中国免疫学杂志
中國免疫學雜誌
중국면역학잡지
CHINESE JOURNAL OF IMMUNOLOGY
2014年
10期
1353-1359
,共7页
朱喜玲%胡微煦%吴梨华%文珠%何丹%吴晓牧%胡国柱
硃喜玲%鬍微煦%吳梨華%文珠%何丹%吳曉牧%鬍國柱
주희령%호미후%오리화%문주%하단%오효목%호국주
过敏性鼻炎%豚鼠%卵白蛋白%肿瘤坏死因子%白细胞介素
過敏性鼻炎%豚鼠%卵白蛋白%腫瘤壞死因子%白細胞介素
과민성비염%돈서%란백단백%종류배사인자%백세포개소
Allergic rhinitis%Guinea pigs%Ovalbumin%TNF-α%IL-1β
目的:探讨抗TNF-α和IL-1βIgY治疗豚鼠过敏性鼻炎的作用及机制。方法:随机分正常对照组( C组,17只)、模型组( M组,27只)、0.1%抗TNF-α和IL-1βIgY治疗组( Z1组,21只)、丙酸氟替卡松治疗组( Z2组,21只);应用卵清白蛋白建立豚鼠过敏性鼻炎模型;分别在治疗后2、4、8 h进行鼻灌洗和支气管肺灌洗,收集鼻灌洗液( NLF)和支气管肺泡灌洗液(BALF),观察炎症细胞;HE染色观察鼻黏膜和肺组织病理改变;免疫组化分析其炎症因子原位表达情况。结果:M组鼻黏膜可见大量嗜酸性粒细胞浸润和炎症改变,肺间质水肿、肺间隔和支气管平滑肌增厚,嗜酸性粒细胞浸润, Z1组和Z2组炎症病理改变明显减轻。 NLF和BALF中嗜酸性粒细胞、淋巴细胞、中性粒细胞在Z1和Z2组显著少于M组( P<0.05)。 Z1组鼻黏膜IL-1β和肺组织IL-1β和TNF-α从2 h开始,而IL-5和IL-33从4 h开始表达显著低于M组( P<0.05)。结论:抗TNF-α和IL-1βIgY滴鼻治疗显著减轻了豚鼠过敏性鼻炎伴过敏性支气管哮喘的炎症病理反应,抑制了嗜酸性粒细胞浸润及炎症细胞因子表达。
目的:探討抗TNF-α和IL-1βIgY治療豚鼠過敏性鼻炎的作用及機製。方法:隨機分正常對照組( C組,17隻)、模型組( M組,27隻)、0.1%抗TNF-α和IL-1βIgY治療組( Z1組,21隻)、丙痠氟替卡鬆治療組( Z2組,21隻);應用卵清白蛋白建立豚鼠過敏性鼻炎模型;分彆在治療後2、4、8 h進行鼻灌洗和支氣管肺灌洗,收集鼻灌洗液( NLF)和支氣管肺泡灌洗液(BALF),觀察炎癥細胞;HE染色觀察鼻黏膜和肺組織病理改變;免疫組化分析其炎癥因子原位錶達情況。結果:M組鼻黏膜可見大量嗜痠性粒細胞浸潤和炎癥改變,肺間質水腫、肺間隔和支氣管平滑肌增厚,嗜痠性粒細胞浸潤, Z1組和Z2組炎癥病理改變明顯減輕。 NLF和BALF中嗜痠性粒細胞、淋巴細胞、中性粒細胞在Z1和Z2組顯著少于M組( P<0.05)。 Z1組鼻黏膜IL-1β和肺組織IL-1β和TNF-α從2 h開始,而IL-5和IL-33從4 h開始錶達顯著低于M組( P<0.05)。結論:抗TNF-α和IL-1βIgY滴鼻治療顯著減輕瞭豚鼠過敏性鼻炎伴過敏性支氣管哮喘的炎癥病理反應,抑製瞭嗜痠性粒細胞浸潤及炎癥細胞因子錶達。
목적:탐토항TNF-α화IL-1βIgY치료돈서과민성비염적작용급궤제。방법:수궤분정상대조조( C조,17지)、모형조( M조,27지)、0.1%항TNF-α화IL-1βIgY치료조( Z1조,21지)、병산불체잡송치료조( Z2조,21지);응용란청백단백건립돈서과민성비염모형;분별재치료후2、4、8 h진행비관세화지기관폐관세,수집비관세액( NLF)화지기관폐포관세액(BALF),관찰염증세포;HE염색관찰비점막화폐조직병리개변;면역조화분석기염증인자원위표체정황。결과:M조비점막가견대량기산성립세포침윤화염증개변,폐간질수종、폐간격화지기관평활기증후,기산성립세포침윤, Z1조화Z2조염증병리개변명현감경。 NLF화BALF중기산성립세포、림파세포、중성립세포재Z1화Z2조현저소우M조( P<0.05)。 Z1조비점막IL-1β화폐조직IL-1β화TNF-α종2 h개시,이IL-5화IL-33종4 h개시표체현저저우M조( P<0.05)。결론:항TNF-α화IL-1βIgY적비치료현저감경료돈서과민성비염반과민성지기관효천적염증병리반응,억제료기산성립세포침윤급염증세포인자표체。
Objective:To investigate therapeutic mechanism of immunoglobulin Yolk (IgY) against tumour necrosis factor alpha ( TNF-α) and interleukin-1 beta ( IL-1β) in guinea pigs with allergic rhinitis.Methods: Hartley guinea pigs were randomly divided into the control group (group C,n=17),the allergic rhinitis model group (group M,n=27),the 0.1%anti-TNF-αand IL-1βIgY treating group (group Z1,n=21) and the fluticasone propionate treating group (group Z2,n=21).The allergic rhinitis model in guinea pigs was established using ovalbumin.After treatment for 2 h,4 h,8 h,nose and bronchial lung were lavaged using 0.9%saline, the nasal lavage fluid (NLF) and bronchoalveolar lavage fluid (BALF) were collected,the precipitated cells were stained using Wright′s,the nasal mucosa and lung tissues were stained using methylene blue and eosin (HE),and TNF-α,IL-1β,IL-5 and IL-33 in nasal mucosa and lung tissues were stained using immunohistochemistry.Results:There were a large amount of eosinophils and more serious inflammation responses in nasal mucosa in the M group compared with the Z 1 and Z2 groups.In the lung tissues,there were more alveolar tube damage ,pulmonary interstitial edema ,interval thickening ,thickening of bronchial smooth muscle and inflammation cell in-filtration in the M group compared with the Z 1 and Z2 groups.The eosinophils ,lymphocytes and neutrophils were significantly decreased in NLF and BALF in the Z1 and Z2 groups compared with the M group (P<0.05).The expressions of IL-1βand TNF-αfrom 2 h to 8 h and IL-5 and IL-33 from 4 h to 8 h significantly decreased in the nasal mucosa and lung tissues in the Z 1 group compared with the M group ( P<0.05 ).Conclusion:The allergic rhinitis in guinea pigs accompany with the allergic asthma.The inhibitory capacity of anti-TNF-αand IL-1βIgY on pathological responses in guinea pigs with allergic rhinitis may be due to the significant decrease in the infiltration of eosinophils and the expressions of inflammatory cytokines in the nasal mucosas and lung tissues .