Tumor Necrosis Factor Causes Increased Pulmonary Permeability and Edema: Comparison to Septic Acute Lung Injury

Stephens, Kenton E.; Ishizaka, Akitoshi; Larrick, James W.; Raffin, Thomas A.

doi:10.1164/ajrccm/137.6.1364

Cited by 322 publications

(117 citation statements)

References 18 publications

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“…This cytokine upregulates endothelial cell adhesion molecules which are required for leucocyte emigration [23], and further activates neutrophils and macrophages for enhanced superoxide radical generation as well as enhanced chemotaxis, phagocytosis and degranulation [20±22]. Furthermore, TNF-á directly increases lung vascular permeability [24] and may promote release of other cytokines and mediators, such as platelet-activating factor, leukotrienes, or nitric oxide [15]. Finally, TNF-á has a potent bronchoconstrictor effect and this may be of particular signi®cance in the PRCV-LPS model.…”

Section: Discussionmentioning

confidence: 99%

A potential role for tumour necrosis factor-α in synergy between porcine respiratory coronavirus and bacterial lipopolysaccharide in the induction of respiratory disease in pigs

Reeth¹,

Nauwynck²,

Pensaert³

2000

Journal of Medical Microbiology

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This study examined whether exposure of pigs to both porcine respiratory coronavirus (PRCV) and bacterial lipopolysaccharide (LPS) can potentiate respiratory disease and lung secretion of tumour necrosis factor-á (TNF-á) and interleukin-1 (IL-1). Caesarianderived colostrum-deprived pigs were inoculated intratracheally with PRCV, with LPS from Escherichia coli O111:B4 (20 ìg=kg), or with a combination of the two, and killed at set times after inoculation. Clinical signs, virus replication and (histo)pathological changes in the lungs, percentage of neutrophils and bioactive TNF-á and IL-1 in broncho-alveolar lavage (BAL)¯uids were examined. The effects of separate virus or LPS inoculations were subclinical and failed to induce high and sustained cytokine levels. In a preliminary study, pigs were inoculated with PRCV and then with LPS 24 h later and killed sequentially. Severe respiratory disease and signi®cantly enhanced TNF-á titres (208±3601 U=ml versus 40±89 U=ml after LPS only) were seen during the ®rst 12 h after LPS inoculation. IL-1 levels (106±1631 U=ml versus 28±654 U=ml after LPS only) were also increased, but persisted for longer after clinical recovery than TNF-á. In a second study, pigs were inoculated with PRCV and subsequently with LPS at various time intervals ranging from 0 to 24 h, and killed 5 h after inoculation with LPS. A time interval of at least 12 h between inoculations was necessary for prominent respiratory signs to develop. Production of TNF-á, but not IL-1, was also dependent on the time interval between inoculations and was tightly correlated with disease. Lung neutrophil in®ltration and pathological changes were comparable after combined PRCV-LPS and single LPS inoculations, and were not associated with disease. These data show that exposure to high endotoxin concentrations in swine buildings can precipitate respiratory disease in PRCV-infected pigs, and that TNF-á is probably an important mediator of these effects. This is the ®rst in-vivo demonstration of synergy between respiratory viruses and LPS.

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Section: Discussionmentioning

confidence: 99%

A potential role for tumour necrosis factor-α in synergy between porcine respiratory coronavirus and bacterial lipopolysaccharide in the induction of respiratory disease in pigs

Reeth¹,

Nauwynck²,

Pensaert³

2000

Journal of Medical Microbiology

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“…These cytokines act synergistically on the stimulation of polymorphonuclear neutrophilic granulocyte migration [31], and stimulate vascular endothelial cells to promote transendothelial passage of neutrophils, albumin, and fluid in vitro and in animal experiments [32][33][34]. TNF-α, IL-1 and LPS induce the expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on endothelial cells, promoting adhesion to granulocytes, monocytes and lymphocytes [35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

Inhalation of swine dust induces cytokine release in the upper and lower airways

Larsson²,

Palmberg³

et al. 1997

Eur Respir J

147

138

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In healthy subjects, acute inhalation of swine dust causes an influx of inflammatory cells into the airways and increased bronchial responsiveness. The exposure may also cause fever and generalized symptoms. It seems likely that proinflammatory cytokines are involved in the response to inhaled swine dust.Nasal and bronchoalveolar lavage (BAL) were performed before, and 7 and 24 h after the start of 3 h exposure to swine dust, during a period of work in a swine confinement building, in 22 healthy subjects. Lavage fluids were analysed with regard to the cellular response and concentrations of interleukin (IL)-1α, IL-1β, IL-6 and tumour necrosis factor-α (TNF-α). Each subject carried personal samplers for exposure measurements. Inhalable dust and airborne endotoxin, 3-hydroxylated (2-OH) fatty acid and muramic acid were measured. Bronchial responsiveness to methacholine was investigated 1-2 weeks before and 7 h after the start of the exposure.Exposure caused fever (>38°C) in three subjects, and approximately 25% of the subjects experienced symptoms. Bronchial responsiveness to methacholine increased by 3.5 (1.6-4.8) doubling doses (median (25th-75th percentile)). Following exposure, granulocytes increased more than 50 fold in BAL fluid and more than 40 fold in nasal lavage fluid. IL-1α and IL-1β increased significantly in BAL fluid (p<0.05) and nasal lavage fluid (p<0.01). IL-6 increased 25 fold in BAL and 15 fold in nasal lavage fluid (p<0.001). TNF-α was below detection limit (0.25 ng·L -1 ) in most subjects before exposure and increased following exposure to 3.8 (2.4-5.7) and 1.3 (0.6-2.3) ng·L -1 in BAL and nasal lavage fluid, respectively, (p<0.001). Total inhalable dust was 20.5 (14.6-30.0) mg·m -3 and the concentrations of airborne endotoxin, 3-OH fatty acid and muramic acid were 1.2 (0.8-1.4), 3.5 (2.2-4.5) and 0.9 (0.3-1.9) µg·m -3 , respectively. There was a significant correlation between the IL-6 response in BAL fluid and exposure to dust endotoxin activity and 3-OH fatty acids (p<0.05). Otherwise, no significant correlations were found between exposure and the cytokine response.We conclude that exposure to swine dust causes an intense upper and lower airway inflammation, which involves the proinflammatory cytokines interleukin-1, interleukin-6 and tumour necrosis factor-α.

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“…Porcine pleuropneumonia is characterized by an intensive inflammation with infiltration of phagocytic cells such as neutrophils and alveolar macrophages, which are the main cells found in affected lungs (17). Previous in vivo studies have shown that A. pleuropneumoniae infection is associated with the production of a large amount of inflammatory mediators (18,19) and proinflammatory cytokines such as IL1, TNF-␣, IL8, and IL6 (20,21) that could be responsible, at least in part, for the lung injuries and tissue destruction observed in porcine pleuropneumonia (20,22). LPS are known as mediators of inflammation (16) as they interact with immune cells and activate the production of inflammatory cytokines (23,24) by these cells.…”

mentioning

confidence: 99%

Truncation of the Lipopolysaccharide Outer Core Affects Susceptibility to Antimicrobial Peptides and Virulence of Actinobacillus pleuropneumoniae Serotype 1

Ramjeet

Deslandes

Michael

et al. 2005

Journal of Biological Chemistry

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We reported previously that the core oligosaccharide region of the lipopolysaccharide (LPS) is essential for optimal adhesion of Actinobacillus pleuropneumoniae, an important swine pathogen, to respiratory tract cells. Rough LPS and core LPS mutants of A. pleuropneumoniae serotype 1 were generated by using a mini-Tn10 transposon mutagenesis system. Here we performed a structural analysis of the oligosaccharide region of three core LPS mutants that still produce the same O-antigen by using methylation analyses and mass spectrometry. We also performed a kinetic study of proinflammatory cytokines production such as interleukin (IL)-6, tumor necrosis factor-␣, IL1-␤, MCP-1, and IL8 by LPS-stimulated porcine alveolar macrophages, which showed that purified LPS of the parent strain, the rough LPS and core LPS mutants, had the same ability to stimulate the production of cytokines. Most interestingly, an in vitro susceptibility test of these LPS mutants to antimicrobial peptides showed that the three core LPS mutants were more susceptible to cationic peptides than both the rough LPS mutant and the wild type parent strain. Furthermore, experimental pig infections with these mutants revealed that the galactose (Gal I) and D,D-heptose (Hep IV) residues present in the outer core of A. pleuropneumoniae serotype 1 LPS are important for adhesion and overall virulence in the natural host, whereas deletion of the terminal GalNAc-Gal II disaccharide had no effect. Our data suggest that an intact core-lipid A region is required for optimal protection of A. pleuropneumoniae against cationic peptides and that deletion of specific residues in the outer LPS core results in the attenuation of the virulence of A. pleuropneumoniae serotype 1.

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Tumor Necrosis Factor Causes Increased Pulmonary Permeability and Edema: Comparison to Septic Acute Lung Injury

Cited by 322 publications

References 18 publications

A potential role for tumour necrosis factor-α in synergy between porcine respiratory coronavirus and bacterial lipopolysaccharide in the induction of respiratory disease in pigs

A potential role for tumour necrosis factor-α in synergy between porcine respiratory coronavirus and bacterial lipopolysaccharide in the induction of respiratory disease in pigs

Inhalation of swine dust induces cytokine release in the upper and lower airways

Truncation of the Lipopolysaccharide Outer Core Affects Susceptibility to Antimicrobial Peptides and Virulence of Actinobacillus pleuropneumoniae Serotype 1

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