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Expression of Th‐2 cytokines interleukin‐4 and −5 and of Th‐1 cytokine interferon‐γ in ovalbumin‐exposed sensitized Brown‐Norway rats
Author(s) -
HACZKU A.,
MACARY P.,
HADDAD E.B.,
HUANG T. J.,
KEMENY D. M.,
MOQBEL R.,
CHUNG K. F.
Publication year - 1996
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.1996.tb00011.x
Subject(s) - ovalbumin , bronchoalveolar lavage , cytokine , interleukin 4 , interferon gamma , immunology , interleukin , interleukin 5 , endocrinology , proinflammatory cytokine , medicine , chemistry , inflammation , lung , immune system
Summary We determined the expression of Th‐2 type cytokines, interleukin‐4 (IL‐4) and IL‐5, and of the Th‐1 type cytokine, interferon‐γ (IFN‐γ), in the Brown‐Norway rat. Rats were intraperitoneally sensitized with ovalbumin and 21 days later were either exposed to ovalbumin or saline aerosol. The value—log PC 300 (PC 300 = concentration of acetylcholine needed to increase baseline lung resistance by 300%) was 2·49 ± 0·15 in sensitized, exposed rats, was higher than in sensitized, saline‐exposed or naive rats (1·54 ± 0·27 and 1·63 ± 0·06 respectively, P < 005). There was a significant increase in eosinophils in bronchoalveolar lavage fluid and in airway submucosal airway tissues in the sensitized exposed group. Reverse‐transcriptase polymerase chain reaction was performed on total lung RNA using primers for IL‐4, IL‐5, IFN‐γ and β‐actin. IL‐4 and IL‐5 mRNA levels in control and sensitized saline‐exposed rats were not detectable, but increased levels were found in sensitized and ovalbumin‐exposed rats with levels of 0·25 ± 0·01 and 0·98 ± 0·02% of β‐actin mRNA as assessed by densitometric measurements. Expression of IFN‐γ mRNA was significantly reduced in sensitized and ovalbumin‐exposed rats. As in asthmatic airways, there is an increased expression of Th‐2 cytokines, IL‐4 and IL‐5, together with a reduction in the Th‐1 cytokine, IFN‐γ, thus supporting a role for Th‐2 cytokines in allergic eosinophilic inflammation.