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在肺炎小鼠模型中,补体C3a过敏毒素受体的消融导致对铜绿假单胞菌的杀伤增强。

Ablation of the complement C3a anaphylatoxin receptor causes enhanced killing of Pseudomonas aeruginosa in a mouse model of pneumonia.

作者信息

Mueller-Ortiz Stacey L, Hollmann Travis J, Haviland David L, Wetsel Rick A

机构信息

Research Center for Immunology and Autoimmune Diseases, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, 77030, USA.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2006 Aug;291(2):L157-65. doi: 10.1152/ajplung.00358.2005. Epub 2006 Feb 3.

Abstract

The C3a anaphylatoxin is a 77-amino acid peptide that is generated by enzymatic cleavage of C3 during activation of the complement system. C3a mediates numerous biological functions on binding its receptor (C3aR), which is present on both myeloid and nonmyeloid cells. To investigate the biological impact of C3a-mediated effects during acute pneumonia caused by Pseudomonas aeruginosa, we subjected C3aR-deficient mice and matched wild-type (WT) mice to P. aeruginosa pulmonary infection. C3aR-deficient mice exhibited increased killing of P. aeruginosa in the lungs, less dissemination of bacteria into the bloodstream, and a decreased inflammatory response to P. aeruginosa pulmonary infection compared with WT mice. To examine whether the absence of C3aR would impact the humoral immune response to P. aeruginosa, we immunized WT and C3aR-deficient mice via intraperitoneal injection with live P. aeruginosa. Both groups of mice developed similar levels of antibody specific to P. aeruginosa. Immunized C3aR-deficient and WT mice were subjected to P. aeruginosa pulmonary infection, and C3aR-deficient mice again displayed increased killing of P. aeruginosa in the lungs, less dissemination of bacteria into the bloodstream, and a decreased inflammatory response in the lungs. Collectively, these data demonstrate that independently of antibody production, absence of C3aR causes enhanced killing of P. aeruginosa despite a diminished inflammatory response in a mouse model of pneumonia.

摘要

C3a过敏毒素是一种由补体系统激活过程中C3酶解产生的含77个氨基酸的肽。C3a与其受体(C3aR)结合后介导多种生物学功能,C3aR存在于髓系细胞和非髓系细胞上。为了研究C3a介导的效应在铜绿假单胞菌引起的急性肺炎中的生物学影响,我们将C3aR缺陷小鼠和配对的野生型(WT)小鼠进行铜绿假单胞菌肺部感染。与WT小鼠相比,C3aR缺陷小鼠肺部对铜绿假单胞菌的杀伤作用增强,细菌向血液中的播散减少,对铜绿假单胞菌肺部感染的炎症反应减弱。为了检验C3aR的缺失是否会影响对铜绿假单胞菌的体液免疫反应,我们通过腹腔注射活的铜绿假单胞菌对WT和C3aR缺陷小鼠进行免疫。两组小鼠产生的针对铜绿假单胞菌的抗体水平相似。对免疫后的C3aR缺陷小鼠和WT小鼠进行铜绿假单胞菌肺部感染,C3aR缺陷小鼠肺部对铜绿假单胞菌的杀伤作用再次增强,细菌向血液中的播散减少,肺部炎症反应减弱。总体而言,这些数据表明,在肺炎小鼠模型中,独立于抗体产生,C3aR的缺失导致对铜绿假单胞菌的杀伤作用增强,尽管炎症反应减弱。

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