IL-37 inhibits IL-4/IL-13-induced CCL11 production and lung eosinophilia in murine allergic asthma

Allergy ◽  
2018 ◽  
Vol 73 (8) ◽  
pp. 1642-1652 ◽  
Author(s):  
J. Lv ◽  
Y. Xiong ◽  
W. Li ◽  
X. Cui ◽  
X. Cheng ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Lung Eosinophilia

Preclinical Safety and Pharmacology of an Anti-Human Interleukin-13 Monoclonal Antibody in Normal Macaques and in Macaques with Allergic Asthma

2008 ◽  
Vol 27 (5) ◽  
pp. 351-358 ◽  
Author(s):  
Pauline L. Martin ◽  
Dusti Fisher ◽  
William Glass ◽  
Karyn O’Neil ◽  
Anuk Das ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Allergic Asthma ◽  
Immunoglobulin E ◽  
Cynomolgus Macaque ◽  
Lavage Fluid ◽  
Antigen Challenge ◽  
Interleukin 13 ◽  
Lung Eosinophilia

Interleukin-13 (IL-13) plays a central role in chronic airway diseases, including asthma. These studies were conducted to evaluate the safety of administration of a human anti-IL-13 monoclonal antibody (mAb) to normal macaques and in macaques with allergic asthma. In addition, serum and bronchioalveolar lavage fluid were collected from allergic cynomolgus macaques in order to identify potential surrogate markers of IL-13 pharmacology that could be useful for subsequent clinical trials. In vitro studies demonstrated that the anti-IL-13 mAb inhibited the pharmacological actions of both human and cynomolgus macaque IL-13. Allergic macaques were treated systemically with 10 mg/kg anti-IL-13 mAb 1 day prior to inhaled Ascaris suum antigen challenge. Normal macaques were dosed intravenously with anti-IL-13 once per week for 3 weeks at doses of 10 or 50 mg/kg. Treatment of macaques with the anti-IL-13 mAb was not associated with any toxicologically significant findings. A slight treatment-related but nonadverse decrease in platelet counts was observed in both the normal and allergic macaques. In allergic macaques, the anti-IL-13 mAb treatment did not affect lung function, lung eosinophilia, or serum or BAL immunoglobulin E (IgE) concentrations but did produce a reduction in BAL and serum eotaxin concentrations ( p < .05) at 6 h post antigen challenge. This study shows that administration of an anti-IL-13 mAb was well tolerated in both normal and allergic asthmatic macaques and that serum eotaxin concentrations may be a useful early in vivo marker for evaluating IL-13 inhibition in patients with asthma.

Dietary lycopene supplementation suppresses Th2 responses and lung eosinophilia in a mouse model of allergic asthma

2011 ◽  
Vol 22 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Leia C. Hazlewood ◽  
Lisa G. Wood ◽  
Philip M. Hansbro ◽  
Paul S. Foster
Keyword(s):  
Mouse Model ◽  
Allergic Asthma ◽  
Th2 Responses ◽  
Lung Eosinophilia

scholarly journals CD4+CD25+ Regulatory T Cells Decreased CD8+IL-4+Cellsin a Mouse Model of Allergic Asthma

2019 ◽  
Author(s):  
Ping Li ◽  
Ze Li ◽  
Guqin Zhang ◽  
Jiong Yang ◽  
Junwen Chen
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Cell Sorting ◽  
Cytotoxic T Cells ◽  
Specific Ige ◽  
Asthma Model ◽  
Cytokine Levels ◽  
Lung Eosinophilia

Interleukin (IL)-4-producing-CD8 (cytotoxic T cells, Tc) contribute to lung eosinophilia and airway hyper-responsiveness (AHR) to an antigen. CD4+CD25+ regulatory T cells (Tregs) attenuate airway inflammation and AHR. This study investigated whether Tregs decrease Tc2frequencies in ovalbumin (OVA)-induced asthma model of mice.  Female C57BL/6 mice were sensitized with OVA intraperitoneally and challenged with OVA intranasally to induce allergic asthma model. Tregs were sorted by fluorescence activated cell sorting (FACS) and magnetic activated cell sorting (MACS) microbeads. OVA-sensitized mice were injected with Tregs or phosphate buffer saline (PBS) by tail vein ahead of the first challenge. Airway inflammation and airway hyper-responsiveness (AHR)were evaluated by histological analysis and invasive method, respectively. OVA-specific IgE and cytokine levels were detected by ELISA. Flow cytometry was used to detect the percentages of Tc1 and Tc2. Gata3 and T-bet mRNA was determined by quantitative PCR (qPCR). OVA-sensitized and challenged mice displayed typical asthma features, which included eosinophilic airway inflammation, higher levels of Th2 cytokines and AHR. Gata3 mRNA, Tc2 frequencies and OVA-specific IgE levels were significantly increased in OVA-sensitized and challenged mice. Compared to PBS treatment, Tregs decreased Tc2 frequencies, airway inflammation, Th2 cytokine levels and AHR in OVA-sensitized and challenged mice. IL-13 levels were negatively correlated with Tc1 frequencies and with IFNg levels in experimental mice. Our results demonstrated that Tregs could prevent airway inflammation and AHR by decreasing Tc2 frequencies and cytokine levels in OVA-induced asthma model of mice, supporting Tregmight be as a potent therapeutic target for alleviating airway inflammation and AHR.

Sequential degranulation of eosinophils induced by antigen or autocoids in allergic humans

1986 ◽  
Vol 44 ◽  
pp. 354-355
Author(s):  
Kate W. Sjoerdsma ◽  
W. James Metzger
Keyword(s):  
Allergic Rhinitis ◽  
Bronchoalveolar Lavage ◽  
Allergic Asthma ◽  
Skin Test ◽  
Positive Skin Test ◽  
Positive Skin ◽  
Human Eosinophil ◽  
Asthmatic Patients ◽  
Allergic Asthmatic ◽  
History Of

Eosinophils are important to the pathogenesis of allergic asthma, and are increased in bronchoalveolar lavage within four hours after bronchoprovocation of allergic asthmatic patients, and remain significantly increased up to 24 hours later. While the components of human eosinophil granules have been recently isolated and purified, the mechanisms of degranulation have yet to be elucidated.We obtained blood from two volunteers who had a history of allergic rhinitis and asthma and a positive skin test (5x5mm wheal) to Alternaria and Ragweed. Eosinophils were obtained using a modification of the method described by Roberts and Gallin.

Therapy of allergic asthma

2001 ◽  
Vol 58 (5) ◽  
pp. 315-320
Author(s):  
C. Bucher ◽  
E. W. J. Russi
Keyword(s):  
Allergic Asthma ◽  
Medikamentöse Therapie ◽  
Asthma Bronchiale ◽  
Spezifische Immuntherapie ◽  
Medikamentöse Behandlung

Asthma bronchiale ist eine chronische entzündliche Erkrankung der Atemwege, die gehäuft bei Atopikern auftritt. Die Therapie des allergischen Asthma bronchiale stützt sich auf drei Pfeiler: Das Vermeiden einer Allergenexposition, eine medikamentöse Therapie sowie in ausgewählten Fällen eine spezifische Immuntherapie (SIT). Ein völliges Meiden des Allergenkontaktes ist in der Regel nicht zu erreichen, weshalb die meisten Asthmatiker eine medikamentöse Behandlung benötigen. Dafür stehen moderne und wirksame Medikamente zur Verfügung. Die SIT hat sich vor allem bei der Pollenallergie bewährt. Wegen des in der Regel chronischen und wechselhaften Verlaufs sowie mitunter lebensbedrohlichen Situationen sollte der Patient über die Natur der Erkrankung, die Therapie, notwendige Kontrollen, sowie Maßnahmen bei einer plötzlichen Verschlechterung sorgfältig instruiert werden. Allgemein gilt für die Therapie des Asthma bronchiale, dass die Compliance des Patienten für den Therapieerfolg entscheidend ist.

TLR ligands alter the phenotype of experimental acute allergic asthma in mice

Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
L Lunding ◽  
C Vock ◽  
H Fehrenbach ◽  
M Wegmann
Keyword(s):  
Allergic Asthma

Distribution and efficacy of a GATA-3-specific DNAzyme in experimental allergic asthma models

Pneumologie ◽  
2012 ◽  
Vol 66 (06) ◽  
Author(s):  
A Turowska ◽  
T Dicke ◽  
N Baumgartl ◽  
J Kuhlmann ◽  
H Renz ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Experimental Allergic Asthma ◽  
Experimental Allergic

Mechanism of bronchopulmonary C-fiber hyperexcitability in allergic asthma: Loss of TRPV1 inhibition by GDNF downregulation?

Pneumologie ◽  
2012 ◽  
Vol 66 (06) ◽  
Author(s):  
R Nandigama ◽  
A Weske ◽  
S Wiegand ◽  
W Kummer ◽  
C Nassenstein
Keyword(s):  
Allergic Asthma ◽  
C Fiber
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