LOGIN TO YOUR ACCOUNT

Username
Password
Remember Me
Or use your Academic/Social account:

CREATE AN ACCOUNT

Or use your Academic/Social account:

Congratulations!

You have just completed your registration at OpenAire.

Before you can login to the site, you will need to activate your account. An e-mail will be sent to you with the proper instructions.

Important!

Please note that this site is currently undergoing Beta testing.
Any new content you create is not guaranteed to be present to the final version of the site upon release.

Thank you for your patience,
OpenAire Dev Team.

Close This Message

CREATE AN ACCOUNT

Name:
Username:
Password:
Verify Password:
E-mail:
Verify E-mail:
*All Fields Are Required.
Please Verify You Are Human:
fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Corteling, R.; Wyss, D.; Trifilieff, A. (2002)
Publisher: BioMed Central
Journal: BMC Pharmacology
Languages: English
Types: Article
Subjects: Methodology Article
BACKGROUND: Evidence suggests that both the migration and activation of neutrophils into the airway is of importance in pathological conditions such as pulmonary emphysema. In the present study, we describe in vivo models of lung neutrophil infiltration and activation in mice and hamsters. RESULTS: BALB/c and C57BL/6 mice were intranasally treated with lipopolysaccharide (0.3 mg/kg). Twenty-four hours after, animals were treated intranasally with N-Formyl-Met-Leu-Phe (0 to 5 mg/kg). Golden Syrian hamsters were treated intratracheally with 0.5 mg/kg of lipopolysaccharide. Twenty-four hours after, animals were treated intratracheally with 0.25 mg/kg of N-Formyl-Met-Leu-Phe. Both mice and hamster were sacrificed two hours after the N-Formyl-Met-Leu-Phe application. In both BALB/c and C57BL/6 mice, a neutrophil infiltration was observed after the sequential application of lipopolysaccharide and N-Formyl-Met-Leu-Phe. However, 5 times less neutrophil was found in C57BL/6 mice when compared to BALB/c mice. This was reflected in the neutrophil activation parameters measured (myeloperoxidase and elastase activities). Despite the presence of neutrophil and their activation status, no lung haemorrhage could be detected in both strains of mice. When compared with mice, the lung inflammation induced by the sequential application of lipopolysaccharide and N-Formyl-Met-Leu-Phe was much greater in the hamster. In parallel with this lung inflammation, a significant lung haemorrhage was also observed. CONCLUSIONS: Both mouse and hamster can be used for pharmacological studies of new drugs or other therapeutics agents that aimed to interfere with neutrophil activation. However, only the hamster model seems to be suitable for studying the haemorrhagic lung injury process
  • The results below are discovered through our pilot algorithms. Let us know how we are doing!

    • 1. Snider GL, Ciccolella DE, Morris SM, Stone PJ, Lucey EC: Putative role of neutrophil elastase in the pathogenesis of emphysema. Ann N Y Acad Sci 1991, 624:45-59
    • 2. Malech HL, Gallin JI: Current concepts: immunology. Neutrophils in human diseases. N Engl J Med 1987, 317:687-694
    • 3. Birkedal-Hansen H: Proteolytic remodeling of extracellular matrix. Curr Opin Cell Biol 1995, 7:728-735
    • 4. Yang RB, Mark MR, Gray A, Huang A, Xie MH, Zhang M, et al: Tolllike receptor-2 mediates lipopolysaccharide-induced cellular signalling. Nature 1998, 395:284-288
    • 5. Kips JC, Tavernier J, Pauwels RA: Tumor necrosis factor causes bronchial hyperresponsiveness in rats. Am Rev Respir Dis 1992, 145:332-336
    • 6. Lefort J, Singer M, Leduc D, Renesto P, Nahori MA, Huerre M, et al: Systemic administration of endotoxin induces bronchopulmonary hyperreactivity dissociated from TNF-alpha formation and neutrophil sequestration into the murine lungs. J Immunol 1998, 161:474-480
    • 7. Miotia JM, Teixeira MM, Hellewell PG: Suppression of acute lung injury in mice by an inhibitor of phosphodiesterase type 4. Am J Respir Cell Mol Biol 1998, 18:411-420
    • 8. Asti C, Ruggieri V, Porzio S, Chiusaroli R, Melillo G, Caselli GF: Lipopolysaccharide-induced lung injury in mice. I. Concomitant evaluation of inflammatory cells and haemorrhagic lung damage. Pulm Pharmacol Ther 2000, 13:61-69
    • 9. Panaro MA, Mitolo V: Cellular responses to FMLP challenging: a mini-review. Immunopharmacol Immunotoxicol 1999, 21:397-419
    • 10. Cavarra E, Martorana PA, Gambelli F, de Santi M, van Even P, Lungarella G: Neutrophil recruitment into the lungs is associated with increased lung elastase burden, decreased lung elastin, and emphysema in alpha 1 proteinase inhibitor-deficient mice. Lab Invest 1996, 75:273-280
    • 11. Olsen UB, Bille-Hansen V: Endotoxin pretreatment enhances neutrophil FMLP-receptor binding and activity in guinea pigs. Agents Actions 1987, 21:177-183
    • 12. Voelkel NF, Czartolomna J, Simpson J, Murphy RC: FMLP causes eicosanoid-dependent vasoconstriction and edema in lungs from endotoxin-primed rats. Am Rev Respir Dis 1992, 145:701- 711
    • 13. Holroyd KJ, Eleff SM, Zhang LY, Jakab GJ, Kleeberger SR: Genetic modeling of susceptibility to nitrogen dioxide-induced lung injury in mice. Am J Physiol 1997, 273:L595-L602
    • 14. Wesselkamper SC, Prows DR, Biswas P, Willeke K, Bingham E, Leikauf GD: Genetic susceptibility to irritant-induced acute lung injury in mice. Am J Physiol 2000, 279:L575-L582
    • 15. Mitsuhashi H, Asano S, Nonaka T, Masuda K, Kiyoki M: Potency of truncated secretory leukoprotease inhibitor assessed in acute lung injury models in hamsters. J Pharmacol Exp Ther 1997, 282:1005-1010
    • 16. Zanardo RC, Costa E, Ferreira HH, Antunes E, Martins AR, Murad F, et al: Pharmacological and immunohistochemical evidence for a functional nitric oxide synthase system in rat peritoneal eosinophils. Proc Natl Acad Sci USA 1997, 94:14111-14114
  • No related research data.
  • Discovered through pilot similarity algorithms. Send us your feedback.

Share - Bookmark

Cite this article