The Pulmonary Air-Blood Barrier of Human Shock Lungs (A Clinical, Ultrastructural and Morphometric Study)

Riede, U. N.; Joachim, Hans; J, Hassenstein; Costabel, Ulrich; Sandritter, W.; Augustín, Peter; Mittermayer, Ch.

doi:10.1016/s0344-0338(78)80130-7

Cited by 48 publications

(13 citation statements)

References 37 publications

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“…Notably, sepsis is the main cause of ARDS, and 30 to 40% of patients with sepsis will eventually develop ARDS41. ARDS has some major features, such as loss of the alveolar-capillary barrier42, alveolar epithelial injury43, inflammatory cell influx44, activation of coagulation and inhibition of fibrinolysis45. Inflammatory cell influx occurs as a result of direct lung injury or as the response to systemic inflammation and cytokine production46.…”

Section: Discussionmentioning

confidence: 99%

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) prevents lipopolysaccharide (LPS)-induced, sepsis-related severe acute lung injury in mice

Takaoka

Goto

Nakano

et al. 2014

Sci Rep

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Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an energy metabolism-related enzyme in the glycolytic pathway. Recently, it has been reported that GAPDH has other physiological functions, such as apoptosis, DNA repair and autophagy. Some in vitro studies have indicated immunological aspects of GAPDH function, although there is no definite study discussing the advantage of GAPDH as a therapeutic target. Here, we show that GAPDH has an anti-inflammatory function by using a lipopolysaccharide (LPS)-induced, sepsis-related severe acute lung injury (ALI) mouse model, which is referred to as acute respiratory distress syndrome (ARDS) in humans. GAPDH pre-injected mice were protected from septic death, and their serum levels of proinflammatory cytokines were significantly suppressed. In lung tissue, LPS-induced acute injury and neutrophil accumulation were strongly inhibited by GAPDH pre-injection. Pulmonary, proinflammatory cytokine gene expression and serum chemokine expression in GAPDH pre-injected mice were also reduced. These data suggest the therapeutic potential of GAPDH for sepsis-related ALI/ARDS.

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Section: Discussionmentioning

confidence: 99%

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) prevents lipopolysaccharide (LPS)-induced, sepsis-related severe acute lung injury in mice

Takaoka

Goto

Nakano

et al. 2014

Sci Rep

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“…Of particular importance is evidence that suggests that PMNs are primary cellular mediators of acute lung injury associated with sepsis. Histological examination of postmortem lungs of PMN-sufficient patients who died from acute respiratory distress syndrome (ARDS) invariably shows large numbers of sequestered PMNs in pulmonary microvasculature (37)(38)(39)(40). Further evidence is provided by studies that show large numbers ofPMNs recovered from BAL fluid of patients suffering from ARDS (41,42).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha blockade prevents neutrophil CD18 receptor upregulation and attenuates acute lung injury in porcine sepsis without inhibition of neutrophil oxygen radical generation.

Windsor

Walsh²,

Mullen³

et al. 1993

J. Clin. Invest.

108

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Tumor necrosis factor (TNFa), both by direct action and by trafficking cells of the immune system, is implicated in cardiopulmonary derangements and PMN-mediated microvascular injury associated with gram-negative sepsis. We examined the effects of pretreatment with a monoclonal antibody to TNFa on PMN function, hemodynamic derangements, and alveolar capillary membrane damage in a septic porcine model. Anti-TNFa profoundly improved hemodynamic consequences in this model. Reduction in PMN CD11 / 18 receptor expression, lung myeloperoxidase activity, and attenuation of peripheral neutropenia (all P < 0.05) indicate that pretreatment significantly reduced lung sequestration of PMNs seen in septic controls. In contrast, PMN oxygen radical (02-) generation was not significantly different from unprotected septic animals. Despite the presence of circulating PMNs primed for 0°-burst, alveolar capillary membrane damage, assessed by bronchoalveolar lavage protein content and arterial Po2 was markedly attenuated in the treatment group (P < 0.05). We conclude that antiTNFa suppresses systemic hemodynamic actions of TNFa. Further, it prevents upregulation of PMN adhesion receptors inhibiting PMN/endothelial cell interaction. This prevents formation of a "microenvironment," protected from circulating oxidant scavengers, into which sepsis-activated PMNs release their toxic products. Pretreatment with anti-TNFa monoclonal antibody thus affords global protection in porcine Gram-negative sepsis. (J. Clin. Invest. 1993. 91:1459-1468

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“…A systemic reaction of connective tissue leading to fibrosis can be observed in protracted shock of man and animals [2,3,11,12,17,18,211. The initiating factors are not known.…”

Section: Discussionmentioning

confidence: 99%

Mesangium in Rats after E. coli Neurotoxin Shock: A Morphometric and Light Microscopic Analysis

Queisser

Drommer

1982

Vet Pathol

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Abstract. The renal corpuscles of 28 specific-pathogen-free Wistar rats fixed by perfusion were examined light microscopically and morphometrically following experimental protracted neurotoxin shock. The mean diameter of the center sections of 420 renal corpuscles was 1 13.0 pm. The mesangial portion occupied 9.5% of the total area of the renal corpuscle in control rats and increased to a maximum of 17.25% in experimental rats. The number of mesangial nuclei per renal corpuscle in rats with protracted shock showed that expansion of the mesangium with compression of capillary loops was not caused solely by an increase in the number of cells. Furthermore, there was an enlargement of the mesangial cytoplasm and matrix. Activation and proliferation of connective tissue in rats with protracted shock could be observed in the interstitium of various organs as well as in the mesangium of the glomerulus.Many publications exist on shock [l, lo], however, little attention has been given to an increase in the mesangium of the glomerulus of the kidney following shock. Morphometric data of mesangial changes after protracted neurotoxin shock in pigs are available [2, 41. Several authors show that in protracted shock a reaction of connective tissue in various organs can be detected [3,18, 221. This study will clarify the reaction of the mesangium as mesenchymal tissue in the rat in long-lasting shock situations. This investigation assesses various parameters of the renal corpuscle of the rat by a quantitative-morphologic method. The rats in this experiment were submitted to various shock intensities and duration by the application of one to four Escherichiu coZi neurotoxin injections. As parameters for a possible mesangial reaction, we determined the area of the glomerulus capsule, the corresponding mesangial area, and the number of mesangial nuclei. In addition to normal values in the rat, we intended to ascertain possible changes in the mesangium. As an alternative to the point-counting method, a simpler, more direct, and thereby faster technique for morphometric evaluations of the glomerulus was used. Materials and MethodsTwenty-eight specific-pathogen-free Wistar rats (13 male, 15 female) were analyzed. Eight of them comprised the control group. The initial body weight of the 55-to 74-day-old rats was between 156 and 218 g. The rats were kept in separate metabolism cages and fed a commercial

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The Pulmonary Air-Blood Barrier of Human Shock Lungs (A Clinical, Ultrastructural and Morphometric Study)

Cited by 48 publications

References 37 publications

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) prevents lipopolysaccharide (LPS)-induced, sepsis-related severe acute lung injury in mice

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) prevents lipopolysaccharide (LPS)-induced, sepsis-related severe acute lung injury in mice

Tumor necrosis factor-alpha blockade prevents neutrophil CD18 receptor upregulation and attenuates acute lung injury in porcine sepsis without inhibition of neutrophil oxygen radical generation.

Mesangium in Rats after E. coli Neurotoxin Shock: A Morphometric and Light Microscopic Analysis

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