Faculty Opinions recommendation of AMD3100, a CxCR4 antagonist, attenuates allergic lung inflammation and airway hyperreactivity.

2002 ◽  
Author(s):  
Steven Kunkel
Keyword(s):  
Lung Inflammation ◽  
Airway Hyperreactivity ◽  
Cxcr4 Antagonist ◽  
Allergic Lung Inflammation

scholarly journals AMD3100, a CxCR4 Antagonist, Attenuates Allergic Lung Inflammation and Airway Hyperreactivity

2002 ◽  
Vol 160 (4) ◽  
pp. 1353-1360 ◽  
Author(s):  
Nicholas W. Lukacs ◽  
Aaron Berlin ◽  
Dominique Schols ◽  
Renato T. Skerlj ◽  
Gary J. Bridger
Keyword(s):  
Lung Inflammation ◽  
Airway Hyperreactivity ◽  
Cxcr4 Antagonist ◽  
Allergic Lung Inflammation

scholarly journals Cutaneous, But Not Airway, Latex Exposure Induces Allergic Lung Inflammation and Airway Hyperreactivity in Mice

2005 ◽  
Vol 125 (5) ◽  
pp. 962-968 ◽  
Author(s):  
Maili Lehto ◽  
Rita Haapakoski ◽  
Henrik Wolff ◽  
Marja-Leena Majuri ◽  
Mika J. Mäkelä ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Airway Hyperreactivity ◽  
Allergic Lung Inflammation

Neutralization of either IL-17A or IL-17F is sufficient to inhibit house dust mite induced allergic asthma in mice

2017 ◽  
Vol 131 (20) ◽  
pp. 2533-2548 ◽  
Author(s):  
Pauline Chenuet ◽  
Louis Fauconnier ◽  
Fahima Madouri ◽  
Tiffany Marchiol ◽  
Nathalie Rouxel ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
House Dust ◽  
House Dust Mite ◽  
Lung Inflammation ◽  
Adaptor Protein ◽  
Airway Hyperreactivity ◽  
Cell Hyperplasia ◽  
Chemokine Production ◽  
Allergic Lung Inflammation ◽  
Dust Mite

T helper (Th)17 immune response participates in allergic lung inflammation and asthma is reduced in the absence of interleukin (IL)-17 in mice. Since IL-17A and IL-17F are induced and bind the shared receptor IL-17RA, we asked whether both IL-17A and IL-17F contribute to house dust mite (HDM) induced asthma. We report that allergic lung inflammation is attenuated in absence of either IL-17A or IL-17F with reduced airway hyperreactivity, eosinophilic inflammation, goblet cell hyperplasia, cytokine and chemokine production as found in absence of IL-17RA. Furthermore, specific antibody neutralization of either IL-17A or IL-17F given during the sensitization phase attenuated allergic lung inflammation and airway hyperreactivity. In vitro activation by HDM of primary dendritic cells revealed a comparable induction of CXCL1 and IL-6 expression and the response to IL-17A and IL-17F relied on IL-17RA signaling via the adaptor protein act1 in fibroblasts. Therefore, HDM-induced allergic respiratory response depends on IL-17RA via act1 signaling and inactivation of either IL-17A or IL-17F is sufficient to attenuate allergic asthma in mice.

scholarly journals Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Luiz Henrique C. Vasconcelos ◽  
Maria da Conceição C. Silva ◽  
Alana C. Costa ◽  
Giuliana A. de Oliveira ◽  
Iara Leão Luna de Souza ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pigs ◽  
Lung Inflammation ◽  
Inflammatory Infiltrate ◽  
Coconut Oil ◽  
Airway Hyperreactivity ◽  
Epithelial Hyperplasia ◽  
Virgin Coconut Oil ◽  
Allergic Lung Inflammation ◽  
Inducible Nos

Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. Therefore, the virgin coconut oil supplementation reverses peribronchial inflammatory infiltrate, epithelial hyperplasia, smooth muscle thickening, and hypercontractility through oxidative stress and its interactions with the NO pathway.

scholarly journals Endogenous Attenuation of Allergic Lung Inflammation by Syndecan-1

2005 ◽  
Vol 174 (9) ◽  
pp. 5758-5765 ◽  
Author(s):  
Jie Xu ◽  
Pyong Woo Park ◽  
Farrah Kheradmand ◽  
David B. Corry
Keyword(s):  
Lung Inflammation ◽  
Allergic Lung Inflammation

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.

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