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Updated: Aug 14, 2026

Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
[Effects of interleukin-18 on asthmatic airway inflammation: experimental study of guinea pig asthmatic model]
1Department of Respiratory Diseases, Union Hospital, Fujian Medical University, Fuzhou 350001, China.
Objective:
To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation.
Methods:
Thirty healthy adult male guinea pigs were randomly divided into 3 equal groups: asthmatic model group (Group A, undergoing intraperitoneally injection of ovalbumin (OVA) once and spraying of OVA aerosol once a day for 5 days; control group (Group B), undergoing intraperitoneally injection of OVA once and spraying of normal saline aerosol once a day for 5 days; and interleukin (IL)-18 intervention group (Group C, undergoing intraperitoneally injection of OVA once and intraperitoneal injection of IL-18 on the days 1, 3, 8. 10. 15, 17, and 19. Twenty-four hours after the final spraying or IL-18 injection the bronchalveolar lavage fluid (BALF) of the left lungs were obtained. HE staining was conducted to the sediment to examine the numbers of eosinophils, neutrophils, and monocytes. ELISA was used to detect the Th1/Th2 cytokines in the BALF. The left lungs underwent pathological examination.
Results:
The number of EOS in BALF of Groups A was (98 +/- 58) x 10(6)/L, significantly higher than those of Group B, (12 +/- 10) x 10(6)/L, and Group C, (29 +/- 10) x 10(6)/L (P < 0.01 and P < 0.05). The numbers of neutrophils in the BALF of Group A was (24 +/- 16) x 10(6)/L, significantly higher than those of Group B and C [(9 +/- 7) x 10(6)/L and (10 +/- 5) x 10(6)/L respectively, both P < 0.05]. The concentration of IFN-gamma and IL-2 in group A were both significantly lower than those of Group B and Group C (P < 0.05 and P < 0.01). The concentration of IL-4 in Group A was significantly higher than those of Groups B and C (both P < 0.05). The concentration of IL-5 of Group A was significantly higher than those of Group Bs and C (both P < 0.01).
Conclusion:
IL-18 effectively inhibits asthmatic airway inflammation by regulating the Th1/Th2 balance.
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