[The effect of glucocorticoid on IL-8 expressing in lung tissue of rat with chronic obstructive pulmonary disease].
OBJECTIVE
To explore the role of IL-8 in the pathogenesis of chronic obstructive pulmonary disease (COPD) and the effect of glucocorticoid on COPD.


METHODS
24 health males of Wistar rats were randomly divided into three groups (group A: normal control group, group B: COPD model group, group C: group pretreated with prednisone), of which each got 8 rats for this study project. Rat COPD model was established by exposing rat to cigarette smoke daily for 120 days. The prednisone was, via stomachal injection, given to the rats of group C with a dose of 5 mg/kg on every other day just before rats exposed to cigarette smoke. After COPD model was set up, the bronchoalveolar lavage (BAL) was performed. The total cells and neutrophils in bronchoalveolar lavage fluid (BALF) were counted for examination, and the levels of IL-8 and TNF-alpha in supernatants of BALF and serum were detected by ELISA. The lung tissue section stained by HE was observed in order to study the alternation of morphology, and also measured in terms of mean lining interval (MLI), mean alveolus number (MAN) and percentage of alveolar area in total area (PAA).


RESULTS
MLI and PAA in group B were higher than those in group A (P < 0.01), and decreased after pretreatment with prednisone (P < 0.01), in which however MAN was just on the contrary. The statistic analysis showed that levels of IL-8 [(114.5 +/- 15.7) pg/mL vs (259.4 +/- 20.1) pg/mL, respectively, P < 0.01], TNF-alpha [(80.5 +/- 9.5) pg/mL vs (145.9 +/- 17.3) pg/ mL, P < 0.01], total cell counts [(1.64 +/- 0.12) x 10(8)/L vs (5.76 +/- 0.29) x 10(8)/L, P < 0.01], neutrophil counts [(0.099 +/- 0.065) x 10(8)/L vs (1.26 +/- 0.25) x 10(8)/L P < 0.01], neutrophil proportion [(5.9 +/- 3. 6)% vs (21.8 +/- 3.7)%, P < 0.05] in BALF of group B were higher than those of group A. After pretreatment with prednisone, the above measured values were significant reduction (P < 0.01 or 0.05). The level of IL-8 in serum of group B was higher than that of group A [(45.2 +/- 13.5) pg/mL vs (85.7 +/- 7.0) pg/mL, P < 0.01], but which, after pretreatment, there was reduction but no significance (P > 0.05). The positive correlation was demonstrated among the levels of IL-8, TNF-alpha and counted neutrophils in BALF of group B, but not between the level of IL-8 and TNF-alpha in serum.


CONCLUSIONS
There is a close correlation between IL-8 in BALF and airway inflammation with COPD. The IL-8 cooperating with TNF-alpha may be responsible for the persistence and amplification of airway inflammation with COPD. By modulating the expression of IL-8 gene, inhibiting granulocyte chemotaxis and degranulation, the prednisone may relieve airway inflammation, and relieve the lesion of airway resulting from inflammatory cytokines and cells, hence postpone the progress of COPD.
Zhang
Yong
Y
Department of Respiratory Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.
Yang
Shao-Rong
SR
Cheng
De-Yun
DY
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D005786:Gene Expression Regulation / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D016209:Interleukin-8 / Q000097:blood / Q000378:metabolism*; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D005938:Glucocorticoids; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha