevance to cytokines secretion from lung structural cells

2020 ◽  
Vol 203 ◽  
pp. 111731 ◽  
Author(s):  
Auriléia Aparecida de Brito ◽  
Elaine Cristina da Silveira ◽  
Nicole Cristine Rigonato-Oliveira ◽  
Stephanie Souza Soares ◽  
Maysa Alves Rodrigues Brandao-Rangel ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Laser Therapy ◽  
Murine Model ◽  
Lung Inflammation ◽  
Airway Remodeling ◽  
Low Level Laser Therapy ◽  
Low Level Laser ◽  
Level Laser ◽  
Cytokines Secretion

scholarly journals Proanthocyanidin from Grape Seed Extract Inhibits Airway Inflammation and Remodeling in a Murine Model of Chronic Asthma

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Dan-Yang Zhou ◽  
Su-Rong Fang ◽  
Chun-Fang Zou ◽  
Qian Zhang ◽  
Wei Gu
Keyword(s):  
Growth Factor ◽  
Airway Inflammation ◽  
Murine Model ◽  
Transforming Growth Factor ◽  
Immunoglobulin E ◽  
Airway Remodeling ◽  
Grape Seed ◽  
Total Serum ◽  
Chronic Asthma ◽  
Tgf Β1

Asthma is characterized by airway inflammation and airway remodeling. Our previous study revealed that grape seed proanthocyanidin extract (GSPE) could inhibit asthmatic airway inflammation and airway hyper-responsiveness by down-regulation of inducible nitric oxide synthase in a murine model of acute asthma. The present study aimed to evaluate GSPE's effects on airway inflammation and airway remodeling in a chronic asthmatic model. BALB/c mice were sensitized with ovalbumin (OVA) and then were challenged three times a week for 8 weeks. Airway responsiveness was measured at 24 h after the last OVA challenge. HE staining, PAS staining, and Masson staining were used to observe any airway inflammation in the lung tissue, airway mucus secretion, and subepithelial fibrosis, respectively. The cytokines levels in the lavage fluid (BALF) in addition to the total serum immunoglobulin E (IgE) levels were detected by ELISA. Furthermore, lung collagen contents, α-smooth muscle actin (α-SMA), and transforming growth factor-β1 (TGF-β1) expression in the airway were assessed by hydroxyproline assay, immunohistochemistry, andWestern blot analysis, respectively. GSPE administration significantly suppressed airway resistance as well as reduced the amount of inflammatory cells, especially the eosinophil count, in BALF. Additionally, the GSPE treatment markedly decreased interleukin (IL)-4, IL-13, and vascular endothelial growth factor (VEGF) levels in BALF in addition to the total serum IgE levels. A histological examination demonstrated that GSPE significantly ameliorated allergen-induced lung eosinophilic inflammation and decreased PAS-positive epithelial cells in the airway. The elevated hydroxyproline contents, lung α-SMA contents, and TGF-β1 protein expression that were observed in the OVA mice were also inhibited by GSPE. In conclusion, GSPE could inhibit airway inflammation and airway remodeling in a murine model of chronic asthma, thus providing a potential treatment for asthma.

scholarly journals Schistosoma japonicumegg antigens stimulate CD4+ CD25+T cells and modulate airway inflammation in a murine model of asthma

Immunology ◽  
2007 ◽  
Vol 120 (1) ◽  
pp. 8-18 ◽  
Author(s):  
Jianghua Yang ◽  
Jiaqing Zhao ◽  
Yanfeng Yang ◽  
Lei Zhang ◽  
Xue Yang ◽  
...  
Keyword(s):  
T Cells ◽  
Airway Inflammation ◽  
Murine Model

MANAGEMENT OF AIRWAY REMODELING IN A MURINE MODEL OF ALLERGIC AIRWAY INFLAMMATION USING EXTRACELLULAR VESICLES FROM HUMAN BONE MARROW-DERIVED MESENCHYMAL STEM CELLS

Cytotherapy ◽  
2021 ◽  
Vol 23 (4) ◽  
pp. 23
Author(s):  
FYI Fragoso ◽  
ABB Angulski ◽  
AC Senegaglia ◽  
LMB Leite ◽  
PV Michelotto ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Airway Inflammation ◽  
Extracellular Vesicles ◽  
Murine Model ◽  
Airway Remodeling ◽  
Allergic Airway Inflammation ◽  
Human Bone ◽  
Human Bone Marrow

scholarly journals Airway delivery of both a BCG prime and adenoviral boost drives CD4 and CD8 T cells into the lung tissue parenchyma

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Daryan A. Kaveh ◽  
M. Carmen Garcia-Pelayo ◽  
Naomi C. Bull ◽  
Pedro J. Sanchez-Cordon ◽  
John Spiropoulos ◽  
...  
Keyword(s):  
T Cells ◽  
Lung Tissue ◽  
Cd8 T Cells ◽  
Murine Model ◽  
Vaccine Development ◽  
Lung Parenchyma ◽  
Boost Vaccination ◽  
Parenteral Delivery ◽  
Promising Strategy ◽  
Intravascular Staining

Abstract Heterologous BCG prime-boost regimens represent a promising strategy for an urgently required improved tuberculosis vaccine. Identifying the mechanisms which underpin the enhanced protection induced by such strategies is one key aim which would significantly accelerate rational vaccine development. Experimentally, airway vaccination induces greater efficacy than parenteral delivery; in both conventional vaccination and heterologous boosting of parenteral BCG immunisation. However, the effect of delivering both the component prime and boost immunisations via the airway is not well known. Here we investigate delivery of both the BCG prime and adenovirus boost vaccination via the airway in a murine model, and demonstrate this approach may be able to improve the protective outcome over parenteral prime/airway boost. Intravascular staining of T cells in the lung revealed that the airway prime regimen induced more antigen-specific multifunctional CD4 and CD8 T cells to the lung parenchyma prior to challenge and indicated the route of both prime and boost to be critical to the location of induced resident T cells in the lung. Further, in the absence of a defined phenotype of vaccine-induced protection to tuberculosis; the magnitude and phenotype of vaccine-specific T cells in the parenchyma of the lung may provide insights into potential correlates of immunity.

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