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Systemic endotoxin suppresses established airway allergic inflammation and airway hyperreactivity via nitric oxide synthase 2 activity (2003)

• Authors:
  • Rodriguez, D.
  • Macedo, Mahasti Sahihi de
  • Keller, A. C.
  • Faquim-Mauro, Eliana Lima
  • Vargaftig, Bernardo Boris Jorge
  • Russo, Momtchilo
• USP affiliated authors: MACEDO, MAHASTI SAHIHI DE - ICB ; RUSSO, MOMTCHILO - ICB
• Unidade: ICB
• Assunto: IMUNOLOGIA
• Language: Português
• Abstract: AIM: Asthma results from an intrapulmonary allergen-driven Th2 response, and is characterized by intermittent airway obstruction, airway hyperreactivity (AHR), and airway inflammation. Either microbial infections, or local administration of the type 1 cytokines, -IL-12 and IFN-g, can prevent allergic responses. The same agents induce nitric oxide (NO) production. In the present work we investigated the effect of bacterial lipopolysaccharide (LPS) on asthma-like responses evaluated by the pulmonary inflammatory reaction, specific antibodies production, cytokine secretion in BAL, mucus secretion by bronchial epithelial cells and AHR determination. METHODS and RESULTS: mice were immunized on days 0 and 7 with 4µgOVA/1,6mgAlum, and challenged on days 14 and 21 with intranasal (i.n.) OVA. Concomitantly with the last OVA challenge, groups of animals were treated with local (i.n.) or systemic (i.v.) LPS.The experiments were performed on day 22. We have found that systemic or local LPS administration suppressed multiple effectors responses of asthma. However, AHR was only blocked by i.v. but not i.n. LPS administration. The suppressive activity of LPS on airway eosinophilic inflammation, mucus production and type 2 cytokine synthesis persisted in IL-12 or IFN-g knockout mouse strains. However, in mice lacking NO synthase 2 (iNOS), the suppressive effects of LPS were not observed. CONCLUSION: These findings identify iNOS as a keyenzyme involved in the suppression of asthma-like responses induced by LPS and suggest that NO inducers may represent a therapeutic strategy for the control of allergic diseases
• Imprenta:
  • Publisher: Comissão de Pesquisa do ICB/USP
  • Publisher place: São Paulo
  • Date published: 2003
• Source:
  • Título: Resumos
• Conference titles: Congresso Instituto Ciências Biomédicas, IV

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How to cite

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• ABNT

  RODRIGUEZ, D. et al. Systemic endotoxin suppresses established airway allergic inflammation and airway hyperreactivity via nitric oxide synthase 2 activity. 2003, Anais.. São Paulo: Comissão de Pesquisa do ICB/USP, 2003. . Acesso em: 26 jan. 2026.

• APA

  Rodriguez, D., Macedo, M. S. de, Keller, A. C., Faquim-Mauro, E. L., Vargaftig, B. B. J., & Russo, M. (2003). Systemic endotoxin suppresses established airway allergic inflammation and airway hyperreactivity via nitric oxide synthase 2 activity. In Resumos. São Paulo: Comissão de Pesquisa do ICB/USP.

• NLM

  Rodriguez D, Macedo MS de, Keller AC, Faquim-Mauro EL, Vargaftig BBJ, Russo M. Systemic endotoxin suppresses established airway allergic inflammation and airway hyperreactivity via nitric oxide synthase 2 activity. Resumos. 2003 ;[citado 2026 jan. 26 ]

• Vancouver

  Rodriguez D, Macedo MS de, Keller AC, Faquim-Mauro EL, Vargaftig BBJ, Russo M. Systemic endotoxin suppresses established airway allergic inflammation and airway hyperreactivity via nitric oxide synthase 2 activity. Resumos. 2003 ;[citado 2026 jan. 26 ]

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