1990 Fiscal Year Final Research Report Summary
A Study for a Role of SRS-A in Pulmonary Allergic Disorders And acute Lung Injury (ARDS)
| Project/Area Number |
01570431
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
ABE. Masayoshi Kyushu University, Medicine, Research Associate, 医学部, 助手 (80131803)
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| Co-Investigator(Kenkyū-buntansha) |
TORISU Motomichi Kyushu University, Medicine, Assistant Professor, 医学部, 講師 (90038810)
TAKAHASHI Hiroko Kyushu University, Medicine, Resident
GOUYA Tomomochi Kyushu University, Medicine, Resident
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| Project Period (FY) |
1989 – 1990
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| Keywords | ARDS model / septic lungs in rats / leukotriene C_4 / leukotriene B_4 / macrophages / endotoxins / superoxide anions / complement |
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| Research Abstract |
We investigated a pathogenesis of septic lung injury (septic-ARDS) focusing on the change of Alveolar Macrophages (AMO). Sepsis was induced in male rats by using the cecal ligation and puncture technique. The protein concentrations in the Bronchoioialveolar Fluid (BALF) increased in parallel with the end otoxin levels in the BALF. The function of AMO was examined according to the time-course following the surgery. The results obtained were the followings ; the septic AM possessed higher adherence, enhanced superoxide anion generation and more release of lysosomal enzymes, suggesting an activation of these cells by endotoxins, On the other hand, the septic AMO generated much smaller amounts of leukotriene B_4, 12- and 5-HETEs while the concentration of LTC_4 was higher in the septic BALF than that in the control. The reduced productivity of LTB_4 by the septic AM may contibute to the increased susceptibility to severe pulmonary infection during the septic state. Next, we compared lipoxy
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genase metabolism between resident and elicited MO by thioglycollate broth. The elicited MO generated more superoxide anions but did fewer amounts of lipoxygenase metabolites including L_4. Furthermore, the elicited MO showed a preferential conversion of exogenous LTA_4 to LTC_4 as compared with the resident cells. These results indicate that the elicited MO may contribute to the progress f inflammation by the preferential generation of vasoactive mediators, sulfidopeptide LTs.
It has been reported that complement activation may play a crucial role in the pathophysiology of ARDS. Therefore, complement activation was evaluated in patients with pre-ARDS and ARDS with emphasis on SC5b-9. Most patients with these illnesses showed elevated SC5b-9 and did and increase in the values in association with exacerbation of the disease. However, some patients with ARDS exhibited lower values of SC5b-9 in spite of progressing to death. The s-protein which is produced in a liver showed the reduced level in these patients, suggesting a contribution of liver dysfunction to the reduced SC5b-9 level.
In conclusion, it is suggested that AM may participate in the occurrence and progression of ARDS by releasing various mediators including LTs, O_2^- and proteases, along with complement activation. Less
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