A murine model of sepsis following smoke inhalation injury

Matthias Lange, Atsumori Hamahata, Daniel L. Traber, Aimalohi Esechie, Collette Jonkam, Kamna Bansal, Yoshimitsu Nakano, Lillian D. Traber, Perenlei Enkhbaatar

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Acute lung injury (ALI) by smoke inhalation with subsequent pneumonia and sepsis represents a major cause of morbidity and mortality in burn patients. The aim of the present study was to develop a murine model of ALI and sepsis to enhance the knowledge of mechanistic aspects and pathophysiological changes in patients with these injuries. In deeply anesthetized female C57BL/6 mice, injury was induced by four sets of cotton smoke using an inhalation chamber. Afterward, live Pseudomonas aeruginosa (3.2 × 107 colony-forming units) was administered intranasally. The indicated dose of bacteria was determined based on the results of a dose-response study (n = 47). The following study groups were monitored for survival over 96 h: (1) sham injury group, (2) only smoke inhalation group, (3) only bacteria group, and (4) smoke inhalation plus bacteria group. Each group included 10 mice. The survival rates were 100%, 90%, 30%, and 10%, respectively. The double hit injury was associated with excessive releases of pro-inflammatory cytokines in the plasma, and enhanced neutrophil accumulation, increased lipid peroxidation, and excessive formation of reactive nitrogen species in the lung. In mice receiving only smoke inhalation injury, no systemic cytokine release and increased lung tissue lipid peroxidation were observed. However, smoke alone significantly increased neutrophil accumulation and formation of reactive nitrogen species in lung tissue. In conclusion, bacterial pneumonia is predominantly responsible for mortality and morbidity in this novel murine model of smoke inhalation and pulmonary sepsis. Reactive oxygen and nitrogen species mediate the severity of lung injury.

Original languageEnglish (US)
Pages (from-to)1555-1560
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume391
Issue number3
DOIs
StatePublished - Jan 15 2010

Fingerprint

Smoke Inhalation Injury
Smoke
Sepsis
Inhalation
Reactive Nitrogen Species
Lung
Acute Lung Injury
Wounds and Injuries
Bacteria
Lipid Peroxidation
Neutrophils
Cytokines
Morbidity
Bacterial Pneumonia
Tissue
Mortality
Lipids
Lung Injury
Inbred C57BL Mouse
Pseudomonas aeruginosa

Keywords

  • Acute lung injury
  • Mice
  • Sepsis
  • Smoke inhalation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

Cite this

A murine model of sepsis following smoke inhalation injury. / Lange, Matthias; Hamahata, Atsumori; Traber, Daniel L.; Esechie, Aimalohi; Jonkam, Collette; Bansal, Kamna; Nakano, Yoshimitsu; Traber, Lillian D.; Enkhbaatar, Perenlei.

In: Biochemical and Biophysical Research Communications, Vol. 391, No. 3, 15.01.2010, p. 1555-1560.

Research output: Contribution to journalArticle

Lange, M, Hamahata, A, Traber, DL, Esechie, A, Jonkam, C, Bansal, K, Nakano, Y, Traber, LD & Enkhbaatar, P 2010, 'A murine model of sepsis following smoke inhalation injury', Biochemical and Biophysical Research Communications, vol. 391, no. 3, pp. 1555-1560. https://doi.org/10.1016/j.bbrc.2009.12.124
Lange M, Hamahata A, Traber DL, Esechie A, Jonkam C, Bansal K et al. A murine model of sepsis following smoke inhalation injury. Biochemical and Biophysical Research Communications. 2010 Jan 15;391(3):1555-1560. https://doi.org/10.1016/j.bbrc.2009.12.124
Lange, Matthias ; Hamahata, Atsumori ; Traber, Daniel L. ; Esechie, Aimalohi ; Jonkam, Collette ; Bansal, Kamna ; Nakano, Yoshimitsu ; Traber, Lillian D. ; Enkhbaatar, Perenlei. / A murine model of sepsis following smoke inhalation injury. In: Biochemical and Biophysical Research Communications. 2010 ; Vol. 391, No. 3. pp. 1555-1560.
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