The role of oxidative stress and innate immunity in O3 and endotoxin-induced human allergic airway disease

2011 ◽  
Vol 242 (1) ◽  
pp. 91-105 ◽  
Author(s):  
David B. Peden
2005 ◽  
Vol 1041 (1) ◽  
pp. 194-196 ◽  
Author(s):  
ISHANEE MOOKERJEE ◽  
MIMI L.K. TANG ◽  
NATASHA SOLLY ◽  
GEOFFREY W. TREGEAR ◽  
CHRISHAN S. SAMUEL

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Anouk K. Gloudemans ◽  
Bart N. Lambrecht ◽  
Hermelijn H. Smits

Allergic asthma is characterized by bronchial hyperresponsiveness, a defective barrier function, and eosinophilic lower airway inflammation in response to allergens. The inflammation is dominated by Th2 cells and IgE molecules and supplemented with Th17 cells in severe asthma. In contrast, in healthy individuals, allergen-specific IgA and IgG4 molecules are found but no IgE, and their T cells fail to proliferate in response to allergens, probably because of the development of regulatory processes that actively suppress responses to allergens. The presence of allergen-specific secretory IgA has drawn little attention so far, although a few epidemiological studies point at a reverse association between IgA levels and the incidence of allergic airway disease. This review highlights the latest literature on the role of mucosal IgA in protection against allergic airway disease, the mechanisms described to induce secretory IgA, and the role of (mucosal) dendritic cells in this process. Finally, we discuss how this information can be used to translate into the development of new therapies for allergic diseases based on, or supplemented with, IgA boosting strategies.


2002 ◽  
Vol 283 (1) ◽  
pp. L198-L204 ◽  
Author(s):  
Jane M. Schuh ◽  
Kate Blease ◽  
Steven L. Kunkel ◽  
Cory M. Hogaboam

Eotaxin/CCL11 is a major chemoattractant for eosinophils and Th2 cells. As such, it represents an attractive target in the treatment of allergic disease. The present study addresses the role of eotaxin/CCL11 during acute and chronic allergic airway responses to the fungus Aspergillus fumigatus. Mice lacking the eotaxin gene (Eo−/−) and wild-type mice (Eo+/+) were sensitized to A. fumigatus and received either an intratracheal challenge with soluble A. fumigatusantigens (acute model) or an intratracheal challenge with live A. fumigatus spores or conidia (chronic model). Airway hyperresponsiveness and eosinophil, but not T cell, recruitment were significantly decreased at 24 h after the soluble allergen in A. fumigatus-sensitized Eo−/− mice compared with similarly sensitized Eo+/+ mice. In contrast, the development of chronic allergic airway disease due to A. fumigatus conidia was not altered by the lack of eotaxin. Together, these data suggest that eotaxin initiates allergic airway disease due to A. fumigatus, but this chemokine did not appear to contribute to the maintenance of A. fumigatus-induced allergic airway disease.


CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 585A
Author(s):  
Mohammad Shameem ◽  
Asrar Ahmad ◽  
Qayyum Hussain ◽  
Rakesh Bhargava ◽  
Zuber Ahmad ◽  
...  

2014 ◽  
Vol 51 (5) ◽  
pp. 615-625 ◽  
Author(s):  
Takehiko Shibata ◽  
Ugur Burcin Ismailoglu ◽  
Nicolai A. Kittan ◽  
Ana Paula Moreira ◽  
Ana Lucia Coelho ◽  
...  

2008 ◽  
Vol 180 (11) ◽  
pp. 7318-7326 ◽  
Author(s):  
Anurag Singh ◽  
William F. Carson ◽  
Eric R. Secor ◽  
Linda A. Guernsey ◽  
Richard A. Flavell ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
pp. 181
Author(s):  
Sanghyun Kim ◽  
Bora Keum ◽  
Junhyoung Byun ◽  
Byoungjae Kim ◽  
Kijeong Lee ◽  
...  

Recent studies on the pathophysiology of irritable bowel syndrome (IBS) have focused on the role of mast cells (MCs) in intestinal mucosal immunity. A link between allergic airway diseases (AADs) and IBS has been suggested because both diseases have similar pathophysiology. We aimed to investigate whether the induction of AAD in mice could lead to inflammation of the colonic mucosa, similar to IBS. We also evaluated whether this inflammatory response could be suppressed by administering a therapeutic agent. Mice were divided into three groups: control, AAD-induced, and salbutamol-treated. An AAD mouse model was established by intraperitoneal injection and nasal challenge with ovalbumin. Mice with AAD were intranasally administered salbutamol. Analyses of cytokine levels, MC count, and tryptase levels in the intestinal mucosa were performed to compare the changes in inflammatory responses among the three groups. Inflammation was observed in the intestinal mucosa of mice in the AAD group. This inflammation in AAD mice was suppressed after salbutamol treatment. Our study demonstrates that AAD induces an inflammatory response similar to that in IBS, suggesting a possible association between IBS and AADs. In patients with IBS with such allergic components, salbutamol may have the potential to alleviate the inflammatory response.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Anurag Singh ◽  
Linda A. Guernsey ◽  
Jeffrey T. Mcnamara ◽  
Eric R. Secor ◽  
Craig M. Schramm ◽  
...  

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