[Effect of exposure to allergen through different duration on a rat asthmatic model].
OBJECTIVE
To investigate the effect of exposure to allergen (ovalbumin, OVA) at different times in infancy on the asthmatic airway inflammation of adult rats, and its possible mechanisms.


METHODS
Newborn rats were classified as asthma model group, day 3, day 7, day 14 after birth allergen exposure groups and control group, and were injected with OVA 1 mg (containing aluminum hydroxide gel 5 mg) subcutaneously on days 3, 7 and 14 after birth respectively. When all rats were kept till six weeks old, all groups but the control group were immunized and provoked via OVA to make asthma model. The pathologic changes of lung tissue and the hyperplasia of mucous cells per bronchiole were observed. The percentage of CD4(+)CD25(+)T cells and forkhead box P3 (Foxp3) transcription factor mRNA in the splenocytes and thymocytes were also measured.


RESULTS
The airway inflammation alleviated significantly and number of mucous cells per bronchiole decreased significantly in day 3 group [(2.29 +/- 0.49) vs(3.50 +/- 0.76),P<0.01] and day 7 group[(1.25+/-0.46) vs (3.50 +/-0.76), P<0.01] compared with asthma group. However, the hyperplasia of mucous cells did not alleviate significantly in day 14 group [(3.00+/-1.16) vs( 3.50+/-0.76), P>0.05]. The CD4(+)CD25(+)T cells and Foxp3 mRNA in the splenocytes increased in day 3 group[(13.68+/-3.54)% vs (7.33+/-3.39)%, P<0.01; (18.46+/-5.01) vs (5.49+/-1.99), P<0.01] and day 7 group [(16.65+/-4.91)% vs (7.33+/-3.39)%,P<0.01; (26.37+/-4.68 )vs( 5.49plusmn;1.99), P<0.01]compared with control group, so did Foxp3 mRNA in thymus in day 7 group [(18.73+/-3.66) vs( 11.13 +/-1.75), P<0.01].But neither the CD4(+)CD25(+)T cells[(11.04+/-2.88)% vs (7.33+/-3.39)%, P>0.05] nor Foxp3 mRNA expression[(8.71 +/- 2.19) vs( 5.49+/-1.99), P>0.05] had a statistically significant increase in day 14 group.


CONCLUSIONS
There exists a "time-window" for inhibiting airway inflammation by early exposure to allergen in the rat asthma model. The possible mechanism could be associated with induced generation of regulatory T cells.
Department of Respiratory Medicine, Peking University First Hospital, Beijing, China.
Yan
Y
Hu
Yun
Y
An
He
H
Huang
Hong Jun
HJ
Hao
Li
L
Su
Yue Dan
YD
Wang
Xin Min
XM
Liu
Hai Chao
HC
Li
D000818:Animals; D000831:Animals, Newborn; D001249:Asthma / Q000139:chemically induced / Q000276:immunology; D004195:Disease Models, Animal; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D010047:Ovalbumin; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D013997:Time Factors
D051858:Forkhead Transcription Factors; C500522:Foxp3 protein, rat; D012333:RNA, Messenger; D010047:Ovalbumin