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Published on: October 22, 2019
[Apoptosis of pulmonary alveolar macrophages in aged and adult rats: a comparative study]
Xiao-shun Qian1, Qing-lei Zhu, Jie Yang
1Institute of Geriatric Cardiology, General Hospital of Chinese People's Liberation Army, Beijing 100853, China.
Objective:
To investigate the role of alveolar macrophages (AM) in the initiation of multiple organ failure in the elderly (MOFE).
Methods:
Three-month-old (adult) and 24-month-old (aged) males SD rats were used as experimental animals. Zymosan 0.5 g/kg was used to establish animal model of MOFE, normal saline were used among the control rats. The rats were divided into 4 groups: aged model group, aged control group, adult model group, and adult control group. Twenty-four hours after the establishment of model, 6 surviving rats from each group were killed. The trachea, bronthi, and lungs were isolated and lavaged with normal saline. One minute later the bronchi-alveolar lavage fluid (BALF) was re-extracted. Cells were collected from the fluid and put into 24-well cell culture plate. The alveolar macrophages (AMs) adhered to the wall were collected, suspended again, cultured, re-collected, centrifuged, and isolated. Apoptosis of the enriched AM was measured by propidium staining and flow cytometry. Fluo-3.AM staining and flow cytometry were used to detect the intracellular free calcium. Mitochondrial membrane electric potential was detected by rhodamine 123 staining with flow cytometry.
Results:
The apoptotic rate (APO) of AM in the aged rat models was 43.4% +/- 8.4%, significantly higher than that of adult model rats (24.2% +/- 3.0%, P < 0.01). Compared with the controls, the intracellular calcium increased, but mitochondrial Dgr;Psim decreased in the 2 model groups.
Conclusion:
The AM APO% of aged MOFE model increases. It may be one of the causes of difficulty to control the inflammation in the lung with MOFE and easiness to induce MOFE in elderly when their lungs are infected or injured. Changes of intracellular calcium and mitochondrial Dgr;Psim may play pivotal roles in apoptosis of AM.
Insights
Alveolar macrophages (AM) show increased apoptosis in aged rats with multiple organ failure (MOFE). This heightened AM apoptosis may contribute to inflammation and MOFE susceptibility in the elderly.
Area of Science:
- Immunology
- Gerontology
- Pathophysiology
Background:
- Multiple organ failure (MOFE) poses a significant health challenge, particularly in the elderly.
- Alveolar macrophages (AM) play a crucial role in pulmonary immunity and inflammation.
- Age-related changes in immune cells can impact susceptibility to critical illness.
Purpose of the Study:
- To investigate the role of alveolar macrophages (AM) in the initiation of multiple organ failure (MOFE) in aged individuals.
- To compare AM apoptosis rates between adult and aged rats modeled for MOFE.
- To explore the cellular mechanisms, including calcium and mitochondrial potential, underlying AM apoptosis in MOFE.
Main Methods:
- Establishment of a MOFE animal model in adult (3-month-old) and aged (24-month-old) Sprague-Dawley rats using zymosan.
- Isolation and culture of alveolar macrophages (AM) from bronchoalveolar lavage fluid (BALF).
- Assessment of AM apoptosis via propidium iodide staining and flow cytometry; intracellular calcium and mitochondrial membrane potential were measured using Fluo-3.AM and rhodamine 123 staining, respectively.
Main Results:
- Aged MOFE rat models exhibited a significantly higher AM apoptotic rate (43.4%) compared to adult MOFE models (24.2%).
- Both adult and aged MOFE models showed increased intracellular calcium levels and decreased mitochondrial membrane potential (ΔΨm) compared to controls.
- These cellular changes suggest a potential mechanism for increased AM apoptosis in aged MOFE.
Conclusions:
- Increased alveolar macrophage (AM) apoptosis is observed in aged rats with MOFE.
- Elevated AM apoptosis may contribute to uncontrolled lung inflammation and increased MOFE susceptibility in the elderly.
- Alterations in intracellular calcium and mitochondrial membrane potential are implicated as key factors in AM apoptosis during MOFE.
