1999 Fiscal Year Final Research Report Summary
BIOLOGICAL AND IMMUNOLOGICAL SPECTS OF HOST FACTORS WHICH ARE RESPONSIBLE FOR THE ESTABLISHMENT OF ANAEROBIC BACTERIAL INFECTION
| Project/Area Number |
10660287
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Miyazaki University |
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Principal Investigator |
SHINJO Toshiharu Miyazaki University, Veterinary Microbiology, Professor, 農学部, 教授 (10040859)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Yoshitaka Miyazaki University, Veterinary Microbiology, Associate Professor, 農学部, 助教授 (30142136)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Fusobacterium necrophorum / liver abscess / cytokine / neutrophil(s) / Inflammatory respnse / endotoxin |
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| Research Abstract |
The study presented has shed some light into the involvement of cytokines in the course of liver abscess formation by Fusobacterium necrophorum. Results likewise indicated that cytokine activity influenced lymphocyte-regulated immune responses and neutrophil-operated inflammatory responses. A difference in the ability to induce mouse lethality by endotoxins from two unequivocally-claimed subspecies of Fusobacterium necrophorum has been presented. Distinct divergence of chemical compositions and endotoxin contents were demonstrated which were could be claimed as correlative factors that highlight its virulence. A better understanding on the simultaneous liver abscess build up by a viable infection to Fusobacterium necrophorum subsp. Necrophorum infection in a fashion consistent with the increment of neutrophils and monocytes in the circulation was provided. Data demonstrating similar effects after sole administration of its endotoxin confirm its significant contribution to these mechanism. In comparison with to Fusobacterium necrophorum subsp. Funduliforme elicited mechanisms prior results exhibiting the simultaneously effects of its endotoxin on the cellular blood components were thwarted in viable infection causing divergence of observed responses.
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