Literature DB >> 20007928

Inducible nitric oxide synthase/CD95L-dependent suppression of pulmonary and bone marrow eosinophilia by diethylcarbamazine.

Tulio Queto1, Pedro Xavier-Elsas, Marcelo Aranha Gardel, Bianca de Luca, Mônica Barradas, Daniela Masid, Patricia Machado R E Silva, Christina A Peixoto, Zilton Meira F Vasconcelos, Eliane P Dias, Maria Ignez Gaspar-Elsas.   

Abstract

RATIONALE: The mechanism of action of diethylcarbamazine (DEC), an antifilarial drug effective against tropical pulmonary eosinophilia, remains controversial. DEC effects on microfilariae depend on inducible NO synthase (iNOS). In eosinophilic pulmonary inflammation, its therapeutic mechanism has not been established. We previously described the rapid up-regulation of bone marrow eosinophilopoiesis in ovalbumin (OVA)-sensitized mice by airway allergen challenge, and further evidenced the down-regulation of eosinophilopoiesis by iNOS- and CD95L-dependent mechanisms.
OBJECTIVES: We investigated whether: (1) DEC can prevent the effects of airway challenge of sensitized mice on lungs and bone marrow, and (2) its effectiveness depends on iNOS/CD95L.
METHODS: OVA-sensitized BALB/c mice were intranasally challenged for 3 consecutive days, with DEC administered over a 12-, 3-, or 2-day period, ending at the day of the last challenge. We evaluated: (1) airway resistance, cytokine (IFN-gamma, IL-4, IL-5, and eotaxin) production, and pulmonary eosinophil accumulation; and (2) bone marrow eosinophil numbers in vivo and eosinophil differentiation ex vivo.
MEASUREMENTS AND MAIN RESULTS: DEC effectively prevented the effects of subsequent challenges on: (1) airway resistance, Th1/Th2 cytokine production, and pulmonary eosinophil accumulation; and (2) eosinophilopoiesis in vivo and ex vivo. Recovery from unprotected challenges included full responses to DEC during renewed challenges. DEC directly suppressed IL-5-dependent eosinophilopoiesis in naive bone marrow. DEC was ineffective in CD95L-deficient gld mice and in mice lacking iNOS activity because of gene targeting or pharmacological blockade.
CONCLUSIONS: DEC has a strong impact on pulmonary eosinophilic inflammation in allergic mice, as well as on the underlying hemopoietic response, suppressing the eosinophil lineage by an iNOS/CD95L-dependent mechanism.

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Year:  2009        PMID: 20007928     DOI: 10.1164/rccm.200905-0800OC

Source DB:  PubMed          Journal:  Am J Respir Crit Care Med        ISSN: 1073-449X            Impact factor:   21.405


  15 in total

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Authors:  Maria Ignez Gaspar-Elsas; Túlio Queto; Daniela Masid-de-Brito; Bruno Marques Vieira; Bianca de Luca; Fernando Queiroz Cunha; Pedro Xavier-Elsas
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6.  Blockage of Eosinopoiesis by IL-17A Is Prevented by Cytokine and Lipid Mediators of Allergic Inflammation.

Authors:  Pedro Xavier-Elsas; Bianca de Luca; Túlio Queto; Bruno Marques Vieira; Daniela Masid-de-Brito; Elizabeth Chen Dahab; José Carlos Alves Filho; Fernando Q Cunha; Maria Ignez C Gaspar-Elsas
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Review 8.  Repurposing Pharmaceuticals Previously Approved by Regulatory Agencies to Medically Counter Injuries Arising Either Early or Late Following Radiation Exposure.

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10.  Essential roles of PKA, iNOS, CD95/CD95L, and terminal caspases in suppression of eosinopoiesis by PGE2 and other cAMP-elevating agents.

Authors:  Bianca de Luca; Pedro Xavier-Elsas; Mônica Barradas; Ricardo A Luz; Túlio Queto; Carla Jones; Maria Augusta Arruda; Thiago Mattar Cunha; Fernando Queiroz Cunha; Maria Ignez Gaspar-Elsas
Journal:  ScientificWorldJournal       Date:  2013-11-24
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