scholarly journals Ultrafine Carbon Black Particles Cause Early Airway Inflammation and Have Adjuvant Activity in a Mouse Allergic Airway Disease Model

2005 ◽  
Vol 87 (2) ◽  
pp. 409-418 ◽  
Author(s):  
Colin de Haar ◽  
Ine Hassing ◽  
Marianne Bol ◽  
Rob Bleumink ◽  
Raymond Pieters
Keyword(s):  
Carbon Black ◽  
Airway Inflammation ◽  
Disease Model ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Adjuvant Activity

Divergent immune responses to house dust mite lead to distinct structural-functional phenotypes

2007 ◽  
Vol 293 (3) ◽  
pp. L730-L739 ◽  
Author(s):  
Jill R. Johnson ◽  
Filip K. Swirski ◽  
Beata U. Gajewska ◽  
Ryan E. Wiley ◽  
Ramzi Fattouh ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Responses ◽  
Airway Remodeling ◽  
Bronchial Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th Cell ◽  
And Function ◽  
Deficient Mice ◽  
Chronic Airway

Asthma is a chronic airway inflammatory disease that encompasses three cardinal processes: T helper (Th) cell type 2 (Th2)-polarized inflammation, bronchial hyperreactivity, and airway wall remodeling. However, the link between the immune-inflammatory phenotype and the structural-functional phenotype remains to be fully defined. The objective of these studies was to evaluate the relationship between the immunologic nature of chronic airway inflammation and the development of abnormal airway structure and function in a mouse model of chronic asthma. Using IL-4-competent and IL-4-deficient mice, we created divergent immune-inflammatory responses to chronic aeroallergen challenge. Immune-inflammatory, structural, and physiological parameters of chronic allergic airway disease were evaluated in both strains of mice. Although both strains developed airway inflammation, the profiles of the immune-inflammatory responses were markedly different: IL-4-competent mice elicited a Th2-polarized response and IL-4-deficient mice developed a Th1-polarized response. Importantly, this chronic Th1-polarized immune response was not associated with airway remodeling or bronchial hyperresponsiveness. Transient reconstitution of IL-4 in IL-4-deficient mice via an airway gene transfer approach led to partial Th2 repolarization and increased bronchial hyperresponsiveness, along with full reconstitution of airway remodeling. These data show that distinct structural-functional phenotypes associated with chronic airway inflammation are strictly dependent on the nature of the immune-inflammatory response.

scholarly journals Dilodendron bipinnatum Radlk. ameliorates airway inflammation through multiple targets in a murine model of ovalbumin-induced allergic airway disease

2018 ◽  
Vol 226 ◽  
pp. 17-25 ◽  
Author(s):  
Ruberlei Godinho de Oliveira ◽  
Fábio Miyajima ◽  
Geovane Roberto de Campos Castilho ◽  
Amílcar Sabino Damazo ◽  
Antonio Macho ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Murine Model ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Multiple Targets

scholarly journals Airway responsiveness in CD38-deficient mice in allergic airway disease: studies with bone marrow chimeras

2015 ◽  
Vol 308 (5) ◽  
pp. L485-L493 ◽  
Author(s):  
Alonso G. P. Guedes ◽  
Joseph A. Jude ◽  
Jaime Paulin ◽  
Laura Rivero-Nava ◽  
Hirohito Kita ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Airway Inflammation ◽  
Surface Protein ◽  
Inflammatory Cells ◽  
Airway Disease ◽  
Airway Responsiveness ◽  
Allergic Airway Disease ◽  
Lower Airway ◽  
Protein Antigens ◽  
Bone Marrow Chimeras

CD38 is a cell-surface protein involved in calcium signaling and contractility of airway smooth muscle. It has a role in normal airway responsiveness and in airway hyperresponsiveness (AHR) developed following airway exposure to IL-13 and TNF-α but appears not to be critical to airway inflammation in response to the cytokines. CD38 is also involved in T cell-mediated immune response to protein antigens. In this study, we assessed the contribution of CD38 to AHR and inflammation to two distinct allergens, ovalbumin and the epidemiologically relevant environmental fungus Alternaria. We also generated bone marrow chimeras to assess whether Cd38+/+inflammatory cells would restore AHR in the CD38-deficient ( Cd38−/−) hosts following ovalbumin challenge. Results show that wild-type (WT) mice develop greater AHR to inhaled methacholine than Cd38−/−mice following challenge with either allergen, with comparable airway inflammation. Reciprocal bone marrow transfers did not change the native airway phenotypic differences between WT and Cd38−/−mice, indicating that the lower airway reactivity of Cd38−/−mice stems from Cd38−/−lung parenchymal cells. Following bone marrow transfer from either source and ovalbumin challenge, the phenotype of Cd38−/−hosts was partially reversed, whereas the airway phenotype of the WT hosts was preserved. Airway inflammation was similar in Cd38−/−and WT chimeras. These results indicate that loss of CD38 on hematopoietic cells is not sufficient to prevent AHR and that the magnitude of airway inflammation is not the predominant underlying determinant of AHR in mice.

Engineered Silica Nanoparticles Promote An Adjuvant Th2/Th17 Response In A Murine Allergic Airway Disease Model

2012 ◽  
Author(s):  
Christina Brandenberger ◽  
Ryan P. Lewandowski ◽  
Nicole L. Rowley ◽  
Lori A. Bramble ◽  
Daven N. Jackson-Humbles ◽  
...  
Keyword(s):  
Silica Nanoparticles ◽  
Disease Model ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th17 Response

scholarly journals Regulatory T cells mediated immunomodulation during asthma: a therapeutic standpoint

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Mohammad Afzal Khan
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Airway Inflammation ◽  
Therapeutic Potential ◽  
Airway Remodeling ◽  
Clinical Manifestations ◽  
Inflammatory Cells ◽  
Airway Disease ◽  
Vital Role ◽  
Allergic Airway Disease

AbstractAsthma is an inflammatory disease of the lung airway network, which is initiated and perpetuated by allergen-specific CD4+ T cells, IgE antibodies, and a massive release of Th2 cytokines. The most common clinical manifestations of asthma progression include airway inflammation, pathological airway tissue and microvascular remodeling, which leads to airway hyperresponsiveness (AHR), and reversible airway obstruction. In addition to inflammatory cells, a tiny population of Regulatory T cells (Tregs) control immune homeostasis, suppress allergic responses, and participate in the resolution of inflammation-associated tissue injuries. Preclinical and clinical studies have demonstrated a tremendous therapeutic potential of Tregs in allergic airway disease, which plays a crucial role in immunosuppression, and rejuvenation of inflamed airways. These findings supported to harness the immunotherapeutic potential of Tregs to suppress airway inflammation and airway microvascular reestablishment during the progression of the asthma disease. This review addresses the therapeutic impact of Tregs and how Treg mediated immunomodulation plays a vital role in subduing the development of airway inflammation, and associated airway remodeling during the onset of disease.

scholarly journals Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation

Thorax ◽  
2020 ◽  
Vol 75 (7) ◽  
pp. 600-605
Author(s):  
Jennifer M Felton ◽  
David A Dorward ◽  
Jennifer A Cartwright ◽  
Philippe MD Potey ◽  
Calum T Robb ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Kinase Inhibitor ◽  
Allergic Airway Inflammation ◽  
Allergic Diseases ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Allergic Airway Disease ◽  
Cyclin Dependent Kinase ◽  
Mucus Production ◽  
Effector Cells

Eosinophils are key effector cells in allergic diseases. Here we investigated Mcl-1 (an anti-apoptotic protein) in experimental allergic airway inflammation using transgenic overexpressing human Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor. Overexpression of Mcl-1 exacerbated allergic airway inflammation, with increased bronchoalveolar lavage fluid cellularity, eosinophil numbers and total protein, and an increase in airway mucus production. Eosinophil apoptosis was suppressed by Mcl-1 overexpression, with this resistance to apoptosis attenuated by cyclin-dependent kinase inhibition which also rescued Mcl-1-exacerbated allergic airway inflammation. We propose that targeting Mcl-1 may be beneficial in treatment of allergic airway disease.

Prophylactic Bifidobacterium adolescentis ATTCC 15703 supplementation reduces partially allergic airway disease in Balb/c but not in C57BL/6 mice

2018 ◽  
Vol 9 (3) ◽  
pp. 465-476 ◽  
Author(s):  
M.C. Casaro ◽  
A.R. Crisma ◽  
A.T. Vieira ◽  
G.H.M. Silva ◽  
E. Mendes ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Asthma ◽  
Therapeutic Potential ◽  
Allergic Airway Inflammation ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Mouse Strains ◽  
Genetic Profile ◽  
Bifidobacterium Adolescentis ◽  
Experimental Allergic

Allergic asthma is a chronic disease mainly characterised by eosinophil inflammation and airway remodelling. Many studies have shown that the gut microbiota of allergic individuals differs from that of non-allergic individuals. Although high levels of bifidobacteria have been associated with healthy persons, Bifidobacterium adolescentis ATCC 15703, a gut bacteria, has been associated with allergic individuals in some clinical studies. The relationship between B. adolescentis ATCC 15703 and asthma or allergies has not been well elucidated, and its effect may be dependent on the host’s genetic profile or disease state. To elucidate this question, we evaluated the role of preventive B. adolescentis ATCC 15703 treatment on experimental allergic airway inflammation in two genetically different mouse strains, Balb/c and C57BL/6 (B6). Balb/c mice display a greater predisposition to develop allergic responses than B6 mice. Oral preventive treatment with B. adolescentis ATCC 15703 modulated experimental allergic airway inflammation, specifically in Balb/c mice, which showed decreased levels of eosinophils in the airway. B6 mice did not exhibit any significant alterations in eosinophils but showed an increased influx of total leukocytes and neutrophils into the airway. The mechanism underlying the beneficial effects of these bacteria in experimental allergic mice may involve products of bacteria metabolism, as dead bacteria did not mimic the ability of live B. adolescentis ATCC 15703 to attenuate the influx of eosinophils into the airway. To conclude, preventive oral B. adolescentis ATCC 15703 treatment can attenuate the major characteristic of allergic asthma, eosinophil airway influx, in Balb/c but not B6 mice. These results suggest that oral treatment with this specific live bacterial strain may have therapeutic potential for the treatment of allergic airway disease, although its effect is mouse-strain-dependent.

Nitrogen dioxide enhances allergic airway inflammation and hyperresponsiveness in the mouse

2006 ◽  
Vol 290 (1) ◽  
pp. L144-L152 ◽  
Author(s):  
Matthew E. Poynter ◽  
Rebecca L. Persinger ◽  
Charles G. Irvin ◽  
Kelly J. Butnor ◽  
Hans van Hirtum ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Recovery Period ◽  
Allergic Airway Inflammation ◽  
Airway Disease ◽  
Air Pollutant ◽  
Allergic Airway Disease ◽  
Eosinophilic Inflammation ◽  
Neutrophilic Inflammation ◽  
Inflammatory Changes ◽  
Cardinal Feature

In addition to being an air pollutant, NO2 is a potent inflammatory oxidant generated endogenously by myeloperoxidase and eosinophil peroxidase. In these studies, we sought to determine the effects of NO2 exposure on mice with ongoing allergic airway disease pathology. Mice were sensitized and challenged with the antigen ovalbumin (OVA) to generate airway inflammation and subsequently exposed to 5 or 25 ppm NO2 for 3 days or 5 days followed by a 20-day recovery period. Whereas 5 ppm NO2 elicited no pathological changes, inhalation of 25 ppm NO2 alone induced acute lung injury, which peaked after 3 days and was characterized by increases in protein, LDH, and neutrophils recovered by BAL, as well as lesions within terminal bronchioles. Importantly, 25 ppm NO2 was also sufficient to cause AHR in mice, a cardinal feature of asthma. The inflammatory changes were ameliorated after 5 days of inhalation and completely resolved after 20 days of recovery after the 5-day inhalation. In contrast, in mice immunized and challenged with OVA, inhalation of 25 ppm NO2 caused a marked augmentation of eosinophilic inflammation and terminal bronchiolar lesions, which extended significantly into the alveoli. Moreover, 20 days postcessation of the 5-day 25 ppm NO2 inhalation regimen, eosinophilic and neutrophilic inflammation, pulmonary lesions, and AHR were still present in mice immunized and challenged with OVA. Collectively, these observations suggest an important role for NO2 in airway pathologies associated with asthma, both in modulation of degree and duration of inflammatory response, as well as in induction of AHR.

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