Effects of LTB4 receptor antagonism on pulmonary inflammation in rodents and non-human primates

Hicks, Alexandra; Goodnow, Robert A.; Cavallo, Gary; Tannu, Shahid; Ventre, Jessica D.; Lavelle, Danielle; Lora, José M.; Satjawatcharaphong, John; Brovarney, Martin; Dabbagh, Karim; Tare, Nadine S.; Oh, Hyesun; Lamb, Martin; Sidduri, Achyutharao; Dominique, Romyr; Qiao, Qi; Lou, Jian Ping; Gillespie, Paul; Fotouhi, Nader; Kowalczyk, Agnieszka; Kurylko, Grazyna; Hamid, Rachid; Wright, Matthew B.; Pamidimukkala, Anjula; Egan, Thomas M.; Gubler, Ueli; Hoffman, Ann F.; Wei, Xinyuan; Li, Ying L.; O’Neil, John J.; Marcano, Ruben; Pozzani, Karen; Molinaro, Tina; Santiago, Jennifer; Singer, Laura; Hargaden, Maureen; Moore, David; Catala, Anne; Chao, Lisa C. F.; Benson, Janet M.; March, Thomas H.; Radhika, V.; Mancebo, Helena; Renzetti, Louis M.

doi:10.1016/j.prostaglandins.2010.02.003

Cited by 25 publications

(19 citation statements)

References 37 publications

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“…However, the very long half-life of this drug has prevented its translation into clinical use 106 . The dual BLT 1 and BLT 2 antagonist RO5101576 inhibited allergen and ozone-induced BAL neutrophilia in non-human primates 107 .…”

Section: Specific Lo Pathway Productsmentioning

confidence: 94%

Lipid mediators and allergic diseases

Fanning

Boyce

2013

Annals of Allergy, Asthma & Immunology

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Section: Specific Lo Pathway Productsmentioning

confidence: 94%

Lipid mediators and allergic diseases

Fanning

Boyce

2013

Annals of Allergy, Asthma & Immunology

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“…However, so far clinical studies in COPD have been negative [98] and, generally, they have not been published. Interestingly, also the dual BLT1 and BLT2 receptor antagonism had no effects on LPS-evoked neutrophilia in guinea pigs and cigarette smoke-evoked neutrophilia in mice and rats [99].…”

Section: Review: Anti-inflammatory Strategies For Copdmentioning

confidence: 95%

Emerging anti-inflammatory strategies for COPD

et al. 2012

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“…This method does not allow for the measurements of the physiological responses to the allergen. Allergen inhalation challenge has become the mainstay for models of asthma developed in many species, including mice [34], rats [35], guinea pigs [36], dogs [37], rabbits [38] and primates [39].…”

Section: Allergen-induced Airway Responsesmentioning

confidence: 99%

Allergen-induced airway responses

2015

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Environmental allergens are an important cause of asthma and can contribute to loss of asthma control and exacerbations. Allergen inhalation challenge has been a useful clinical model to examine the mechanisms of allergen-induced airway responses and inflammation. Allergen bronchoconstrictor responses are the early response, which reaches a maximum within 30 min and resolves by 1-3 h, and late responses, when bronchoconstriction recurs after 3-4 h and reaches a maximum over 6-12 h. Late responses are followed by an increase in airway hyperresponsiveness. These responses occur when IgE on mast cells is cross-linked by an allergen, causing degranulation and the release of histamine, neutral proteases and chemotactic factors, and the production of newly formed mediators, such as cysteinyl leukotrienes and prostaglandin D 2 . Allergen-induced airway inflammation consists of an increase in airway eosinophils, basophils and, less consistently, neutrophils. These responses are mediated by the trafficking and activation of myeloid dendritic cells into the airways, probably as a result of the release of epithelial cell-derived thymic stromal lymphopoietin, and the release of pro-inflammatory cytokines from type 2 helper T-cells. Allergen inhalation challenge has also been a widely used model to study potential new therapies for asthma and has an excellent negative predictive value for this purpose. @ERSpublications Environmental allergens are an important cause of asthma

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Effects of LTB4 receptor antagonism on pulmonary inflammation in rodents and non-human primates

Cited by 25 publications

References 37 publications

Lipid mediators and allergic diseases

Lipid mediators and allergic diseases

Emerging anti-inflammatory strategies for COPD

Allergen-induced airway responses

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