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Lipid peroxidation by alveolar macrophages challenged with Cryptococcus neoformans, Candida albicans or Aspergillus
N T Gross1, K Hultenby, S Mengarelli
1Department of Immunology, Microbiology, Pathology and Infectious Diseases, Huddinge University Hospital, Sweden. Norma.Gross@impi.ki.se
Abstract:
Increased formation of oxygen radicals has previously been shown for alveolar macrophages (AM) challenged with Cryptococcus neoformans cells opsonized with fresh serum or polyclonal immunoglobulin G. AM show similar responses to Candida albicans or Aspergillus fumigatus. Oxygen radicals are capable of damaging various macromolecules, including lipids. In the present study, lipid peroxidation (LPO) caused by AM incubated with the fungi was examined in the presence and absence of lung surfactant. The level of malonaldehyde was used as an indicator of LPO. AM damage was examined by electron microscopy (EM), by trypan blue exclusion and by counting the AM loss from culture dish to supernatant. Stimulation of AM by each fungus increased cellular LPO but did not affect AM viability. A slight surfactant LPO induced by AM alone was shown with significantly increased values after addition of each fungus. EM studies showed that dense lipid droplets, presumably consisting of oxidized lipids, were ingested in high amounts together with C. neoformans cells that had been opsonized in fresh serum, and in low amounts in combination with C. albicans. These processes were accompanied by increased numbers of AM in the supernatants. LPO and detachment of AM were counteracted by vitamin E. In the lungs, AM exposed to one of these fungal pathogens might promote peroxidation of surfactant lipids.
Insights
Alveolar macrophages (AM) exposed to fungi like Cryptococcus neoformans and Candida albicans cause lipid peroxidation, damaging lung surfactant. Vitamin E can counteract this fungal-induced damage to AM and surfactant.
Area of Science:
- Immunology
- Pulmonary Medicine
- Biochemistry
Background:
- Alveolar macrophages (AM) generate oxygen radicals when challenged with fungi.
- Oxygen radicals can damage lipids, a process known as lipid peroxidation (LPO).
- Lung surfactant is a crucial component of the pulmonary system susceptible to oxidative damage.
Purpose of the Study:
- To investigate lipid peroxidation (LPO) in AM incubated with fungi, with and without lung surfactant.
- To assess the impact of fungal challenge on AM viability and integrity.
- To determine the role of vitamin E in mitigating fungal-induced LPO and AM damage.
Main Methods:
- Measurement of malonaldehyde as an indicator of LPO.
- Assessment of AM damage using electron microscopy (EM), trypan blue exclusion, and supernatant cell counts.
- Incubation of AM with Cryptococcus neoformans, Candida albicans, and Aspergillus fumigatus in the presence and absence of lung surfactant.
- Evaluation of vitamin E's protective effects.
Main Results:
- Fungal stimulation increased LPO in AM but did not affect AM viability.
- Significant LPO of lung surfactant was observed after AM were exposed to fungi.
- Electron microscopy revealed ingestion of oxidized lipid droplets with fungi, correlating with AM detachment.
- Vitamin E counteracted LPO and AM detachment.
Conclusions:
- AM challenged with fungi can induce lipid peroxidation in lung surfactant.
- Fungal-induced LPO may contribute to AM damage and detachment in the lungs.
- Vitamin E demonstrates a protective effect against fungal-induced LPO and AM damage.