scholarly journals Role of the phosphoinositide 3-kinase p110δ in generation of type 2 cytokine responses and allergic airway inflammation

2007 ◽  
Vol 37 (2) ◽  
pp. 416-424 ◽  
Author(s):  
Baher F. Nashed ◽  
Tingting Zhang ◽  
Monther Al-Alwan ◽  
Ganesh Srinivasan ◽  
Andrew J. Halayko ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Cytokine Responses ◽  
Phosphoinositide 3 Kinase

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 O21 - The role of DNA damage and repair in allergic airway inflammation

2014 ◽  
Vol 4 (Suppl 1) ◽  
pp. O21
Author(s):  
Tze Khee Chan ◽  
Xin Yi Loh ◽  
Daniel WS Tan ◽  
Bevin P Engelward ◽  
Fred WS Wong
Keyword(s):  
Dna Damage ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Dna Damage And Repair

Chitinase 3-like-1 protects airway function despite promoting type 2 inflammation during fungal-associated allergic airway inflammation

2021 ◽  
Author(s):  
Joseph J. Mackel ◽  
Jaleesa M. Garth ◽  
MaryJane Jones ◽  
Diandra A. Ellis ◽  
Jonathan P. Blackburn ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Periodic Acid ◽  
Acute Infection ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Allergic Airway Inflammation ◽  
Lung Edema ◽  
Periodic Acid Schiff ◽  
Wide Range ◽  
Type 2 Inflammation

Exposure to fungi can result in a wide range of comorbidities depending on the immune status of the host. Chronic exposure and reactivity to fungi such as Aspergillus fumigatus can result in conditions such as severe asthma with fungal sensitization (SAFS) or allergic bronchopulmonary aspergillosis (ABPA). However, the pathophysiology of SAFS and ABPA are not well understood. Here, we report that the chitinase-like protein YKL-40 is elevated in lung lavage fluid from human asthmatics that are sensitized to fungi. Initial studies demonstrated that mice deficient in the murine ortholog of YKL-40, breast regression protein-39 (BRP-39, chitinase-3-like 1, Chi3l1), were not more susceptible to acute infection with A. fumigatus. However, in an experimental model of fungal-associated allergic airway inflammation (fungal asthma), Chi3l1-/- mice had significantly increased airway hyperresponsiveness (AHR). Surprisingly, increased AHR in Chi3l1-/- mice occurred in the presence of significantly lower type 2 responses (decreased eosinophil numbers and decreased IL-4, IL-5, IL-33, CCL17 and CCL22 levels), although type 1 and type 17 responses were not different. Increased AHR was not associated with differences in Periodic-acid-Schiff staining of lung tissue, differences in the expression of Muc5ac and Clca3, nor differences in lung edema. Bone marrow chimera studies revealed that the presence of BRP-39 in either the hematopoietic or non-hematopoietic compartment was sufficient for controlling AHR during fungal asthma. Collectively, these results indicate that BRP-39 protects against AHR during fungal asthma despite contributing to type 2 inflammation, thus highlighting an unexpected protective role for BRP-39 in allergic fungal asthma.

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 75 Role of the IL1 signaling pathway in the development of type 2 airway inflammation in juvenile Scnn1b-Tg mice

2017 ◽  
Vol 16 ◽  
pp. S83
Author(s):  
R. Brown ◽  
S. Schmidt ◽  
J. Schatterny ◽  
S. Hirtz ◽  
M.A. Mall
Keyword(s):  
Airway Inflammation ◽  
Signaling Pathway

scholarly journals Multi-Faceted Notch in Allergic Airway Inflammation

2019 ◽  
Vol 20 (14) ◽  
pp. 3508
Author(s):  
Miao-Tzu Huang ◽  
Chiao-Juno Chiu ◽  
Bor-Luen Chiang
Keyword(s):  
Embryonic Development ◽  
Notch Signaling ◽  
Airway Inflammation ◽  
Cell Activity ◽  
Adult Life ◽  
Allergic Airway Inflammation ◽  
T Cell Subsets ◽  
Cell Fate Decisions ◽  
Physiological Processes

Notch is an evolutionarily conserved signaling family which iteratively exerts pleiotropic functions in cell fate decisions and various physiological processes, not only during embryonic development but also throughout adult life. In the context of the respiratory system, Notch has been shown to regulate ciliated versus secretory lineage differentiation of epithelial progenitor cells and coordinate morphogenesis of the developing lung. Reminiscent of its role in development, the Notch signaling pathway also plays a role in repair of lung injuries by regulation of stem cell activity, cell differentiation, cell proliferation and apoptosis. In addition to functions in embryonic development, cell and tissue renewal and various physiological processes, including glucose and lipid metabolism, Notch signaling has been demonstrated to regulate differentiation of literally almost all T-cell subsets, and impact on elicitation of inflammatory response and its outcome. We have investigated the role of Notch in allergic airway inflammation in both acute and chronic settings. In this mini-review, we will summarize our own work and recent advances on the role of Notch signaling in allergic airway inflammation, and discuss potential applications of the Notch signaling family in therapy for allergic airway diseases.

scholarly journals Role of Interleukin-25 in allergic airway inflammation and vascular damage

2011 ◽  
Vol 31 (5) ◽  
pp. 420-424
Author(s):  
Hiroshi Nakajima ◽  
Saki Kawashima ◽  
Tomohiro Tamachi ◽  
Kentaro Takahashi ◽  
Koichi Hirose
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Vascular Damage ◽  
Interleukin 25

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

scholarly journals The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Morris Nechama ◽  
Jeahoo Kwon ◽  
Shuo Wei ◽  
Adrian Tun Kyi ◽  
Robert S. Welner ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Type 2 Immunity

scholarly journals Exacerbation of Allergic Airway Inflammation in Mice Lacking ECTO-5′-Nucleotidase (CD73)

2020 ◽  
Vol 11 ◽  
Author(s):  
Elisabetta Caiazzo ◽  
Ida Cerqua ◽  
Maria Antonietta Riemma ◽  
Roberta Turiello ◽  
Armando Ialenti ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Sensitization ◽  
Adaptive Immune Response ◽  
Allergic Airway Inflammation ◽  
Individual Response ◽  
Type I ◽  
Target Tissue ◽  
Extracellular Adenosine ◽  
Reduced Frequency

The airways are a target tissue of type I allergies and atopy is the main etiological factor of bronchial asthma. A predisposition to allergy and individual response to allergens are dependent upon environmental and host factors. Early studies performed to clarify the role of extracellular adenosine in the airways highlighted the importance of adenosine-generating enzymes CD73, together with CD39, as an innate protection system against lung injury. In experimental animals, deletion of CD73 has been associated with immune and autoimmune diseases. Our experiments have been performed to investigate the role of CD73 in the assessment of allergic airway inflammation following sensitization. We found that in CD73−/− mice sensitization, induced by subcutaneous ovalbumin (OVA) administration, increased signs of airway inflammation and atopy developed, characterized by high IgE plasma levels and increased pulmonary cytokines, reduced frequency of lung CD4+CD25+Foxp3+ T cells, but without bronchial hyperreactivity, compared to sensitized wild type mice. Our results provide evidence that the lack of CD73 causes an uncontrolled allergic sensitization, suggesting that CD73 is a key molecule at the interface between innate and adaptive immune response. The knowledge of host immune factors controlling allergic sensitization is of crucial importance and might help to find preventive interventions that could act before an allergy develops.

Sign in / Sign up

Export Citation Format

Share Document