Appearance of cytokine-induced neutrophil chemoattractant isoforms and immunolocalization of them in lipopolysaccharide-induced acute lung inflammation in rats

Mitsuhashi, Hiroaki; Hata, J. Steven; Asano, Satoshi; Kishimoto, Tadashi

doi:10.1007/s000110050508

Cited by 27 publications

(20 citation statements)

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“…Several experimental studies have suggested that CINCs play an important role in acute inflammatory response [11 -16]. For example, CINC-1 is increased in lung tissue and bronchoalveolar lavage (BAL) fluid in LPSinduced rat lung injury model, and intratracheal administration of anti-CINC-1 antibody reduced the lung damage [15,16]. These results suggest that CINC-1 is a major contributor to LPS-induced lung injury in rats.…”

Section: Introductionmentioning

confidence: 74%

“…Yamasawa et al [15] reported that anti-CINC-1 antibody significantly reduced the total cell count and number of neutrophils in BAL fluids in LPSinduced rat lung injury. They also suggested that CINC-3 as well as CINC-1 was involved in the lung injury, however, Mitsuhashi et al could not detect CINC-3 in lung homogenate after LPS-treatment [16]. Ulich et al [12] reported that intratracheal LPS injection increased CINC-1 mRNA and protein expression in the lung, and anti-CINC-1 antibody inhibited LPS-induced neutrophil emigration into BAL fluid.…”

Section: Discussionmentioning

confidence: 99%

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Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

et al. 2002

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Section: Introductionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

et al. 2002

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“…The important role of these cytokines in the pathogenesis of lung injury has been previously demonstrated (31)(32)(33)(34)(35)(36).…”

Section: Discussionmentioning

confidence: 91%

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Avlonitis

Wigfield

Kirby

et al. 2005

American Journal of Transplantation

156

123

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Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by a -adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.

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“…TNF-␣ and IL-1␤ are among the best characterized of the cytokines and can be regulated as archetypal acute inflammatory cytokines. Cytokine-induced neutrophil chemoattractant factor-1 (CINC-1), a member of the IL-8 family (23), is a potent neutrophil chemotactic and activating factor (29). Therefore, in this descriptive study, we investigate the influence of CO 2 and buffering pH on LPS-stimulated synthesis and/or secretion of TNF-␣, IL-1␤, and CINC-1 proteins in cultured rat AM.…”

mentioning

confidence: 99%

Effect of CO₂on LPS-induced cytokine responses in rat alveolar macrophages

Lang¹,

Dong²,

Hosszu³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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veolar macrophages (AM) may be exposed to a range of CO 2 and pH levels depending on their location in the alveoli and the health of the lung. Cytokines produced by AM contribute to inflammation in acute lung injury (ALI). Current ventilatory practices for the management of ALI favor low tidal volumes, which can give rise to increases in CO2 and changes in pH of the alveolar microenvironment. Here we examined the effect of CO2 on cytokine release from LPS-stimulated rat AM. AM were incubated for 1-4 h under different atmospheric gas mixtures ranging from 2.5-20% CO2. To distinguish between effects of pH and CO 2, the culture media were also buffered to pH 7.2 with NaHCO 3. Cell metabolic activity, but not cell viability, decreased and increased significantly after 4 h at 20 and 2.5% CO 2, respectively. Increasing CO 2 decreased TNF-␣ secretion but had no effect on lysate TNF-␣. Buffering the media abated the effects of CO 2 on TNF-␣ secretion. CO 2 increased cytokine-induced neutrophil chemoattractant factor-1 secretion only when the pH was buffered to 7.2. Effects of CO2 on cytokine responses were reversible. In conclusion, the effects of CO 2 on cytokine lysate levels and/or secretion in AM are cytokine specific and, depending on both the cytokine and the immediate

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Appearance of cytokine-induced neutrophil chemoattractant isoforms and immunolocalization of them in lipopolysaccharide-induced acute lung inflammation in rats

Abstract: These findings suggest that CINC-1 is the major isoform among the four CINCs in lipopolysaccharide-induced acute lung inflammation in rats. Its sources are likely to be bronchial noncilliated cells and certain infiltrating neutrophils.

Cited by 27 publications

References 30 publications

Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Effect of CO₂on LPS-induced cytokine responses in rat alveolar macrophages

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Appearance of cytokine-induced neutrophil chemoattractant isoforms and immunolocalization of them in lipopolysaccharide-induced acute lung inflammation in rats

Abstract: These findings suggest that CINC-1 is the major isoform among the four CINCs in lipopolysaccharide-induced acute lung inflammation in rats. Its sources are likely to be bronchial noncilliated cells and certain infiltrating neutrophils.

Cited by 27 publications

References 30 publications

Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

Prophylactic effect of JTE-607 on LPS-induced acute lung injury in rats with CINC-1 inhibition

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Effect of CO2on LPS-induced cytokine responses in rat alveolar macrophages

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Product

Resources

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Effect of CO₂on LPS-induced cytokine responses in rat alveolar macrophages