OBJECTIVE: To establish a model of secondary bacterial pneumonia following gastric aspiration and to identify possible mechanisms involved in the suppressed antibacterial defenses following the initial pulmonary insult. DESIGN: A controlled, in vivo laboratory study. SETTING: Research laboratory of a health sciences university. SUBJECTS: Ninety-five Long-Evans rats. INTERVENTIONS: Animals were anesthetized for neck dissection and placement of a 14-gauge catheter in the trachea. Gastric aspirate (1.2 mL/kg of saline, pH 1.25, and 40 mg/mL sterile rat gastric particles) or an equal amount of normal saline (pH 5.3) was instilled intratracheally. One minute after this insult, animals received an intratracheal instillation of either 5.6 x 10 colony-forming units of Escherichia coli or an equal volume of normal saline. The animals remained in room air until kill at 4 hrs or 24 hrs after the intratracheal instillation. The lungs were homogenized for quantitative bacterial cultures. Bronchoalveolar lavage fluid was obtained for cell counts and measurements of albumin, tumor necrosis factor-alpha, interleukin-1 beta, cytokine-induced neutrophil chemoattractant-1, macrophage inflammatory protein-2, monocyte chemoattractant protein-1, and interleukin 10. MEASUREMENTS AND MAIN RESULTS: Animals that received gastric aspirate (followed by normal saline or E. coli) had increased injury as assessed by significant reductions in oxygenation and elevations in bronchoalveolar lavage albumin. At 24 hrs, animals that received gastric aspirate inoculation followed by E. coli had significantly higher pulmonary bacterial counts compared with animals that received E. coli alone. Gastric aspiration injury followed by bacterial inoculation also resulted in acute, but transient, increases in tumor necrosis factor-alpha, interleukin-1 beta, cytokine-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 and more sustained elevations of monocyte chemoattractant protein-1 and interleukin-10. CONCLUSIONS: Lung injury increases and bacterial clearance decreases in this experimental model of E. coli pneumonia following gastric aspiration. Cytokine profiles suggest possible mechanisms for the impaired antibacterial host defense.
OBJECTIVE: To establish a model of secondary bacterial pneumonia following gastric aspiration and to identify possible mechanisms involved in the suppressed antibacterial defenses following the initial pulmonary insult. DESIGN: A controlled, in vivo laboratory study. SETTING: Research laboratory of a health sciences university. SUBJECTS: Ninety-five Long-Evans rats. INTERVENTIONS: Animals were anesthetized for neck dissection and placement of a 14-gauge catheter in the trachea. Gastric aspirate (1.2 mL/kg of saline, pH 1.25, and 40 mg/mL sterile rat gastric particles) or an equal amount of normal saline (pH 5.3) was instilled intratracheally. One minute after this insult, animals received an intratracheal instillation of either 5.6 x 10 colony-forming units of Escherichia coli or an equal volume of normal saline. The animals remained in room air until kill at 4 hrs or 24 hrs after the intratracheal instillation. The lungs were homogenized for quantitative bacterial cultures. Bronchoalveolar lavage fluid was obtained for cell counts and measurements of albumin, tumor necrosis factor-alpha, interleukin-1 beta, cytokine-induced neutrophil chemoattractant-1, macrophage inflammatory protein-2, monocyte chemoattractant protein-1, and interleukin 10. MEASUREMENTS AND MAIN RESULTS: Animals that received gastric aspirate (followed by normal saline or E. coli) had increased injury as assessed by significant reductions in oxygenation and elevations in bronchoalveolar lavage albumin. At 24 hrs, animals that received gastric aspirate inoculation followed by E. coli had significantly higher pulmonary bacterial counts compared with animals that received E. coli alone. Gastric aspiration injury followed by bacterial inoculation also resulted in acute, but transient, increases in tumor necrosis factor-alpha, interleukin-1 beta, cytokine-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 and more sustained elevations of monocyte chemoattractant protein-1 and interleukin-10. CONCLUSIONS:Lung injury increases and bacterial clearance decreases in this experimental model of E. coli pneumonia following gastric aspiration. Cytokine profiles suggest possible mechanisms for the impaired antibacterial host defense.
Authors: F Puig; R Herrero; R Guillamat-Prats; M N Gómez; J Tijero; L Chimenti; O Stelmakh; L Blanch; A Serrano-Mollar; M A Matthay; A Artigas Journal: Am J Physiol Lung Cell Mol Physiol Date: 2016-06-17 Impact factor: 5.464
Authors: Madathilparambil V Suresh; George Yalamanchili; Tejeshwar C Rao; Sinan Aktay; Alex Kralovich; Yatrik M Shah; Krishnan Raghavendran Journal: FASEB Bioadv Date: 2022-01-12
Authors: Stanley F Fernandez; Christopher Fung; Jadwiga D Helinski; Ravi Alluri; Bruce A Davidson; Paul R Knight Journal: Biomed Res Int Date: 2013-10-30 Impact factor: 3.411