Saturday, 17 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Kyung Eun Lee, PhD
,
Department of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea
Jung Yeon Hong
,
Department of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea
Mi Na Kim
,
Department of Pediatrics and Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea
Kyung Won Kim, MD, PhD
,
Department of Pediatrics and Institute of Allergy, Yonsei University College of Medicine, Seoul, South Korea
Kyu-Earn Kim, MD, PhD
,
Department of Pediatrics and Institute of Allergy, Yonsei University College of Medicine, Seoul, South Korea
Hye Mi Jee, MD
,
Department of Pediatrics, Bundang CHA Medical Center, CHA University School of Medicine, Seongnam, South Korea
Myung Hyun Sohn, MD, PhD
,
Department of Pediatrics and Institute of Allergy, Yonsei University College of Medicine, Seoul, South Korea
Background: Cockroaches contain or produce many proteins including proteases from feces, saliva and the bodies, which have been recognized to induce cellular different responses. Matrix metalloproteinases (MMPs), a family of extracellular matrix-degrading enzymes are released by various stimuli and play important roles in inflammation, tissue remodeling, angiogenensis, wound healing, and tumor invasion.
Purpose: We aimed to determine if German cockroach extract (GCE) can activate MMPs and then, GCE-stimulated MMPs influence tight and adherence junction in airway epithelial cells.
Methods: The mRNA and protein levels of MMPs were assessed by quantitative PCR and enzyme linked immunosorbent assay in human airway epithelial cells cultured in the presence of German cockroach extract. Immunoblotting and immunofluorescent staining were performed for identifying airway epithelial integrity and the structure of intercellular junction. Transepithelial resistance was measured to determine epithelial barrier function.
Results: GCE significantly increased MMP-1 and MMP-9 mRNA and protein in airway epithelial cells. This extract also attenuated the integrity of ZO-1 and Occludin protein, and induced epithelial ZO-1 and Occludin delocalization profoundly. In addition, prolonged exposure to GCE decreased significantly epithelial resistance. These GCE-induced degradations were dramatically prohibited by a MMP inhibitor known as a potent inhibitor of collagenases.
Conclusion: This study shows that GCE-activated MMP-1 and MMP-9 can alter junctional proteins and epithelial barrier function, thereby facilitating stimuli penetration.
