Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs

Sadatomo Tasaka, Akitoshi Ishizaka, Koichi Sayama, Fumio Sakamaki, Hidetoshi Nakamura, Takeshi Terashima, Yasuhiro Waki, Kenzo Soejima, Morio Nakamura, Hiroaki Matsubara, Seitaro Fujishima, Minoru Kanazawa

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Corynebacterium parvum (CP) is known to increase susceptibility to endotoxin, which is associated with increased production of tumor necrosis factor (TNF). We investigated the effect of CP-priming on the pathogenesis of acute lung injury caused by intratracheal Escherichia coli endotoxin (lipopolysaccharide [LPS]). Guinea pigs were divided into four groups: (1) control (n = 6), (2) CP-alone (n = 6), (3) LPS-alone (n = 6), and (4) CP + LPS (n = 6). A CP dose of 4 mg/kg was injected intraperitoneally 7 d before the study. Animals were observed for 4 h after intratracheal administration of 0.02 mg/kg of LPS. The lung wet-to-dry weight ratio (W/D), [125I]albumin concentration ratio of lung tissue to plasma (T/P) and of bronchoalveolar lavage (BAL) fluid to plasma (B/P) and differential cell count in BAL fluid were examined. In the LPS-alone group, neither excess lung water nor increased albumin leakage was observed. The CP + LPS group showed increased lung water and albumin leakage as compared with the other three groups (p < 0.05). We also observed increased cell counts in BAL fluid (p < 0.05), in the CP + LPS group. The spleen weight was increased in guinea pigs pretreated with CP, indicating reticuloendothelial system (RES) activation. In the CP + LPS group, the TNF level was increased in both plasma and BAL fluid. We conclude that pretreatment with CP enhances LPS-induced acute lung injury in parallel with increasing TNF production, which suggests that the activation of mononuclear phagocytes contributes to increased susceptibility to intratracheal endotoxin in guinea pigs.

Original languageEnglish
Pages (from-to)1047-1055
Number of pages9
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume153
Issue number3
Publication statusPublished - 1996

Fingerprint

Propionibacterium acnes
Lung Injury
Endotoxins
Guinea Pigs
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Hot Temperature
Bronchoalveolar Lavage Fluid
Albumins
Acute Lung Injury
Lung
Cell Count
Weights and Measures
Mononuclear Phagocyte System
Water
Pulmonary Edema
Phagocytes
Spleen

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Tasaka, S., Ishizaka, A., Sayama, K., Sakamaki, F., Nakamura, H., Terashima, T., ... Kanazawa, M. (1996). Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs. American Journal of Respiratory and Critical Care Medicine, 153(3), 1047-1055.

Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs. / Tasaka, Sadatomo; Ishizaka, Akitoshi; Sayama, Koichi; Sakamaki, Fumio; Nakamura, Hidetoshi; Terashima, Takeshi; Waki, Yasuhiro; Soejima, Kenzo; Nakamura, Morio; Matsubara, Hiroaki; Fujishima, Seitaro; Kanazawa, Minoru.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 153, No. 3, 1996, p. 1047-1055.

Research output: Contribution to journalArticle

Tasaka, S, Ishizaka, A, Sayama, K, Sakamaki, F, Nakamura, H, Terashima, T, Waki, Y, Soejima, K, Nakamura, M, Matsubara, H, Fujishima, S & Kanazawa, M 1996, 'Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs', American Journal of Respiratory and Critical Care Medicine, vol. 153, no. 3, pp. 1047-1055.
Tasaka, Sadatomo ; Ishizaka, Akitoshi ; Sayama, Koichi ; Sakamaki, Fumio ; Nakamura, Hidetoshi ; Terashima, Takeshi ; Waki, Yasuhiro ; Soejima, Kenzo ; Nakamura, Morio ; Matsubara, Hiroaki ; Fujishima, Seitaro ; Kanazawa, Minoru. / Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs. In: American Journal of Respiratory and Critical Care Medicine. 1996 ; Vol. 153, No. 3. pp. 1047-1055.
@article{2e792f1cc61e4fb38b8ffb4039e8a084,
title = "Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs",
abstract = "Corynebacterium parvum (CP) is known to increase susceptibility to endotoxin, which is associated with increased production of tumor necrosis factor (TNF). We investigated the effect of CP-priming on the pathogenesis of acute lung injury caused by intratracheal Escherichia coli endotoxin (lipopolysaccharide [LPS]). Guinea pigs were divided into four groups: (1) control (n = 6), (2) CP-alone (n = 6), (3) LPS-alone (n = 6), and (4) CP + LPS (n = 6). A CP dose of 4 mg/kg was injected intraperitoneally 7 d before the study. Animals were observed for 4 h after intratracheal administration of 0.02 mg/kg of LPS. The lung wet-to-dry weight ratio (W/D), [125I]albumin concentration ratio of lung tissue to plasma (T/P) and of bronchoalveolar lavage (BAL) fluid to plasma (B/P) and differential cell count in BAL fluid were examined. In the LPS-alone group, neither excess lung water nor increased albumin leakage was observed. The CP + LPS group showed increased lung water and albumin leakage as compared with the other three groups (p < 0.05). We also observed increased cell counts in BAL fluid (p < 0.05), in the CP + LPS group. The spleen weight was increased in guinea pigs pretreated with CP, indicating reticuloendothelial system (RES) activation. In the CP + LPS group, the TNF level was increased in both plasma and BAL fluid. We conclude that pretreatment with CP enhances LPS-induced acute lung injury in parallel with increasing TNF production, which suggests that the activation of mononuclear phagocytes contributes to increased susceptibility to intratracheal endotoxin in guinea pigs.",
author = "Sadatomo Tasaka and Akitoshi Ishizaka and Koichi Sayama and Fumio Sakamaki and Hidetoshi Nakamura and Takeshi Terashima and Yasuhiro Waki and Kenzo Soejima and Morio Nakamura and Hiroaki Matsubara and Seitaro Fujishima and Minoru Kanazawa",
year = "1996",
language = "English",
volume = "153",
pages = "1047--1055",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "3",

}

TY - JOUR

T1 - Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs

AU - Tasaka, Sadatomo

AU - Ishizaka, Akitoshi

AU - Sayama, Koichi

AU - Sakamaki, Fumio

AU - Nakamura, Hidetoshi

AU - Terashima, Takeshi

AU - Waki, Yasuhiro

AU - Soejima, Kenzo

AU - Nakamura, Morio

AU - Matsubara, Hiroaki

AU - Fujishima, Seitaro

AU - Kanazawa, Minoru

PY - 1996

Y1 - 1996

N2 - Corynebacterium parvum (CP) is known to increase susceptibility to endotoxin, which is associated with increased production of tumor necrosis factor (TNF). We investigated the effect of CP-priming on the pathogenesis of acute lung injury caused by intratracheal Escherichia coli endotoxin (lipopolysaccharide [LPS]). Guinea pigs were divided into four groups: (1) control (n = 6), (2) CP-alone (n = 6), (3) LPS-alone (n = 6), and (4) CP + LPS (n = 6). A CP dose of 4 mg/kg was injected intraperitoneally 7 d before the study. Animals were observed for 4 h after intratracheal administration of 0.02 mg/kg of LPS. The lung wet-to-dry weight ratio (W/D), [125I]albumin concentration ratio of lung tissue to plasma (T/P) and of bronchoalveolar lavage (BAL) fluid to plasma (B/P) and differential cell count in BAL fluid were examined. In the LPS-alone group, neither excess lung water nor increased albumin leakage was observed. The CP + LPS group showed increased lung water and albumin leakage as compared with the other three groups (p < 0.05). We also observed increased cell counts in BAL fluid (p < 0.05), in the CP + LPS group. The spleen weight was increased in guinea pigs pretreated with CP, indicating reticuloendothelial system (RES) activation. In the CP + LPS group, the TNF level was increased in both plasma and BAL fluid. We conclude that pretreatment with CP enhances LPS-induced acute lung injury in parallel with increasing TNF production, which suggests that the activation of mononuclear phagocytes contributes to increased susceptibility to intratracheal endotoxin in guinea pigs.

AB - Corynebacterium parvum (CP) is known to increase susceptibility to endotoxin, which is associated with increased production of tumor necrosis factor (TNF). We investigated the effect of CP-priming on the pathogenesis of acute lung injury caused by intratracheal Escherichia coli endotoxin (lipopolysaccharide [LPS]). Guinea pigs were divided into four groups: (1) control (n = 6), (2) CP-alone (n = 6), (3) LPS-alone (n = 6), and (4) CP + LPS (n = 6). A CP dose of 4 mg/kg was injected intraperitoneally 7 d before the study. Animals were observed for 4 h after intratracheal administration of 0.02 mg/kg of LPS. The lung wet-to-dry weight ratio (W/D), [125I]albumin concentration ratio of lung tissue to plasma (T/P) and of bronchoalveolar lavage (BAL) fluid to plasma (B/P) and differential cell count in BAL fluid were examined. In the LPS-alone group, neither excess lung water nor increased albumin leakage was observed. The CP + LPS group showed increased lung water and albumin leakage as compared with the other three groups (p < 0.05). We also observed increased cell counts in BAL fluid (p < 0.05), in the CP + LPS group. The spleen weight was increased in guinea pigs pretreated with CP, indicating reticuloendothelial system (RES) activation. In the CP + LPS group, the TNF level was increased in both plasma and BAL fluid. We conclude that pretreatment with CP enhances LPS-induced acute lung injury in parallel with increasing TNF production, which suggests that the activation of mononuclear phagocytes contributes to increased susceptibility to intratracheal endotoxin in guinea pigs.

UR - http://www.scopus.com/inward/record.url?scp=9044247855&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=9044247855&partnerID=8YFLogxK

M3 - Article

C2 - 8630544

AN - SCOPUS:9044247855

VL - 153

SP - 1047

EP - 1055

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 3

ER -