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1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Korea University Medical College, Seoul, Korea, Republic of
2 Departmant of Nursing, College of Medicine, Pochon CHA University, Pochon, Korea, Republic of
3 Institute of Human Genomic Study, Korea University Ansan Hospital, Ansan, Korea, Republic of
4 Department of Clinical Pathology, Kangwon National University Medical College, Chuncheon, Korea, Republic of
* To whom correspondence should be addressed. E-mail: kkhchest{at}korea.ac.kr.
Neutrophils are considered to play a central role in the ventilator-induced lung injury (VILI). However, the pulmonary consequences of neutrophil accumulation have not been fully elucidated. Matrix metalloproteinase-9 (MMP-9) had been postulated to participate in neutrophil transmigration. The purpose of this study was to investigate the role of MMP-9 in the neutrophilic inflammation of VILI. Male Sprague-Dawley rats were divided into three groups: (1) low tidal volume (LVT), 7 mL/Kg of tidal volume (VT); (2) high tidal volume (HVT), 30 mL/Kg of VT; and (3) high tidal volume with MMP inhibitor (HVT+MMPI). As a MMPI, CMT-3 was administered daily from three days before mechanical ventilation. Degree of VILI was assessed by wet-to-dry weight ratio and acute lung injury (ALI) scores. Neutrophilic inflammation was determined from the neutrophil count in the lung tissue and myeloperoxidase (MPO) activity in the bronchoalveolar lavage fluid (BALF). MMP-9 expression and activity were examined by immunohistochemical staining and gelatinase zymography, respectively. The wet-to-dry weight ratio, ALI score, neutrophil infiltration, and MPO activity were increased significantly in the HVT group. However, in the HVT+MMPI group, pretreatment with MMPI decreased significantly the degree of VILI, as well as neutrophil infiltration and MPO activity. These changes correlated significantly with MMP-9 immunoreactivity and MMP-9 activity. Most outcomes were significantly worse in the HVT+MMPI group compared to the LVT group. In conclusion, VILI mediated by neutrophilic inflammation is closely related to MMP-9 expression and activity. The inhibition of MMP-9 protects against the development of VILI through the downregulation of neutrophil-mediated inflammation.
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