Intrapulmonary neutrophil apoptosis in a pig model of pneumonia
T T Bauer1, Y Arce, C-H Marquette
1Abt. für Pneumologie, Allergologie und Schlafmedizin, Bergmannsheil, Klinikum der Ruhr-Universität, Bochum, Germany.
Background:
Apoptosis and necrosis are two distinct cell death modalities. Polymorphonuclear leukocytes (PMNL) play an important role in pneumonia and little information is available on whether these cells are cleared by necrosis or apoptosis. We therefore compared the proportion of apoptotic PMNL in lung tissues with and without pneumonia. In addition, the association of PMNL apoptosis and mechanical ventilation (MV) was investigated.
Methods:
Samples obtained from a pig model developed to tracheobronchial stenting were analysed. Pneumonia was induced with that model in 10 animals (white-Landrace piglets, Pittman-Moore or Göttingen minipigs). Animals were sacrificed when clinical parameters of pneumonia became evident and 17 lung samples could be analysed for histologic evidence of pneumonia, growth of micro-organisms, and the apoptotic index (proportion of apoptotic PMNL over all PMNL in a 400-power field). In addition, lung samples (n = 7) from two pigs without stent implantation on mechanically ventilated for more than 48 h were studied.
Results:
A total of 9/17 samples (53%) showed histologic evidence of pneumonia, 11/17 (65%) had significant bacterial growth (> 10(3) cfu/g), and 7/17 (41%) fulfilled both criteria. The apoptotic index was not significantly different in samples with and without histologic evidence of pneumonia (pneumonia: 25.3 +/- 6.1% vs. No pneumonia: 25.2 +/- 11.9%; 95%CI: -9.7 - 9.5, p = 0.989) or in samples with and without significant bacterial growth (significant bacterial growth: 23.5+/-9.3% vs. No significant bacterial growth: 28.5+/-8.2%; 95%CI: -4.6 - 16.7; p = 0.284). However, the apoptotic index was higher in samples of pigs, mechanically ventilated for more than 48 h, compared to the stent group (MV: 36.9+/-10.7% vs. Stent: 25.2 +/- 9.0%; 95% CI: -20.5 - -2.9; p = 0.012).
Conclusion:
In an animal model, the proportion of apoptotic PMNL was not different in lung samples with and without histologic or bacterial pneumonia. However, MV for more than 48 h was associated with a higher proportion of apoptotic PMNL in lung tissue. This study may be helpful for the understanding of the evolution of lung tissue damage induced by bacterial pneumonia and MV.
Insights
In pneumonia, polymorphonuclear leukocytes (PMNL) are not cleared via apoptosis. However, mechanical ventilation (MV) for over 48 hours increases apoptotic PMNL in lung tissue.
Area of Science:
- Cell Biology
- Pulmonary Medicine
- Immunology
Background:
- Polymorphonuclear leukocytes (PMNL) are crucial in pneumonia pathogenesis.
- The clearance mechanism of PMNL in pneumonia (apoptosis vs. necrosis) is not well understood.
- This study investigates PMNL apoptosis in pneumonia and its relation to mechanical ventilation.
Purpose of the Study:
- To compare the proportion of apoptotic PMNL in lung tissues with and without pneumonia.
- To investigate the association between PMNL apoptosis and mechanical ventilation (MV).
Main Methods:
- Utilized a pig model with induced pneumonia via tracheobronchial stenting.
- Analyzed 17 lung samples for histologic pneumonia, microbial growth, and apoptotic index (AI).
- Compared AI in pigs with pneumonia vs. controls, and in mechanically ventilated pigs vs. a stent group.
Main Results:
- Histologic pneumonia and/or bacterial growth were present in 53-65% of samples.
- No significant difference in AI was found between samples with or without pneumonia (25.3% vs. 25.2%).
- A significantly higher AI (36.9%) was observed in pigs mechanically ventilated for >48 hours compared to the stent group (25.2%).
Conclusions:
- The proportion of apoptotic PMNL does not differ in lung tissue with or without pneumonia.
- Mechanical ventilation exceeding 48 hours is associated with increased PMNL apoptosis in lung tissue.
- Findings contribute to understanding lung tissue damage in bacterial pneumonia and MV.
