IMMUNOTOXICITY OF ACID ANHYDRIDES IN THE LUNG

酸酐在肺中的免疫毒性

基本信息

  • 批准号:
    6043474
  • 负责人:
  • 金额:
    $ 19.52万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1996
  • 资助国家:
    美国
  • 起止时间:
    1996-08-01 至 2000-07-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION: (Adapted from the Investigator's Abstract) Acid anhydrides, used in a number of industries, cause the immunotoxic response of allergy. The long term goal is to understand the mechanism of immunotoxicity of the acid anhydrides in the lung so rational therapeutic approaches can be designed. A guinea pig model of trimellitic anhydride (TMA)-induced allergy will be used because it mimics many symptoms seen in the allergic human. Animals will be sensitized ID with TMA and 3 wk later challenged intratracheally with antigen (TMA coupled to serum albumin). Components of the immunotoxic response to TMA which will be monitored include: broncho-constriction and an immediate decrease in circulating platelets; increased airway microvascular and pulmonary vascular permeability; lung hemorrhage; and eosinophil, neutrophil and mononuclear cell infiltration into the lung. The hypothesis is that TMA-GPSA combines with cytophilic IgG1 and/or non-cytophilic IgG2 Ab in the airspace and/or the circulation to cause complement activation with a resultant decrease in circulating platelets: both of which are required for the immunotoxic response to TMA. TMA- GPSA-specific IgG1 and IgG2 will be measured by ELISA in the serum and bronchoalveolar lavage (BAL) of actively-sensitized animals and correlated with the immunotoxic response. The ability of purified IgG1/IgG2 Ab to mediate the immunotoxic response will be determined in passively-sensitized animals. To determine which antibody mediates complement participation, animals will be passively sensitized with IgG1 or IgG2, depleted of complement with Cobra Venom Factor, and the response to TMA assessed. To determine if complement activation occurs in the circulation or airspace, complement cleavage product C3a will be assayed in plasma and BAL by a Western blot method. In vitro studies will determine combinations of antigen, Ab, and BAL cells which result in C3a generation or BAL cell activation. An isolated tracheal preparation will be used to determine if antigen movement (with or without Ab and C) is limited by epithelial permeability. The importance of platelets will be assessed by determining if platelets sequester in the lung and whether depleting platelets or preventing their aggregation affects the immunotoxic response. These studies will determine if cytophilic Ab can evoke participation of the complement system and if cytophilic plus non-cytophilic Ab can predict the immunotoxic response.
描述:(改编自研究者摘要)酸

项目成果

期刊论文数量(11)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Trimellitic anhydride (TMA) dust induces airway obstruction and eosinophilia in non-sensitized guinea pigs.
偏苯三酸酐 (TMA) 粉尘会导致非致敏豚鼠气道阻塞和嗜酸性粒细胞增多。
  • DOI:
    10.1016/s0300-483x(02)00190-7
  • 发表时间:
    2002
  • 期刊:
  • 影响因子:
    4.5
  • 作者:
    Larsen,ChristenP;Regal,JeanF
  • 通讯作者:
    Regal,JeanF
Role of the complement system in pulmonary disorders.
补体系统在肺部疾病中的作用。
  • DOI:
    10.1016/s0162-3109(97)00058-1
  • 发表时间:
    1997
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Regal,JF
  • 通讯作者:
    Regal,JF
Primary prevention of asthma: age and sex influence sensitivity to allergen-induced airway inflammation and contribute to asthma heterogeneity in Guinea pigs.
哮喘的一级预防:年龄和性别影响对过敏原引起的气道炎症的敏感性,并导致豚鼠哮喘的异质性。
The role of IgG1 and IgG2 in trimellitic anhydride-induced allergic response in the guinea pig lung.
IgG1 和 IgG2 在偏苯三酸酐诱导的豚鼠肺过敏反应中的作用。
  • DOI:
    10.1006/taap.1998.8419
  • 发表时间:
    1998
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Fraser,DG;Graziano,FM;Larsen,CP;Regal,JF
  • 通讯作者:
    Regal,JF
Trimellitic anhydride-induced cellular infiltration into Guinea pig lung varies with age but not gender.
偏苯三酸酐诱导的豚鼠肺细胞浸润随年龄而变化,但不随性别而变化。
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JEAN F. REGAL其他文献

JEAN F. REGAL的其他文献

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{{ truncateString('JEAN F. REGAL', 18)}}的其他基金

Complement activation and angiogenic imbalance in pregnancy and hypertension
妊娠和高血压中的补体激活和血管生成失衡
  • 批准号:
    8179940
  • 财政年份:
    2011
  • 资助金额:
    $ 19.52万
  • 项目类别:
Complement Activation in Pregnancy and Hypertension
妊娠和高血压中的补体激活
  • 批准号:
    8574333
  • 财政年份:
    2011
  • 资助金额:
    $ 19.52万
  • 项目类别:
IMMUNOTOXICITY OF ACID ANHYDRIDES IN THE LUNG
酸酐在肺中的免疫毒性
  • 批准号:
    2459007
  • 财政年份:
    1996
  • 资助金额:
    $ 19.52万
  • 项目类别:
IMMUNOTOXICITY OF ACID ANHYDRIDES IN THE LUNG
酸酐在肺中的免疫毒性
  • 批准号:
    2156803
  • 财政年份:
    1996
  • 资助金额:
    $ 19.52万
  • 项目类别:
IMMUNOTOXICITY OF ACID ANHYDRIDES IN THE LUNG
酸酐在肺中的免疫毒性
  • 批准号:
    2749675
  • 财政年份:
    1996
  • 资助金额:
    $ 19.52万
  • 项目类别:
ROLE OF C3A/C5A IN ANTIGEN-INDUCED BRONCHOCONSTRICTION
C3A/C5A 在抗原诱导的支气管收缩中的作用
  • 批准号:
    3339812
  • 财政年份:
    1981
  • 资助金额:
    $ 19.52万
  • 项目类别:
ROLE OF C3A/C5A IN ANTIGEN-INDUCED BRONCHOCONSTRICTION
C3A/C5A 在抗原诱导的支气管收缩中的作用
  • 批准号:
    3339806
  • 财政年份:
    1981
  • 资助金额:
    $ 19.52万
  • 项目类别:
ROLE OF C3A/C5A IN ANTIGEN-INDUCED BRONCHOCONSTRICTION
C3A/C5A 在抗原诱导的支气管收缩中的作用
  • 批准号:
    3339813
  • 财政年份:
    1981
  • 资助金额:
    $ 19.52万
  • 项目类别:
ROLE OF C3A/C5A IN ANTIGEN-INDUCED BRONCHOCONSTRICTION
C3A/C5A 在抗原诱导的支气管收缩中的作用
  • 批准号:
    3339814
  • 财政年份:
    1981
  • 资助金额:
    $ 19.52万
  • 项目类别:
ROLE OF C3A/C5A IN ANTIGEN-INDUCED BRONCHOCONSTRICTION
C3A/C5A 在抗原诱导的支气管收缩中的作用
  • 批准号:
    3339811
  • 财政年份:
    1981
  • 资助金额:
    $ 19.52万
  • 项目类别:
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