scholarly journals Electronic Cigarettes and Asthma: What Do We Know So Far?

2021 ◽  
Vol 11 (8) ◽  
pp. 723
Author(s):  
Serafeim-Chrysovalantis Kotoulas ◽  
Paraskevi Katsaounou ◽  
Renata Riha ◽  
Ioanna Grigoriou ◽  
Despoina Papakosta ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Lung Function ◽  
Airway Inflammation ◽  
Clinical Characteristics ◽  
Electronic Cigarettes ◽  
T Helper ◽  
Asthmatic Patients ◽  
Asthma Symptoms ◽  
Th2 Inflammation

Electronic cigarettes (EC) are a novel product, marketed as an alternative to tobacco cigarette. Its effects on human health have not been investigated widely yet, especially in specific populations such as patients with asthma. With this review, we use the existing literature in order to answer four crucial questions concerning: (1) ECs’ role in the pathogenesis of asthma; (2) ECs’ effects on lung function and airway inflammation in patients with asthma; (3) ECs’ effects on asthma clinical characteristics in asthmatics who use it regularly; and (4) ECs’ effectiveness as a smoking cessation tool in these patients. Evidence suggests that many EC compounds might contribute to the pathogenesis of asthma. Lung function seems to deteriorate by the use of EC in this population, while airway inflammation alters, with the aggravation of T-helper-type-2 (Th2) inflammation being the most prominent but not the exclusive effect. EC also seems to worsen asthma symptoms and the rate and severity of exacerbations in asthmatics who are current vapers, whilst evidence suggests that its effectiveness as a smoking cessation tool might be limited. Asthmatic patients should avoid using EC.

Contrasting roles for the receptor for advanced glycation end-products on structural cells in allergic airway inflammation vs. airway hyperresponsiveness

2015 ◽  
Vol 309 (8) ◽  
pp. L789-L800 ◽  
Author(s):  
Akihiko Taniguchi ◽  
Nobuaki Miyahara ◽  
Koichi Waseda ◽  
Etsuko Kurimoto ◽  
Utako Fujii ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Allergic Airway Inflammation ◽  
T Helper ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Group 2 ◽  
Airway Responses

The receptor for advanced glycation end-products (RAGE) is a multiligand receptor that belongs to the immunoglobulin superfamily. RAGE is reported to be involved in various inflammatory disorders; however, studies that address the role of RAGE in allergic airway disease are inconclusive. RAGE-sufficient (RAGE+/+) and RAGE-deficient (RAGE−/−) mice were sensitized to ovalbumin, and airway responses were monitored after ovalbumin challenge. RAGE−/− mice showed reduced eosinophilic inflammation and goblet cell metaplasia, lower T helper type 2 (Th2) cytokine production from spleen and peribronchial lymph node mononuclear cells, and lower numbers of group 2 innate lymphoid cells in the lung compared with RAGE+/+ mice following sensitization and challenge. Experiments using irradiated, chimeric mice showed that the mice expressing RAGE on radio-resistant structural cells but not hematopoietic cells developed allergic airway inflammation; however, the mice expressing RAGE on hematopoietic cells but not structural cells showed reduced airway inflammation. In contrast, absence of RAGE expression on structural cells enhanced innate airway hyperresponsiveness (AHR). In the absence of RAGE, increased interleukin (IL)-33 levels in the lung were detected, and blockade of IL-33 receptor ST2 suppressed innate AHR in RAGE−/− mice. These data identify the importance of RAGE expressed on lung structural cells in the development of allergic airway inflammation, T helper type 2 cell activation, and group 2 innate lymphoid cell accumulation in the airways. RAGE on lung structural cells also regulated innate AHR, likely through the IL-33-ST2 pathway. Thus manipulating RAGE represents a novel therapeutic target in controlling allergic airway responses.

scholarly journals IFITM proteins drive type 2 T helper cell differentiation and exacerbate allergic airway inflammation

2018 ◽  
Vol 49 (1) ◽  
pp. 66-78 ◽  
Author(s):  
Diana C. Yánez ◽  
Hemant Sahni ◽  
Susan Ross ◽  
Anisha Solanki ◽  
Ching-In Lau ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper

scholarly journals Critical Involvement of CD44 in T Helper Type 2 Cell-Mediated Eosinophilic Airway Inflammation in a Mouse Model of Acute Asthma

2022 ◽  
Vol 12 ◽  
Author(s):  
Shigeki Katoh
Keyword(s):  
Monoclonal Antibodies ◽  
Airway Inflammation ◽  
Th17 Cells ◽  
Acute Asthma ◽  
Mite Allergen ◽  
Th2 Cells ◽  
T Helper ◽  
Th2 Cell ◽  
Helper Type

Interactions between CD44 and hyaluronan (HA) are crucial for recruiting leukocytes to inflamed tissues. This review summarizes findings from our studies of the roles of CD44-HA interactions in leukocyte trafficking, with a particular focus on airway T helper type 2 (Th2) cells in mouse models of acute asthma. In a mite allergen-induced model of acute asthma, intraperitoneal injection of anti-CD44 monoclonal antibodies blocked lymphocytes and eosinophils from accumulating in the lung, and suppressed both the antigen-induced increase in Th2 cytokines in the bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness (AHR). CD44 deficiency was associated with decreased mite allergen-induced Th2 cell-mediated airway inflammation and AHR in sensitized mice. Asthmatic responses to antigen-sensitized splenic CD4+ T cells transferred from CD44-deficient mice were weaker than in wild-type mice. Administration of anti-CD44 monoclonal antibodies preferentially suppressed the airway accumulation of antigen-specific Th2 cells induced by antigen challenge, without affecting Th1 and Th17 cells. Increased HA-binding ability of CD44 and expression of Neu1 sialidase were observed on antigen-specific Th2 cells compared with antigen-specific Th1 and Th17 cells. Finally, in a mouse model of acute asthma, neuraminidase 1-deficient SM/J mice exhibited a lower Th2 cytokine concentration and a lower absolute Th2 cell number in the BALF, as well as an attenuated AHR. Our findings indicate that CD44 critically contributes to the antigen challenge-induced airway accumulation of antigen-specific Th2 cells, without affecting Th1 and Th17 cells, in mice. Furthermore, neuraminidase 1 activity is necessary for the interaction between HA and CD44, and Th2 cell-mediated airway inflammation.

scholarly journals Effects of personal air pollution exposure on asthma symptoms, lung function and airway inflammation

2018 ◽  
Vol 48 (7) ◽  
pp. 798-805 ◽  
Author(s):  
L. Chambers ◽  
J. Finch ◽  
K. Edwards ◽  
A. Jeanjean ◽  
R. Leigh ◽  
...  
Keyword(s):  
Air Pollution ◽  
Lung Function ◽  
Airway Inflammation ◽  
Asthma Symptoms ◽  
Air Pollution Exposure ◽  
Pollution Exposure

Lung function and respiratory symptoms in a randomized smoking cessation trial of electronic cigarettes

2016 ◽  
Vol 130 (21) ◽  
pp. 1929-1937 ◽  
Author(s):  
Fabio Cibella ◽  
Davide Campagna ◽  
Pasquale Caponnetto ◽  
Maria Domenica Amaradio ◽  
Massimo Caruso ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Lung Function ◽  
Respiratory Symptoms ◽  
Electronic Cigarettes ◽  
Controlled Trial ◽  
Substantial Reduction ◽  
Cigarette Consumption ◽  
Phenotype Classification ◽  
Quitting Smoking

Quitting smoking is the most important step smokers can take to improve their health. Nonetheless, there is little information on long-term improvements in lung function and/or respiratory symptoms after smoking cessation. Here we illustrate long-term changes in spirometric indices as well as in respiratory symptoms in smokers invited to quit or reduce their cigarette consumption by switching to electronic cigarettes (ECs). Prospective evaluation of cigarette consumption, spirometry and symptoms was performed in a 1-year randomized controlled trial of smokers receiving EC containing 2.4%, 1.8% or 0% nicotine. Spirometric data are presented on the basis of participants’ pooled continuous smoking phenotype classification (Quitters, Reducers, Failures), whereas respiratory symptoms on the basis of their point prevalence-smoking phenotype. Smoking phenotype classification (Quitters, Reducers, Failures) had no significant effect on spirometric indices (FEV1, FVC and FEV1/FVC) with the exception of FEF25–75%, which significantly (P  =0.034) increased over the time among Quitters; their FEF25–75% (% predicted) improving from (means±S.D.) 85.7±15.6% at baseline (BL) to 100.8±14.6%. High prevalence of cough/phlegm (43.1%) and shortness of breath (SoB; 34.8%) was reported at BL with substantial reduction in their frequency at subsequent follow-up visits. These symptoms virtually disappeared very quickly in both quitters and reducers. Smokers invited to switch to ECs who completely abstained from smoking showed steady progressive improvements in their FEF25–75%. Normalization of peripheral airways function was associated with improvement in respiratory symptoms, adding to the notion that abstaining from smoking can reverse tobacco harm in the lung.

scholarly journals Basophils as a primary inducer of the T helper type 2 immunity in ovalbumin-induced allergic airway inflammation

Immunology ◽  
2014 ◽  
Vol 142 (2) ◽  
pp. 202-215 ◽  
Author(s):  
Wenwei Zhong ◽  
Wen Su ◽  
Yanjie Zhang ◽  
Qi Liu ◽  
Jinhong Wu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
T Helper ◽  
Type 2 Immunity ◽  
Helper Type

scholarly journals 552The lung function and airway inflammation markers associated with short-term pollen exposure- A systematic review

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
N. Sabrina Idrose ◽  
Caroline Lodge ◽  
Jennifer Koplin ◽  
Don Vicendese ◽  
Jo Douglass ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Inflammation ◽  
Meta Analysis ◽  
Qualitative Synthesis ◽  
Short Term ◽  
Cross Sectional ◽  
Random Effects Models ◽  
Newcastle Ottawa Scale ◽  
Pollen Exposure

Abstract Background Experimental challenge studies have shown that pollen can affect the lungs and airways. Here, we systematically reviewed community-based studies investigating outdoor pollen exposure, lung function and/or airway inflammation. Methods Four online databases were searched. The search strategy included terms relating to both exposure and outcomes. Inclusion criteria were studies published in English that were representative of the community. We only considered cross-sectional or short-term longitudinal studies which investigated pollen exposure by levels or season. Study quality assessment was performed using the Newcastle-Ottawa scale. Meta-analysis was conducted using random-effects models. Results We included 27 of 6,551 studies identified from the search. Qualitative synthesis indicated associations between pollen exposure and predominantly type-2 inflammation in both the upper and lower airways, but little evidence for lung function changes. People with ever asthma and/or seasonal allergic rhinitis (SAR) were at higher risk of such airway inflammation. Meta-analysis confirmed a positive relationship between pollen season and eosinophilic airway inflammation in people with ever SAR but the results between studies were highly variable. Heterogeneity was reduced after further subgrouping by age and the forest plots indicated that eosinophilic airway inflammation to outdoor pollen exposure increased with age. Conclusion Among people with ever asthma and ever SAR, exposure to increased ambient pollen triggers type-2 airway inflammation rather than a non-specific or innate inflammation. Key messages This review indicates pollen exposure influences predominantly type-2 airway inflammation, but little evidence on lung function.

Calcium Channel Blocker Prevents T Helper Type 2 Cell–mediated Airway Inflammation

2007 ◽  
Vol 175 (11) ◽  
pp. 1117-1124 ◽  
Author(s):  
Bruno Gomes ◽  
Marilena Djata Cabral ◽  
Alexandra Gallard ◽  
Magali Savignac ◽  
Pierre Paulet ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Airway Inflammation ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
T Helper ◽  
Helper Type
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