Increased expression of inflammatory cytokines and adhesion molecules by alveolar macrophages of human lung allograft recipients with acute rejection: decline with resolution of rejection

2000 ◽  
Vol 19 (9) ◽  
pp. 858-865 ◽  
Author(s):  
Monica Rizzo ◽  
Krovvidi S.R SivaSai ◽  
Michael A Smith ◽  
Elbert P Trulock ◽  
John P Lynch ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Alveolar Macrophages ◽  
Human Lung

Surfactant downregulates synthesis of DNA and inflammatory mediators in normal human lung fibroblasts

1996 ◽  
Vol 270 (1) ◽  
pp. L159-L163 ◽  
Author(s):  
M. J. Thomassen ◽  
J. M. Antal ◽  
B. P. Barna ◽  
L. T. Divis ◽  
D. P. Meeker ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Human Lung ◽  
Thymidine Incorporation ◽  
Interleukin 1 ◽  
S Phase ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblast ◽  
Normal Human

The initial inflammatory event in the adult respiratory distress syndrome (ARDS) is followed by fibroproliferation and a cascade of fibroblast-derived mediators. Because lung fibroblasts may be exposed to surfactant as well as inflammatory cytokines during ARDS, we hypothesized that surfactant might modulate fibroblast activity. We previously demonstrated that surfactant inhibited production of inflammatory cytokines from endotoxin-stimulated human alveolar macrophages. In the current study the effects of surfactant on normal human lung fibroblast proliferative capacity and mediator production were examined. Both synthetic (Exosurf) and natural (Survanta) surfactant inhibited fibroblast [3H]thymidine incorporation. Examination of pre-S-phase events indicated stimulation of the immediate response gene, c-fos, and no effect on the G1/S cyclin, cyclin D1, suggesting that the surfactant block occurred elsewhere before S phase. The antioxidant N-acetyl-L-cysteine (NAC), like surfactant, inhibited [3H]thymidine incorporation. Furthermore, menadione, a generator of intracellular H2O2, stimulated fibroblast [3H]thymidine incorporation, and this was inhibited by surfactant. Interleukin-1 (IL-1)-stimulated secretion of the inflammatory mediators, IL-6 and prostaglandin E2, was also inhibited by surfactant. These data suggest that surfactant may modify lung fibroblast participation in ARDS sequelae by downregulating DNA synthesis and secondary inflammatory mediator production.

scholarly journals Characterization of Early Stages of Human Alveolar Infection by the Q Fever AgentCoxiella burnetii

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Amanda L. Dragan ◽  
Richard C. Kurten ◽  
Daniel E. Voth
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Human Lung ◽  
Q Fever ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Human Lung Tissue ◽  
Content Type ◽  
Alveolar Epithelial

ABSTRACTHuman Q fever is caused by the intracellular bacterial pathogenCoxiella burnetii. Q fever presents with acute flu-like and pulmonary symptoms or can progress to chronic, severe endocarditis. After human inhalation,C. burnetiiis engulfed by alveolar macrophages and transits through the phagolysosomal maturation pathway, resisting the acidic pH of lysosomes to form a parasitophorous vacuole (PV) in which to replicate. Previous studies showed thatC. burnetiireplicates efficiently in primary human alveolar macrophages (hAMs) inex vivohuman lung tissue. AlthoughC. burnetiireplicates in most cell typesin vitro, the pathogen does not grow in non-hAM cells of human lung tissue. In this study, we investigated the interaction betweenC. burnetiiand other pulmonary cell types apart from the lung environment.C. burnetiiformed a prototypical PV and replicated efficiently in human pulmonary fibroblasts and in airway, but not alveolar, epithelial cells. Atypical PV expansion in alveolar epithelial cells was attributed in part to defective recruitment of autophagy-related proteins. Further assessment of theC. burnetiigrowth niche showed that macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response toC. burnetiiand ultimately shifted to an M2-polarized phenotype characteristic of anti-inflammatory macrophages. Considering our findings together, this study provides further clarity on the uniqueC. burnetii-lung dynamic during early stages of human acute Q fever.

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