The Role of Keratinocyte-derived Chemokine in Hemorrhage-induced Acute Lung Injury in Mice

Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytok...

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Published inJournal of Korean medical science Vol. 24; no. 5; pp. 775 - 781
Main Authors Lee, Byoung Hoon, Lee, Tae Jin, Jung, Jae Woo, Oh, Dong Jin, Choi, Jae Chol, Shin, Jong Wook, Park, In Won, Choi, Byoung Whui, Kim, Jae Yeol
Format Journal Article
LanguageEnglish
Published Korea (South) The Korean Academy of Medical Sciences 01.10.2009
대한의학회
Subjects
Acute Lung Injury - etiology
Acute Lung Injury - metabolism
Animals
Antibodies - immunology
Antibodies - metabolism
Chemokine CXCL2 - analysis
Chemokines - analysis
Chemokines - blood
Chemokines - physiology
Chickens
HMGB1 Protein - metabolism
Humans
Interleukin-1beta - analysis
Lipopolysaccharides - toxicity
Mice
Mice, Inbred BALB C
Neutrophils - immunology
Neutrophils - metabolism
NF-kappa B - metabolism
Original
Peroxidase - analysis
Shock, Hemorrhagic - complications
Time Factors
Tumor Necrosis Factor-alpha - analysis
의학일반
Keratinocyte-derived Chemokines
Hemorrhage
Acute Lung Injury
LPS
Online AccessGet full text
ISSN1011-8934
1598-6357
1598-6357
DOI10.3346/jkms.2009.24.5.775

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Abstract Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expression were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappaB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.
AbstractList Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expressison were evaluated in LPS- or hemorrhage-induced ALI models of BALB/ c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4±13.0 and 56.5±16.4 U/g, respectively. NF-κB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-α, MIP-2, and IL-1β were increased by LPS injection. However, there was only a minimal increase in IL-1β and no expressions of TNF-α or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1±12.3 vs. 14.2±1.6 pg/mL/mg by ELISA) ( P <0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.
Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage- induced ALI. In this study, lung injury and cytokine expressison were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4±13.0 and 56.5±16.4 U/g, respectively. NF-κB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-α, MIP-2, and IL-1β were increased by LPS injection. However, there was only a minimal increase in IL-1β and no expressions of TNF-αor MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1±12.3 vs. 14.2± 1.6 pg/mL/㎎ by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI. KCI Citation Count: 8
Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expression were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappaB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.
Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expression were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappaB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expression were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappaB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.
Author Choi, Jae Chol
Lee, Byoung Hoon
Jung, Jae Woo
Choi, Byoung Whui
Kim, Jae Yeol
Oh, Dong Jin
Shin, Jong Wook
Park, In Won
Lee, Tae Jin
AuthorAffiliation 1 Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea
2 Department of Pathology, Chung-Ang University College of Medicine, Seoul, Korea
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Issue 5
Keywords Keratinocyte-derived Chemokines
Hemorrhage
Acute Lung Injury
LPS
Language English
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Snippet Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine...
Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine...
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StartPage 775
SubjectTerms Acute Lung Injury - etiology
Acute Lung Injury - metabolism
Animals
Antibodies - immunology
Antibodies - metabolism
Chemokine CXCL2 - analysis
Chemokines - analysis
Chemokines - blood
Chemokines - physiology
Chickens
HMGB1 Protein - metabolism
Humans
Interleukin-1beta - analysis
Lipopolysaccharides - toxicity
Mice
Mice, Inbred BALB C
Neutrophils - immunology
Neutrophils - metabolism
NF-kappa B - metabolism
Original
Peroxidase - analysis
Shock, Hemorrhagic - complications
Time Factors
Tumor Necrosis Factor-alpha - analysis
의학일반
Title The Role of Keratinocyte-derived Chemokine in Hemorrhage-induced Acute Lung Injury in Mice
URI https://www.ncbi.nlm.nih.gov/pubmed/19794970
https://www.proquest.com/docview/733615319
https://pubmed.ncbi.nlm.nih.gov/PMC2752755
https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001376536
Volume 24
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ispartofPNX Journal of Korean Medical Science, 2009, 24(5), 132, pp.775-781
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