Source:http://linkedlifedata.com/resource/pubmed/id/19797856
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
2009-10-2
|
pubmed:abstractText |
Diesel exhaust particles (DEP), a well-known air pollutant, exacerbate type I hypersensitivity conditions, such as asthma and pollen allergy. In this study, we examined the effect of diesel exhaust (DE) exposure on delayed-type hypersensitivity (DTH), a type IV hypersensitivity, induced with methyl-bovine serum albumin (mBSA) in C57BL/6 mice. Mice were exposed to DE containing DEP at a dose of 1.78 mg/m(3) in an inhalation chamber for 14 days. On Day 7, DTH mice and DE-exposed DTH mice were injected s.c. with 200 microl of 1.25 mg/ml mBSA emulsified with CFA in the dorsal region as initial sensitization. On Day 14, mice were injected s.c. into one footpad with 20 microl of 10 mg/ml mBSA dissolved in PBS as challenge. On Day15, footpad thickness and spleen weight were measured. Significant footpad swelling (%) was observed in DTH mice compared with normal control mice, and this swelling was significantly augmented by DE exposure. The levels of pro-inflammatory cytokines, including IFN-gamma, TNF-alpha, and IL-6, in DTH mice were significantly higher than in normal mice, and were also further enhanced by DE exposure. DE exposure increased production of IL-17, which enhances local tissue inflammation through up-regulation of pro-inflammatory cytokines, while production of IL-10, which inhibits local tissue inflammation through suppression of immune cell proliferation, was unchanged. No change was observed in the percentage of CD4(+)CD25(+)Foxp3(+)T regulatory (Treg) cells in splenic lymphocytes following DE exposure. IL-6 production was increased by DE, and this would facilitate the differentiation of naïve T cells to IL-17-producing Th17 cells, while concomitantly suppressing the competing differentiation pathway to IL-10-producing Treg cells. Our results indicate that DE inhalation may, in part, exacerbate the pathological symptoms of DTH and induction of pro-inflammatory cytokines such as IFN-gamma, TNF-alpha, IL-6 and IL-17.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Particulate Matter,
http://linkedlifedata.com/resource/pubmed/chemical/Serum Albumin, Bovine,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Vehicle Emissions,
http://linkedlifedata.com/resource/pubmed/chemical/methylated bovine serum albumin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
1880-3989
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:volume |
34
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
483-92
|
pubmed:meshHeading |
pubmed-meshheading:19797856-Animals,
pubmed-meshheading:19797856-Cytokines,
pubmed-meshheading:19797856-Hypersensitivity, Delayed,
pubmed-meshheading:19797856-Interferon-gamma,
pubmed-meshheading:19797856-Interleukin-17,
pubmed-meshheading:19797856-Interleukin-6,
pubmed-meshheading:19797856-Male,
pubmed-meshheading:19797856-Mice,
pubmed-meshheading:19797856-Mice, Inbred C57BL,
pubmed-meshheading:19797856-Particle Size,
pubmed-meshheading:19797856-Particulate Matter,
pubmed-meshheading:19797856-Serum Albumin, Bovine,
pubmed-meshheading:19797856-Splenomegaly,
pubmed-meshheading:19797856-Tumor Necrosis Factor-alpha,
pubmed-meshheading:19797856-Vehicle Emissions
|
pubmed:year |
2009
|
pubmed:articleTitle |
Diesel exhaust (DE) aggravates pathology of delayed-type hypersensitivity (DTH) induced by methyl-bovine serum albumin (mBSA) in mice.
|
pubmed:affiliation |
Department of Radiation Biosciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science (TUS) Noda-shi, Chiba, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|