| pubmed-article:7927780 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0026339 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0038402 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0348801 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:7927780 | lifeskim:mentions | umls-concept:C0441836 | lld:lifeskim |
| pubmed-article:7927780 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:7927780 | pubmed:dateCreated | 1994-11-22 | lld:pubmed |
| pubmed-article:7927780 | pubmed:abstractText | Previous studies have shown that tumor necrosis factor alpha (TNF-alpha) plays a pathophysiologic role in sepsis induced in rat pups by group B streptococci (GBS). In this model, TNF-alpha is also partially responsible for the induction of interleukin-6 (IL-6). The present study was undertaken to investigate the role of IL-6 in neonatal BALB/c mice infected with type III GBS. The effect of anti-IL-6 monoclonal antibodies and recombinant IL-6 on lethality and TNF-alpha production was investigated. In mouse pups infected with GBS strain COH1, plasma IL-6 reached levels of 3,067 +/- 955 and 1,923 +/- 891 U/ml when measured at 22 and 48 h, respectively (P < 0.05 compared with uninfected controls). Pretreatment with 25 micrograms of anti-IL-6 antibodies totally prevented the increase in circulating IL-6 bioactivity at both 22 and 48 h after infection (P < 0.05). Treatment with anti-IL-6 also induced a moderate decrease in survival time of mice infected with lethal doses of strains COH1 and COH31, as evidenced by increased lethality (P < 0.05) at 24 to 48 h but not at 96 h. Mouse recombinant IL-6 (12,500 U) given 6 h before challenge with strains COH1 and COH31 consistently increased survival time, as evidenced by decreased (P < 0.05) lethality at 48 to 72 h but not at 96 h. The effects of IL-6 pretreatment were dose dependent, since no protection was observed with doses lower than 12,500 U. In addition, no effects on lethality were noted when IL-6 was given at the time of challenge or at later times. TNF-alpha elevations (P < 0.05 compared with uninfected controls) were measured at 12, 22, and 48 h after challenge with strain COH1 (68 +/- 28, 233 +/- 98, and 98 +/- 34 U, respectively). Pretreatment with IL-6 significantly (P < 0.05) decreased plasma TNF-alpha levels at 12 and 22 h, with 55 and 69% inhibitions, respectively. Anti-IL-6 had an opposite effect, as evidenced by a 145% increase (P < 0.05) in TNF-alpha levels at 48 h after challenge. Collectively, our data are compatible with the hypothesis that IL-6 is involved in negative feedback regulation of plasma TNF-alpha levels in experimental GBS sepsis. In this model, IL-6 pretreatment can increase survival time. Future studies will be needed to investigate the mechanisms underlying this effect. | lld:pubmed |
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| pubmed-article:7927780 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7927780 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7927780 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7927780 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7927780 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7927780 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:TomaselloFF | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:CookJ AJA | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:TetiGG | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:MancusoGG | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:CochranJJ | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:DelfinoDD | lld:pubmed |
| pubmed-article:7927780 | pubmed:author | pubmed-author:MigliardoMM | lld:pubmed |
| pubmed-article:7927780 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7927780 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:7927780 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7927780 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7927780 | pubmed:pagination | 4997-5002 | lld:pubmed |
| pubmed-article:7927780 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7927780 | pubmed:meshHeading | pubmed-meshheading:7927780-... | lld:pubmed |
| pubmed-article:7927780 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7927780 | pubmed:articleTitle | Beneficial effects of interleukin-6 in neonatal mouse models of group B streptococcal disease. | lld:pubmed |
| pubmed-article:7927780 | pubmed:affiliation | Istituto di Microbiologia, Facoltà di Medicina e Chirurgia, Università degli Studi di Messina, Italy. | lld:pubmed |
| pubmed-article:7927780 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7927780 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7927780 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:23855 | entrezgene:pubmed | pubmed-article:7927780 | lld:entrezgene |
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