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Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine.

Li R, Navab K, Hough G, Daher N, Zhang M, Mittelstein D, Lee K, Pakbin P, Saffari A, Bhetraratana M, Sulaiman D, Beebe T, Wu L, Jen N, Wine E, Tseng CH, Araujo JA, Fogelman A, Sioutas C, Navab M, Hsiai TK - Environ. Health Perspect. (2014)

Bottom Line: However, little is known about the effects of air pollution on gastrointestinal disorders.Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA.Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

ABSTRACT

Background: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders.

Objective: We sought to assess whether exposure to ambient UFP (diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine.

Methods: Ldlr- mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles, California, site that was heavily affected by vehicular emissions; the exposure was carried out for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal chow diet.

Results: Compared with FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid (AA) and prostaglandin D2 (PGD2) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA. Although exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration.

Conclusions: Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.

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Related in: MedlinePlus

UFP exposure modulated the plasma levels of inflammatory markers. The plasma levels of SAA and TNF-α in mice on chow diet were measured (exposure 2). NS, no significant difference. (A) UFP increased SAA levels, which were significantly attenuated by administration of D-4F (n = 6). (B) TNF-α levels were not significantly elevated in mice on the normal chow diet (n = 6).
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f6: UFP exposure modulated the plasma levels of inflammatory markers. The plasma levels of SAA and TNF-α in mice on chow diet were measured (exposure 2). NS, no significant difference. (A) UFP increased SAA levels, which were significantly attenuated by administration of D-4F (n = 6). (B) TNF-α levels were not significantly elevated in mice on the normal chow diet (n = 6).

Mentions: Plasma measures of inflammation in response to UFP exposure. UFP exposure promoted systemic inflammation as indicated by increased plasma levels of SAA in mice on both high-fat diet [first exposure study, as previously reported (Li et al. 2013), and chow diet (second exposure study) Figure 6A], and administration of D-4F significantly attenuated these effects (Li et al. 2013) (Figure 6A). Although UFP significantly increased plasma TNF-α levels in the fat-fed mice (Li et al. 2013), a similar trend in the chow-fed mice did not reach statistical significance (Figure 6B). Administration of D-4F had no significant effects on plasma TNF-α levels in both high-fat (Li et al. 2013) and chow-fed mice (Figure 6B).


Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine.

Li R, Navab K, Hough G, Daher N, Zhang M, Mittelstein D, Lee K, Pakbin P, Saffari A, Bhetraratana M, Sulaiman D, Beebe T, Wu L, Jen N, Wine E, Tseng CH, Araujo JA, Fogelman A, Sioutas C, Navab M, Hsiai TK - Environ. Health Perspect. (2014)

UFP exposure modulated the plasma levels of inflammatory markers. The plasma levels of SAA and TNF-α in mice on chow diet were measured (exposure 2). NS, no significant difference. (A) UFP increased SAA levels, which were significantly attenuated by administration of D-4F (n = 6). (B) TNF-α levels were not significantly elevated in mice on the normal chow diet (n = 6).
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4286268&req=5

f6: UFP exposure modulated the plasma levels of inflammatory markers. The plasma levels of SAA and TNF-α in mice on chow diet were measured (exposure 2). NS, no significant difference. (A) UFP increased SAA levels, which were significantly attenuated by administration of D-4F (n = 6). (B) TNF-α levels were not significantly elevated in mice on the normal chow diet (n = 6).
Mentions: Plasma measures of inflammation in response to UFP exposure. UFP exposure promoted systemic inflammation as indicated by increased plasma levels of SAA in mice on both high-fat diet [first exposure study, as previously reported (Li et al. 2013), and chow diet (second exposure study) Figure 6A], and administration of D-4F significantly attenuated these effects (Li et al. 2013) (Figure 6A). Although UFP significantly increased plasma TNF-α levels in the fat-fed mice (Li et al. 2013), a similar trend in the chow-fed mice did not reach statistical significance (Figure 6B). Administration of D-4F had no significant effects on plasma TNF-α levels in both high-fat (Li et al. 2013) and chow-fed mice (Figure 6B).

Bottom Line: However, little is known about the effects of air pollution on gastrointestinal disorders.Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA.Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

ABSTRACT

Background: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders.

Objective: We sought to assess whether exposure to ambient UFP (diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine.

Methods: Ldlr- mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles, California, site that was heavily affected by vehicular emissions; the exposure was carried out for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal chow diet.

Results: Compared with FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid (AA) and prostaglandin D2 (PGD2) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA. Although exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration.

Conclusions: Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.

Show MeSH
Related in: MedlinePlus