Literature DB >> 2492173

Bronchoalveolar macrophages from patients with idiopathic pulmonary fibrosis are unable to kill facultative intracellular bacteria.

D Savici1, P A Campbell, T E King.   

Abstract

The accumulation of inflammatory and immune effector cells in the lungs of patients at early stages of interstitial lung disease has been well documented, but little is known about the functional activity of these cells, particularly alveolar macrophages. The purpose of the experiments described here was to determine whether alveolar macrophages from patients with idiopathic pulmonary fibrosis (IPF) differed from alveolar macrophages of normal subjects using a model system that assesses a component of cell-mediated immunity. Alveolar macrophages were tested for their ability to phagocytose and kill the facultative intracellular bacterium Listeria monocytogenes. Because this system requires the stimulation of macrophages by antigen-specific T-cells, it allows the assessment of effector functions of macrophages found in the lower respiratory tract of patients with IPF. Data showed that alveolar macrophages from normal subjects both phagocytosed and killed those bacteria. However, alveolar macrophages from patients with IPF phagocytosed bacteria normally but expressed little bactericidal or bacteriostatic activity. Further, we found no difference in HLA-DR expression by normal and IPF alveolar macrophages. Therefore, it does not appear that this defect in bactericidal activity in IPF macrophages results from a defect in the antigen-presenting function of these cells. These data suggest that alveolar macrophages from patients with IPF express a functional deficiency in their ability to kill facultative intracellular bacteria.

Entities:  

Mesh:

Substances:

Year:  1989        PMID: 2492173     DOI: 10.1164/ajrccm/139.1.22

Source DB:  PubMed          Journal:  Am Rev Respir Dis        ISSN: 0003-0805


  2 in total

1.  Effect of Co-trimoxazole (Trimethoprim-Sulfamethoxazole) vs Placebo on Death, Lung Transplant, or Hospital Admission in Patients With Moderate and Severe Idiopathic Pulmonary Fibrosis: The EME-TIPAC Randomized Clinical Trial.

Authors:  Andrew M Wilson; Allan B Clark; Tony Cahn; Edwin R Chilvers; William Fraser; Matthew Hammond; David M Livermore; Toby M Maher; Helen Parfrey; Ann Marie Swart; Susan Stirling; David R Thickett; Moira Whyte
Journal:  JAMA       Date:  2020-12-08       Impact factor: 56.272

2.  Fibrotic lung disease inhibits immune responses to staphylococcal pneumonia via impaired neutrophil and macrophage function.

Authors:  Helen I Warheit-Niemi; Summer J Edwards; Shuvasree SenGupta; Carole A Parent; Xiaofeng Zhou; David N O'Dwyer; Bethany B Moore
Journal:  JCI Insight       Date:  2022-02-22
  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.