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Updated: Jun 10, 2026

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A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Traumatic Brain Injury Enhances Susceptibility to Lung Bacterial Infection in Mice and Pigs by Modulating the Innate
Anupamaa J Seshadri1, Paula Alves1, Hyo In Kim1,2
1Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Critical Care Medicine
|June 9, 2026
Summary
Traumatic brain injury (TBI) impairs lung bacterial clearance, despite increased neutrophils. TBI plasma, including extracellular vesicles, causes neutrophil dysfunction, increasing infection risk.
Area of Science:
- Immunology
- Neuroscience
- Pulmonary Medicine
Background:
- Traumatic brain injury (TBI) disrupts immune homeostasis, increasing infection susceptibility.
- Neutrophils (PMNs) are critical for bacterial clearance, but their function may be impaired post-TBI.
Purpose of the Study:
- To investigate the impact of TBI on lung bacterial clearance in murine and porcine models.
- To assess the effect of TBI on neutrophil (PMN) function, particularly in response to plasma from human TBI patients.
Main Methods:
- Mild TBI was induced in C57BL6 mice and Yucatan mini swine, followed by bacterial lung inoculation.
- Bronchoalveolar lavage, blood, and lung tissue were collected for analysis.
- In vitro assays evaluated PMN function using plasma from human TBI patients and healthy volunteers.
Main Results:
- TBI models showed reduced pulmonary bacterial clearance despite elevated PMN counts in the lungs and blood.
- Plasma and extracellular vesicles (EVs) from TBI patients impaired PMN function in vitro, reducing chemokinesis, reactive oxygen species production, and phagocytosis.
Conclusions:
- TBI compromises lung bacterial clearance, linked to systemic factors in plasma, including EVs, that cause PMN dysfunction.
- These findings highlight a mechanism contributing to increased bacterial lung infection risk after TBI.
- Further research is needed to elucidate the TBI-PMN dysfunction pathway and therapeutic targets.

