中华儿科杂志
中華兒科雜誌
중화인과잡지
Chinese Journal of Pediatrics
2009年
8期
628-631
,共4页
廖竞%农光民%蒋敏%张毓娴%梁秀安%刘静
廖競%農光民%蔣敏%張毓嫻%樑秀安%劉靜
료경%농광민%장민%장육한%량수안%류정
哮喘%细胞凋亡%中性白细胞
哮喘%細胞凋亡%中性白細胞
효천%세포조망%중성백세포
Asthma%Apoptosis%Neutrophils
目的 探讨儿童重度哮喘气道中性粒细胞(NEU)炎症的发生机制.方法 选择轻-中度哮喘患儿28例和重度哮喘患儿16例,健康对照组16例,进行肺功能测定,采用诱导痰检查方法对痰炎性细胞进行分类计数;采用酶联免疫吸附测定法检测痰和外周血IL-8浓度;同时在NEU中分别加入痰上清液、IL-8、地塞米松、米非司酮、磷酸盐缓冲液(PBS)、脂多糖(LPS)进行培养,观察NEU凋亡的变化.结果 (1)重度哮喘组诱导痰NEU百分比(%)为59.54(41.99~74.65),高于轻-中度哮喘组[30.03(15.94~47.71)]和健康对照组[29.72(16.53~45.74)](P均<0.01);重度哮喘组痰上清IL-8(ng/L)为2907.78(331.67~3457.93),高于轻-中度哮喘组[287.58(130.75~656.84)]和健康对照组[179.2(58.55~346.59)](P均<0.01).(2)体外培养NEU凋亡率(%):LPS+NEU组(10.57±1.97)、重度哮喘痰上清+NEU组(11.82±2.96)、地塞米松+NEU组(9.93±1.95)、IL-8+NEU组(10.47±1.93)、重度哮喘痰上清+米非司酮+NEU组(12.15±2.86)均低于PBS+NEU组(17.98±2.27)、健康对照痰上清+NEU组(17.37±2.50)、轻-中度哮喘痰上清+NEU组(16.35±3.26)、米非司酮+NEU组(17.89±2.38)、地塞米松+米非司酮+NEU组(17.06±2.59)(P均<0.01).结论 部分重度哮喘患者气道NEU增多可能与NEU凋亡受抑制有关,并同时伴有痰IL-8浓度的升高.
目的 探討兒童重度哮喘氣道中性粒細胞(NEU)炎癥的髮生機製.方法 選擇輕-中度哮喘患兒28例和重度哮喘患兒16例,健康對照組16例,進行肺功能測定,採用誘導痰檢查方法對痰炎性細胞進行分類計數;採用酶聯免疫吸附測定法檢測痰和外週血IL-8濃度;同時在NEU中分彆加入痰上清液、IL-8、地塞米鬆、米非司酮、燐痠鹽緩遲液(PBS)、脂多糖(LPS)進行培養,觀察NEU凋亡的變化.結果 (1)重度哮喘組誘導痰NEU百分比(%)為59.54(41.99~74.65),高于輕-中度哮喘組[30.03(15.94~47.71)]和健康對照組[29.72(16.53~45.74)](P均<0.01);重度哮喘組痰上清IL-8(ng/L)為2907.78(331.67~3457.93),高于輕-中度哮喘組[287.58(130.75~656.84)]和健康對照組[179.2(58.55~346.59)](P均<0.01).(2)體外培養NEU凋亡率(%):LPS+NEU組(10.57±1.97)、重度哮喘痰上清+NEU組(11.82±2.96)、地塞米鬆+NEU組(9.93±1.95)、IL-8+NEU組(10.47±1.93)、重度哮喘痰上清+米非司酮+NEU組(12.15±2.86)均低于PBS+NEU組(17.98±2.27)、健康對照痰上清+NEU組(17.37±2.50)、輕-中度哮喘痰上清+NEU組(16.35±3.26)、米非司酮+NEU組(17.89±2.38)、地塞米鬆+米非司酮+NEU組(17.06±2.59)(P均<0.01).結論 部分重度哮喘患者氣道NEU增多可能與NEU凋亡受抑製有關,併同時伴有痰IL-8濃度的升高.
목적 탐토인동중도효천기도중성립세포(NEU)염증적발생궤제.방법 선택경-중도효천환인28례화중도효천환인16례,건강대조조16례,진행폐공능측정,채용유도담검사방법대담염성세포진행분류계수;채용매련면역흡부측정법검측담화외주혈IL-8농도;동시재NEU중분별가입담상청액、IL-8、지새미송、미비사동、린산염완충액(PBS)、지다당(LPS)진행배양,관찰NEU조망적변화.결과 (1)중도효천조유도담NEU백분비(%)위59.54(41.99~74.65),고우경-중도효천조[30.03(15.94~47.71)]화건강대조조[29.72(16.53~45.74)](P균<0.01);중도효천조담상청IL-8(ng/L)위2907.78(331.67~3457.93),고우경-중도효천조[287.58(130.75~656.84)]화건강대조조[179.2(58.55~346.59)](P균<0.01).(2)체외배양NEU조망솔(%):LPS+NEU조(10.57±1.97)、중도효천담상청+NEU조(11.82±2.96)、지새미송+NEU조(9.93±1.95)、IL-8+NEU조(10.47±1.93)、중도효천담상청+미비사동+NEU조(12.15±2.86)균저우PBS+NEU조(17.98±2.27)、건강대조담상청+NEU조(17.37±2.50)、경-중도효천담상청+NEU조(16.35±3.26)、미비사동+NEU조(17.89±2.38)、지새미송+미비사동+NEU조(17.06±2.59)(P균<0.01).결론 부분중도효천환자기도NEU증다가능여NEU조망수억제유관,병동시반유담IL-8농도적승고.
Objective To investigate the changes of neutrophils in airway inflammation in children with severe asthma. Method Children with mild to moderate asthma (n=23), severe asthma (n=16) and healthy control subjects (n=16) underwent lung function tests and sputum induction. The sputum specimens were assayed for cellular differential count, the supematant and peripheral blood were assayed for the concentrations of IL-8 by "sandwich" enzyme linked immunosorbent assay (ELISA). Sputum supernatant, IL-8 and mifepristone were assessed for their abilities to prolong the in vitro survival of blood-derived neutrophils. Result The percentage of sputum neutrophils was significantly higher in severe asthmatics [59.54 (41.99-74.65) %] than mild-moderate asthmatics [30.03 (15.94-47.71)%] and healthy control subjects [29.72 (16.53-45.74)%] (P<0.01) ; the level of IL-8 in sputum was significantly higher in severe asthmatics [2907.78 (331.67-3457.93) ng/L] than mild-moderate asthmatics [287.58 (130.75-656.84) ng/L] and healthy control subjects [179.2 (58.55-346.59) ng/L] (P<0.01) ; the percentages of neutrophilic apoptosis respectively cultured with LPS [(10.57±1.97) % ], severe asthmatics supematant [ (11.82±2.96) % ], IL-8 [(10.47±1.93) % ], dexamethasone [(9.93±1.95)% ] ,severe asthma supernatant + mifepristone [(12.15±2.86)% ] in vitro were lower than that cultured with PBS [(17.98±2.27) % ], healthy control supernatant [(17.37±2.50) % ], mild-moderate asthmatics supematant [ (16.35±3.26) % ], mifepristone [(17.89±2.38) % ], and dexamethasone + mifepristone [ ( 17.06±2.59) % ] ( P<0.01 ). Conclusion Suppression of neutrophilic apoptosis seems to play a potential role in airway neutrophilic inflammation in severe asthmatics, and the level of IL-8 in sputum was significantly higher in patients with severe asthmatics.