|
KMID : 0350519950480041017
|
|
Journal of Catholic Medical College
1995 Volume.48 No. 4 p.1017 ~ p.1030
|
|
|
The Role of Interleukin 6 and Interleukin 8 in the Pathogenesis of Endotoxin-Induced Acute Lung Injury in Rats
|
|
|
|
|
Abstract
|
|
|
The acute respiratory distress syndrome (ARDS) is a form of acute lung injury (ALI) characterized by high-permeability, low-pressure pulmonary edema, refractory hypoxemia, and respiratory failure. Much has been learned about the pathophysiology
of
ARDS
in the past 25 years, but ARDS mortality of present days remains still high mainly due to our incomplete understanding of the pathophysiology of the ALI and ARDS. Although the pathogenesis of ARDS is undoubtedly complex, and poorly understood,
several
observations point to an important role of polymorphonuclear leukocytes (PMNs). And some chemotactic factors are needed to migrate PMNs to the site of local inflammation. The results of seeral recent investigations have suggested that certain
cytokines,
including interleuin 6 (IL-6) and interleukin 8 (IL-8), may play a role in the pathogenesis of ALI or ARDS because these humoral substances have powerful effects on PMN function.
Lipopolysaccharide (LPS) is one of the most important causes of ARDS and can cause release of various inflammatory cytokines leading to ALI. There have been reports measuring IL-6 and IL-8 levels in serum or bronchoalveolar lavage fluind (BALF)
from
patients with sepsis or APDS. But, to our knowledge, IL-6 and IL-8 levels have not been investigated in the rat model with LPS-induced acute lung injury.
To gain further insight into the pathogenetic role of IL-6 and IL-8 in ALI, we measured IL-6 and IL-S levels in the sera and BALFs obtained from rats at 4, 8, 12, and 24 hours after LPS injection. We also performed histological examinationsl of
the
lung
tissue to observe the relationshop between these cytokine levels and the degree of PMN infiltrations in the lung.
@ES The results were as follows :
@EN 1. The PMN percentages in the peripheral blood were significantly increased at 4 and 8 hours after LPS injection compared to the control (p<0.05). The PMN percentages in the BALFs were significantly increased at 8 hours after LPS injection
and
remained high thereafter compared to the control (p<0.05).
2. The protein concentration in the BALFs were significaantly increased at 8 and 12 hours after LPS injection compared to the control (p<0.05).
3. The wet/dry ratios of lung weight were significantly increased at 4 hours after LPS injection and remained high thereafter compared to the control (p<0.05).
4. IL-6 concentrations in the serum and BAPFs were very low in all groups.
5. IL-8 concentrations in the BALFs were significantly increased at 4 after LPS injection and remained high thereafter compared to the control (p<0.05). IL-8 concentrations in the serum were significantly decreased at 24 hours after LPS
injection
compared to the control (p<0.05).
6. PMN infiltrations in the interstitium were significantly increased in all LPS-treated groups (p<0.05).
7. There was significant correlation between the PMN percentages in the BALFs and IL-8 concentrations in the BALFs (p<0.05).
These results suggest that PMN is the major effector cell in the PLS-induced acute lung injury in rats and IL-8, rather than IL-6, is a main cytokine involved in the chemotaxis, activation and local accumulation of PMN.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|