Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease
Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Ex...
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| Veröffentlicht in: | Journal of immunotoxicology 2009-12, Vol.6 (4), p.266-275 |
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| creator | Tan, Hui-Hui Fiel, M. Isabel Sun, Qinghua Guo, Jinsheng Gordon, Ronald E. Chen, Lung-Chi Friedman, Scott L. Odin, Joseph A. Allina, Jorge |
| description | Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters |
| doi_str_mv | 10.3109/15476910903241704 |
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Isabel ; Sun, Qinghua ; Guo, Jinsheng ; Gordon, Ronald E. ; Chen, Lung-Chi ; Friedman, Scott L. ; Odin, Joseph A. ; Allina, Jorge</creator><creatorcontrib>Tan, Hui-Hui ; Fiel, M. Isabel ; Sun, Qinghua ; Guo, Jinsheng ; Gordon, Ronald E. ; Chen, Lung-Chi ; Friedman, Scott L. ; Odin, Joseph A. ; Allina, Jorge</creatorcontrib><description>Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters < 2.5 μm (PM2.5) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM2.5 induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM2.5 exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00 ± 0.00 vs. 1.50 ± 0.71, P < 0.001) and fibrosis stage (1.00 ± 0.00 vs. 0.60 ± 0.52, P = 0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00 ± 0.94 vs. 0.20 ± 0.42, respectively, P < 0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4−/− Kupffer cells (P < 0.050). In conclusion, ambient PM2.5 exposure may be a significant risk factor for NAFLD progression.</description><identifier>ISSN: 1547-691X</identifier><identifier>EISSN: 1547-6901</identifier><identifier>DOI: 10.3109/15476910903241704</identifier><identifier>PMID: 19908945</identifier><language>eng</language><publisher>Informa UK Ltd</publisher><subject>fibrosis ; IL-6 ; kupffer cell ; steatohepatitis ; Toll-like receptor</subject><ispartof>Journal of immunotoxicology, 2009-12, Vol.6 (4), p.266-275</ispartof><rights>2009 Informa UK Ltd 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-64d57d6d79e0de7d9a322b31c8b37698f3c85f8e57ab57a34a75ff44d32a46383</citedby><cites>FETCH-LOGICAL-c514t-64d57d6d79e0de7d9a322b31c8b37698f3c85f8e57ab57a34a75ff44d32a46383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.3109/15476910903241704$$EPDF$$P50$$Ginformaworld$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.3109/15476910903241704$$EHTML$$P50$$Ginformaworld$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,59647,60436,61221,61402</link.rule.ids></links><search><creatorcontrib>Tan, Hui-Hui</creatorcontrib><creatorcontrib>Fiel, M. Isabel</creatorcontrib><creatorcontrib>Sun, Qinghua</creatorcontrib><creatorcontrib>Guo, Jinsheng</creatorcontrib><creatorcontrib>Gordon, Ronald E.</creatorcontrib><creatorcontrib>Chen, Lung-Chi</creatorcontrib><creatorcontrib>Friedman, Scott L.</creatorcontrib><creatorcontrib>Odin, Joseph A.</creatorcontrib><creatorcontrib>Allina, Jorge</creatorcontrib><title>Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease</title><title>Journal of immunotoxicology</title><description>Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters < 2.5 μm (PM2.5) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM2.5 induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM2.5 exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00 ± 0.00 vs. 1.50 ± 0.71, P < 0.001) and fibrosis stage (1.00 ± 0.00 vs. 0.60 ± 0.52, P = 0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00 ± 0.94 vs. 0.20 ± 0.42, respectively, P < 0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4−/− Kupffer cells (P < 0.050). In conclusion, ambient PM2.5 exposure may be a significant risk factor for NAFLD progression.</description><subject>fibrosis</subject><subject>IL-6</subject><subject>kupffer cell</subject><subject>steatohepatitis</subject><subject>Toll-like receptor</subject><issn>1547-691X</issn><issn>1547-6901</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp9kdtKHjEQx0OpVKt9gN7lBbZNNtlDaBFEehAFbxS8C7M59ItkN0uS_eq-fbN8RZBiA0NmMvP7D5NB6CMlnxgl4jNteNeK4hFWc9oR_gadbG9VKwh9--zTh2P0PqVHQmpBGXmHjqkQpBe8OUHpepmtNREr4z0Gld0esgsTHlYM4-DMlDG4iGeI2anFQzZ4hJwLYZ7mkJa4xWsJQJk4bOkpTBV4FXbBO4VtKV6xd_tCaJcMJHOGjiz4ZD78vU_R_fdvd5c_q5vbH1eXFzeVaijPVct10-lWd8IQbTotgNX1wKjqB1bG7i1TfWN703QwFGMcusZazjWrgbesZ6fo_KA7L8NotCqzRPByjm6EuMoATr7MTG4nf4W9rPty6rYI0IOAiiGlaOwzS4ncNiD_2UBhvh4YN9kQR_gdotcyw-pDtBEm5dKGvo5_eYHvDPi8UxCNfAxLnMp__af5Hz-7oJ0</recordid><startdate>200912</startdate><enddate>200912</enddate><creator>Tan, Hui-Hui</creator><creator>Fiel, M. 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Isabel</creatorcontrib><creatorcontrib>Sun, Qinghua</creatorcontrib><creatorcontrib>Guo, Jinsheng</creatorcontrib><creatorcontrib>Gordon, Ronald E.</creatorcontrib><creatorcontrib>Chen, Lung-Chi</creatorcontrib><creatorcontrib>Friedman, Scott L.</creatorcontrib><creatorcontrib>Odin, Joseph A.</creatorcontrib><creatorcontrib>Allina, Jorge</creatorcontrib><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of immunotoxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tan, Hui-Hui</au><au>Fiel, M. Isabel</au><au>Sun, Qinghua</au><au>Guo, Jinsheng</au><au>Gordon, Ronald E.</au><au>Chen, Lung-Chi</au><au>Friedman, Scott L.</au><au>Odin, Joseph A.</au><au>Allina, Jorge</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease</atitle><jtitle>Journal of immunotoxicology</jtitle><date>2009-12</date><risdate>2009</risdate><volume>6</volume><issue>4</issue><spage>266</spage><epage>275</epage><pages>266-275</pages><issn>1547-691X</issn><eissn>1547-6901</eissn><abstract>Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters < 2.5 μm (PM2.5) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM2.5 induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM2.5 exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00 ± 0.00 vs. 1.50 ± 0.71, P < 0.001) and fibrosis stage (1.00 ± 0.00 vs. 0.60 ± 0.52, P = 0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00 ± 0.94 vs. 0.20 ± 0.42, respectively, P < 0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4−/− Kupffer cells (P < 0.050). In conclusion, ambient PM2.5 exposure may be a significant risk factor for NAFLD progression.</abstract><pub>Informa UK Ltd</pub><pmid>19908945</pmid><doi>10.3109/15476910903241704</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | fibrosis IL-6 kupffer cell steatohepatitis Toll-like receptor |
| title | Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease |
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