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Updated: Jul 2, 2026
Mouse Pneumonectomy Model of Compensatory Lung Growth
Published on: December 17, 2014
Occult injury in the residual lung after pneumonectomy in mice
Atsushi Tajima1, Mitsutomo Kohno, Masazumi Watanabe
1Department of Surgery, Saiseikai Utsunomiya Hospital, Tochigi, Japan.
Objectives:
We aimed to determine the acute phase impact of pneumonectomy with respect to injury in the remaining lung using a murine model, and to investigate the profiles of inflammatory mediators including high mobility group box 1 protein (HMGB1) following surgery and administration of low dose intratracheal lipopolysaccharide.
Methods:
Mice received left pneumonectomy with intratracheal administration of either saline or lipopolysaccharide. Lung permeability index, lung wet-to-dry weight ratio, pathological findings, HMGB1 levels in bronchoalveolar lavage fluid (BALF) and plasma, and cytokine profiles in BALF were assessed 24 h after surgery.
Results:
Index of capillary permeability, lung water content, and neutrophil and macrophage counts in BALF were significantly increased by pneumonectomy. These parameters were highest in the mice with pneumonectomy with intratracheal administration of lipopolysaccharide. On lung pathology, neutrophil infiltration was prominent in the residual lung after pneumonectomy. HMGB1 levels were significantly higher in both BALF and plasma in the mice with pneumonectomy, and were highest in those with pneumonectomy and intratracheal administration of lipopolysaccharide. Pro-inflammatory cytokine levels including interferon-gamma significantly increased in BALF in the mice with pneumonectomy.
Conclusions:
It was suggested that pneumonectomy itself may cause occult lung injury in the acute phase (24 h) of post-surgery which could be enhanced by inflammatory stimulus, such as bacterial component, leading to significant lung injury. HMGB1 might be involved in the pathogenesis of the occult lung injury.
Insights
Pneumonectomy can cause lung injury, worsened by inflammation. High mobility group box 1 protein (HMGB1) may play a role in this post-surgery damage.
Area of Science:
- Pulmonary Medicine
- Surgical Research
- Immunology
Background:
- Pneumonectomy, the surgical removal of a lung, can lead to complications in the remaining lung.
- Understanding the acute inflammatory response post-pneumonectomy is crucial for patient outcomes.
- High mobility group box 1 protein (HMGB1) is implicated in various inflammatory conditions.
Purpose of the Study:
- To evaluate the acute impact of pneumonectomy on the remaining lung in a murine model.
- To investigate the role of inflammatory mediators, including HMGB1, after pneumonectomy and lipopolysaccharide challenge.
Main Methods:
- Mice underwent left pneumonectomy with intratracheal administration of saline or lipopolysaccharide.
- Assessed lung permeability index, wet-to-dry weight ratio, and histopathology 24 hours post-surgery.
- Measured HMGB1 levels in bronchoalveolar lavage fluid (BALF) and plasma, alongside BALF cytokine profiles.
Main Results:
- Pneumonectomy significantly increased lung permeability, water content, and inflammatory cell counts (neutrophils, macrophages) in BALF.
- These parameters were exacerbated by co-administration of lipopolysaccharide.
- Elevated HMGB1 levels were observed in BALF and plasma post-pneumonectomy, peaking with lipopolysaccharide treatment.
- Pro-inflammatory cytokines, including interferon-gamma, increased in BALF following pneumonectomy.
Conclusions:
- Pneumonectomy itself may induce subclinical lung injury in the acute phase (24 hours).
- This injury can be amplified by inflammatory stimuli, such as bacterial components.
- HMGB1 is a potential mediator in the pathogenesis of post-pneumonectomy lung injury.
