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항대식세포혈청이 마우스의 급성면역 복합체성 사구체신염에 미치는 영향

Other Titles
 Effect of antimacrophage serum(AMS) on acute immune complex glomerulonephritis in mice 
Authors
 정현주 
Issue Date
1987
Description
의학과/박사
Abstract
[한글]

단핵구,/대식세포는 이물질을 제거하는 기능 및 여러 효소와 물질을 분비하는 기능이있어 면역학적인 사구체 손상의 매개체로도 작용할 가능성이 높으므로, 본 연구는 항대식세포혈청을 사용하여 마우스의 급성 사구체신염에 미치는 단핵구/대식세포의 역할을 알아보고자 하였다.

체중 20gm 내외의 ICR마우스 42마리를 5군으로 나누어, 1군과 2군은 각 5마리로서 정상백서혈청 또는 항대식세포혈청을 정맥주사하여 10일째 도살하였고, 3군은 bovine serum albumin(BSA)을 정맥주사하여 10일과 12일째 도살하였다. 4군은 BSA를 주사후 10일과 11일째 항대식세포혈청을 주사하여 다음날 도살하였으며, 5군은 항대식세포혈청의 작용과 비교하기 위해 BSA 주사후 10일째 prednisolone를 1 mg 근육주사하고 다음날 도살하였다.도살당시 임상검사로 소변내 단백과 혈청 creatinine치를 측정하였고, 신장의 광학현미경적, 면역형광현미경적 및 전자현미경적 검색을 시행하여 다음의 결과를 얻었다.

1. 항대식세포혈청 또는 정상백서혈청 단독투여군에서는 대부분 단백뇨가 검출되지 않거나 미량이었으며, 광학현미경적 소견은 정상이었으나 사구체 맥관막내 미량의 IgG 침착이 관찰되었다.

2. BSA 투여군에서는 단백뇨와 함께 사구체내 세포증가 및 맥관막과 모세혈관고리에 IgG와 C^^3 가 침착되었으며 드물게 간질내 혈관에도 C^^3 가 침착되었다.

3. BSA 투여후 항대식세포혈청처치군에서는 BSA 투여군에 비해 단백뇨가 소실되거나 감소되었으며, 사구체내 세포수 및 면역글로블린의 침착도 감소되거나 소실되었다.

4. BSA 투여후 prednisolone처치군에서는 약 반수에서 단백뇨가 감소되었으나, IgG 침착은 BSA 투여군과 동일하거나 일부에서는 맥관막내에 증가되었다.

이상의 결과로 마우스의 급성 면역복합체성 사구체 신염에 단핵구/대식세포가 관여함을 알 수 있었다. 항대식세포혈청은 선택적으로 대식세포에 의한 조직손상 정도를 억제하여 단백뇨를 감소시키고 사구체내 세포증가 및 면역글로블린 침착을 감소시키며, prednisolone은 단백뇨는 감소시키지만 혈관투과력을 감소시켜 면역복합체의 제거속도를 늦춤으로써 일부에서 사구체 맥관막내 IgG 침착을 증가시키는 것으로 생각되었다.













Effect of Antimacrophage Serum (AMS) on Acute Immune Complex Glomerulonephritis in

Mice



Hyeon Joo Jeong

Department of Medical Science The Graduate School, Yonsei University

(Directed by Professor In Joon Choi, M.D.)



Macrophages are important not only in antigen processing but also may act as

effector cells in glomerular injury due to their phagocytic activity, synthesis

and/or secretion of various degradative enzymes and substances.

Studies on monocytic involement in glomerulonephritis were initiated by Okumura

et al in 1971, and it wart known that monocytes infiltrated in the glomeruli in

some forms of experimental and human glomerulonephritis.

To investigate the role of monocytes/macrophages in glomerular injury, male ICR

mice, with bovine serum albumin(BSA) induced acute glomerulonephritis were treated

with antimacrophage serum(AMS), and the results were compared with those treated

with prednisolone.

AMS was prepared in rats immunized with mouse peritoneal macrophages. Peritoneal

exudate was cultured for 4 hrs at 37℃. The adhesive cells were detached from the

glass and suspended in a saline concentration of 10^^7 /ml. Approximately 10**7

macrophages were injected subcutaneously into rate weekly for 3 weeks. One week

later serum collected from the rats was serially precipitated with ammonium

sulfate, heated at 56℃ for 30 minutes and used for injection.

Forty two ICR mice were separated into 5 groups. The first and second groups were

injected with 0.2 ml of either normal rat serum or AMS and sacrificed on the 10th

day. The third group was injected with 0.2mg of BSA intravenously and sacrificed on

the 10th & 12th day. The fourth group was treated with AMS on the 10th and 11th

days post BSA administration, while the fifth group was given 1 mg of prednisolone

intramuscularly on the 10th day post BSA administration and sacrificed the next

day. Urinary protein and serum creatinine were measured and the kidneys were

examined by light, immunefluorescent and electron microscopy.

The results were as follows :

1. The AMS or normal rat serum administered groups showed no significant

proteinuria, or glomerular hypercellularity except an occasional minimal deposit of

IgG in the mesangium .

2. The BSA treated group exhibited proteinuria, glomerular hypercellularity, and

IgG and C^^3 deposits along the loop and in mesangium. The increased cells had

oval, vesicular nuclei, but were difficult to discriminate by light or electron

microscopy.

3. AMS treatment in acute glomerulonephritis produced decreases in proteinuria,

glomerular cellularity and immune deposits.

4. Prednsiolone treatment resulted in a decrease in proteinuria in half the mice,

but immune deposits were the some as those of the BSA administered group and

increased in 2 mice.

These results indicate that macrophages/monocytes participate in glomerular

injury in acute glomerulonephritis of mice. AMS seems to suppress macrophages and

their effects. Prednisolone increases the glomerular deposits of IgG in a few cases

by decreasing capillary permeability and increasing the half life of the

circulating immune complex.

[영문]

Macrophages are important not only in antigen processing but also may act as effector cells in glomerular injury due to their phagocytic activity, synthesis and/or secretion of various degradative enzymes and substances.

Studies on monocytic involement in glomerulonephritis were initiated by Okumura et al in 1971, and it wart known that monocytes infiltrated in the glomeruli in some forms of experimental and human glomerulonephritis.

To investigate the role of monocytes/macrophages in glomerular injury, male ICR mice, with bovine serum albumin(BSA) induced acute glomerulonephritis were treated with antimacrophage serum(AMS), and the results were compared with those treated

with prednisolone.

AMS was prepared in rats immunized with mouse peritoneal macrophages. Peritoneal exudate was cultured for 4 hrs at 37℃. The adhesive cells were detached from the glass and suspended in a saline concentration of 10^^7 /ml. Approximately 10**7

macrophages were injected subcutaneously into rate weekly for 3 weeks. One week later serum collected from the rats was serially precipitated with ammonium sulfate, heated at 56℃ for 30 minutes and used for injection.

Forty two ICR mice were separated into 5 groups. The first and second groups were injected with 0.2 ml of either normal rat serum or AMS and sacrificed on the 10th day. The third group was injected with 0.2mg of BSA intravenously and sacrificed on the 10th & 12th day. The fourth group was treated with AMS on the 10th and 11th days post BSA administration, while the fifth group was given 1 mg of prednisolone intramuscularly on the 10th day post BSA administration and sacrificed the next day. Urinary protein and serum creatinine were measured and the kidneys were

examined by light, immunefluorescent and electron microscopy.

The results were as follows :

1. The AMS or normal rat serum administered groups showed no significant proteinuria, or glomerular hypercellularity except an occasional minimal deposit of IgG in the mesangium .

2. The BSA treated group exhibited proteinuria, glomerular hypercellularity, and IgG and C^^3 deposits along the loop and in mesangium. The increased cells had oval, vesicular nuclei, but were difficult to discriminate by light or electron microscopy.

3. AMS treatment in acute glomerulonephritis produced decreases in proteinuria, glomerular cellularity and immune deposits.

4. Prednsiolone treatment resulted in a decrease in proteinuria in half the mice, but immune deposits were the some as those of the BSA administered group and increased in 2 mice.

These results indicate that macrophages/monocytes participate in glomerular injury in acute glomerulonephritis of mice. AMS seems to suppress macrophages and their effects. Prednisolone increases the glomerular deposits of IgG in a few cases by decreasing capillary permeability and increasing the half life of the circulating immune complex.
Full Text
https://ymlib.yonsei.ac.kr/catalog/search/book-detail/?cid=CAT000000045430
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 3. Dissertation
Yonsei Authors
Jeong, Hyeon Joo(정현주) ORCID logo https://orcid.org/0000-0002-9695-1227
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/127465
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