Update in Asthma 2005

Wenzel, Sally E.; Covar, Ronina

doi:10.1164/rccm.2601007

Cited by 22 publications

(18 citation statements)

References 116 publications

(115 reference statements)

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“…Material of >95% purity was qualified using a synthetic LXA 4 standard by 1 H‐NMR, HPLC coinjection with photodiode array UV‐visible detection (two methods), and LC‐MS‐MS. HPLC analyses were carried out on a LUNA 5 µ C18(2) column (250×4.60 mm) using a gradient of methanol in water containing 0.1% acetic acid on a Varian ProStar HPLC equipped with a diode array detector. The plasma half‐life of ATLa after i.v.…”

Section: Methodsmentioning

confidence: 99%

Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

et al. 2007

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Cellular recruitment during inflammatory/immune responses is tightly regulated. The ability to dampen inflammation is imperative for prevention of chronic immune responses, as in asthma. Here we investigated the ability of lipoxin A4 (LXA4) stable analogs to regulate airway responses in two allergen-driven models of inflammation. A 15-epi-LXA4 analog (ATLa) and a 3-oxa-15-epi-LXA4 analog (ZK-994) prevented excessive eosinophil and T lymphocyte accumulation and activation after mice were sensitized and aerosol-challenged with ovalbumin. At <0.5 mg/kg, these LXA4 analogs reduced leukocyte trafficking into the lung by >50% and to a greater extent than equivalent doses of the CysLT1 receptor antagonist montelukast. Distinct from montelukast, ATLa treatment led to marked reductions in cysteinyl leukotrienes, interleukin-4 (IL-4), and IL-10, and both ATLa and ZK-994 inhibited levels of IL-13. In cockroach allergen-induced airway responses, both intraperitoneal and oral administration of ZK-994 significantly reduced parameters of airway inflammation and hyper-responsiveness in a dose-dependent manner. ZK-994 also significantly changed the balance of Th1/Th2-specific cytokine levels. Thus, the ATLa/LXA4 analog actions are distinct from CysLT1 antagonism and potently block both allergic airway inflammation and hyper-reactivity. Moreover, these results demonstrate these analogs' therapeutic potential as new agonists for the resolution of inflammation.

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Section: Methodsmentioning

confidence: 99%

Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

et al. 2007

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“…Furthermore, relapse after therapy withdrawal is common [12], and the effects of these drugs are not always satisfactory in clinical practice because of local or systemic side effects [13–15]. On the other hand, although corticosteroids improve asthma symptoms, they do not alter the progression of asthma or cure the disease [16].…”

Section: Introductionmentioning

confidence: 99%

Puerarin Attenuates Ovalbumin‐Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

Dong

Wang

Duan

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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Aim. We aimed to investigate and evaluate the preventive activity of puerarin on the ovalbumin-induced asthma rat model. Materials and Methods. Male Wistar rats were sensitized intraperitoneally on days 0, 7, and 14 and challenged to ovalbumin intratracheally on day 21. Groups of sensitized rats were treated randomly either with placebo, puerarin, dexamethasone, or puerarin combined with dexamethasone, from days 15 to 20. Inflammatory markers, including cell counts in bronchoalveolar lavage fluid (BALF), inflammatory cytokines, histopathology, and coagulation parameters, such as coagulation tests and the activity of coagulation factors, were analyzed. Results. Puerarin significantly inhibited the recruitment of inflammatory cells in BALF and lung tissue. At the same time, the release of IL-4, IL-10, and IFN-γ in serum and the expression of mRNAs in lung tissue homogenate were changed by puerarin. Administration of puerarin also effectively rectified the coagulation disorder in asthmatic rats, such as prothrombin time (PT) (P < 0.01), thrombin time (TT) (P < 0.05), fibrinogen (FIB) (P < 0.01),the activity of factor II (FII) (P < 0.01), the activity of factor V (FV) (P < 0.05), the activity of factor VII (FVII) (P < 0.05), the activity of factor X (FX) (P < 0.05), the activity of factor VIII (FVIII) (P < 0.01), the activity of factor IX (FIX) (P < 0.05), and the activity of factor XII (FXII) (P < 0.05). Conclusions. Our results provide a clue that puerarin was useful for the preventive of allergic airway disease in rodents.

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“…1,2 However, the specific mechanisms that mediate its induction and persistence are unclear. Patients with severe asthma have major handicaps in their daily life, and their care accounts for most of the health care costs associated with asthma.…”

mentioning

confidence: 99%

An ex vivo model of severe asthma using reconstituted human bronchial epithelium

Gras

Bourdin

Vachier

et al. 2012

Journal of Allergy and Clinical Immunology

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Update in Asthma 2005

Cited by 22 publications

References 116 publications

Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

Puerarin Attenuates Ovalbumin‐Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

An ex vivo model of severe asthma using reconstituted human bronchial epithelium

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Update in Asthma 2005

Cited by 22 publications

References 116 publications

Lipoxin A4stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

Lipoxin A4stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

Puerarin Attenuates Ovalbumin‐Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

An ex vivo model of severe asthma using reconstituted human bronchial epithelium

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Product

Resources

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Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism

Lipoxin A₄stable analogs reduce allergic airway responsesviamechanisms distinct from CysLT1 receptor antagonism