Open AccessRespiratory effects of lipopolysaccharide‐induced inflammatory lung injury in mice
Author(s) -
Faffe D.S.,
Seidl V.R.,
Chagas P.S.C,
Gonçalves de Moraes V.L,
Capelozzi V.L.,
Rocco P.R.M.,
Zin W.A.
Publication year - 2000
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.2000.15a16.x
Subject(s) - bronchoalveolar lavage , histopathology , lipopolysaccharide , lung , inhalation , medicine , tumor necrosis factor alpha , infiltration (hvac) , respiratory system , pathology , saline , inflammation , necrosis , anesthesia , physics , thermodynamics
The pathogenic mechanisms of lipopolysaccharide (LPS)‐induced lung injury have not been classified. This study examined the physiological changes after endotoxin inhalation and related those to features of pulmonary inflammation in mice. Pulmonary mechanics, histopathology, and bronchoalveolar lavage fluid (BALF) from BALB/c mice were analysed at different occasions (3, 24, 48 and 72 h) after inhalation of saline or LPS from Excherichia coli (0.3 (L0.3) or 10 mg·mL ‐1 (L10)). Mice were sedated, anaesthetized, and ventilated. After chest wall resection static ( E st) and dynamic ( E dyn) elastances, Δ E ( E dyn‐ E st), resistive (Δ P 1) and viscoelastic/inhomogeneous pressures (Δ P 2), and Δ P 1+Δ P 2 (Δ P tot) were obtained by end‐inflation occlusion method. Lungs were prepared for histopathology. In parallel groups, tumour necrosis factor (TNF)‐α, neutrophils, and protein were evaluated in the BALF. L0.3 and L10 showed a time‐dependent production of TNF‐α preceding a massive neutrophil infiltration. In L10 BALF there was an increase in protein level at 24 and 48 h. E st and E dyn increased early in L0.3 (65%, 63%) and L10 (41%, 51%). In L10 Δ E , Δ P 2, and Δ P tot showed a gradual rise. At 72 h all groups were similar. L0.3 showed an early increase in cellularity, which returned to normal at 72 h. L10 presented the same pattern with the cell count remaining elevated until 72 h. In conclusion, lipopolysaccharide inhalation led to elastic and viscoelastic pulmonary changes together with tumour necrosis factor‐α production and neutrophil infiltration in mouse lung.