rdf:type |
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lifeskim:mentions |
|
pubmed:issue |
5
|
pubmed:dateCreated |
2000-6-13
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pubmed:abstractText |
Our previous study showed that gamma interferon (IFN-gamma), a T-helper 1 (Th1)-type cytokine, plays a detrimental role in Staphylococcus aureus infection in mice. In this study, the role of Th2-type cytokines such as interleukin-4 (IL-4) and IL-10 in S. aureus infection was investigated. IL-10 mRNA was induced in parallel with IFN-gamma in the spleens and kidneys of mice during S. aureus infection, whereas IL-4 mRNA was induced in the spleens but not in the kidneys of these animals. Spleen cells obtained from S. aureus-infected mice produced lower titers of IFN-gamma and higher titers of IL-4 and IL-10 in response to heat-killed S. aureus than did those from uninfected mice. Administration of anti-IL-4 monoclonal antibody (MAb) or anti-IL-10 MAb inhibited the elimination of S. aureus cells from the kidneys of mice. IFN-gamma mRNA expression was enhanced in the spleens of anti-IL-4 MAb- or anti-IL-10 MAb-treated mice and also in the kidneys of anti-IL-4 MAb-treated animals. Next, we evaluated the role of IFN-gamma in S. aureus infection in IFN-gamma(-/-) mice. An increase in survival rates, a decrease in bacterial numbers in the kidneys, and an amelioration of histologic abnormalities in these organs were observed in IFN-gamma(-/-) mice compared with those in IFN-gamma(+/+) mice. Administration of MAb against IL-4 or IL-10 failed to affect bacterial growth in the spleens and kidneys of IFN-gamma(-/-) mice irrespective of the expression of Th2 response. These results suggest that S. aureus infection induced a Th2 response and that IL-4 and IL-10 might play a protective role through the regulation of IFN-gamma in S. aureus infection.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-10354370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-10358772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-10458752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-1385868,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-1535368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-1602140,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-1833466,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-2112583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-2440339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-2521244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-7499861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-7593621,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/10768926-9783259
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0019-9567
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2424-30
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10768926-Animals,
pubmed-meshheading:10768926-Antibodies, Monoclonal,
pubmed-meshheading:10768926-Cells, Cultured,
pubmed-meshheading:10768926-Gene Expression,
pubmed-meshheading:10768926-Immunity, Innate,
pubmed-meshheading:10768926-Interferon-gamma,
pubmed-meshheading:10768926-Interleukin-10,
pubmed-meshheading:10768926-Interleukin-4,
pubmed-meshheading:10768926-Mice,
pubmed-meshheading:10768926-Mice, Inbred C57BL,
pubmed-meshheading:10768926-Mice, Knockout,
pubmed-meshheading:10768926-RNA, Messenger,
pubmed-meshheading:10768926-Spleen,
pubmed-meshheading:10768926-Staphylococcal Infections
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pubmed:year |
2000
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pubmed:articleTitle |
Interleukin-4 and interleukin-10 are involved in host resistance to Staphylococcus aureus infection through regulation of gamma interferon.
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pubmed:affiliation |
Department of Bacteriology, Hirosaki University School of Medicine, Hirosaki, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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