Pathology of Adult Respiratory Distress Syndrome: Implications Regarding Therapy

Pratt, Philip C.

doi:10.1055/s-2007-1012470

Cited by 20 publications

(12 citation statements)

References 7 publications

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“…In terms of the histology performed during AE, the major histological finding was DAD, predominantly in the organising phase, as is well described in the pathology literature [32,33]. While the appearances in a given microscopic field are identical to those seen in intra-alveolar organisation due to other causes such as COP, the presence of coexistent acute respiratory failure, and the HRCT data, plus the areas with the adjacent hyaline membranes in three of the four cases, indicate that the features represented organising DAD.…”

Section: Acute Exacerbation Of Ipf Ds Kim Et Almentioning

confidence: 62%

Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features

et al. 2006

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Although acute exacerbations of idiopathic pulmonary fibrosis are well recognised, there are no studies documenting their prevalence or identifying pre-existing risk factors.This study analysed the clinical, radiological and pathological data of 11 patients who satisfied the criteria for acute exacerbation among 147 patients with biopsy-proven idiopathic pulmonary fibrosis. There were five additional patients who had similar demographics, radiology and surgical lung biopsy pathology, but had clinically less severe disease, and so were not included. The 2-yr frequency of acute exacerbation was 9.6% after the diagnosis. Most exacerbations were idiopathic, although two cases presented after surgical lung biopsy and one after bronchoalveolar lavage.No significant risk factor was found by univariate proportional hazard analysis. Imaging revealed diffuse bilateral ground-glass opacification superimposed on subpleural reticular and honeycombing densities. The biopsies of four patients taken during acute exacerbation exhibited diffuse alveolar damage superimposed upon usual interstitial pneumonia.The findings of this study demonstrate that acute exacerbation of idiopathic pulmonary fibrosis is rather common and this exacerbation is likely to have a spectrum of severity.

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Section: Acute Exacerbation Of Ipf Ds Kim Et Almentioning

confidence: 62%

Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features

et al. 2006

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“…ARDS is an acute deterioration of lung function in individuals with severe underlying conditions such as sepsis, and many neutrophils accumulate within the lungs in the early phase of the acute lung injury [19]. Neutrophils are sequestered in the lung capillaries [20,21], causing a transient decrease in the number of circulating neutrophils [22]. Some of the sequestered neutrophils migrate from the lung capillaries into the interstitium and alveolar spaces [23,24].…”

Section: Discussionmentioning

confidence: 99%

Peptide inhibitor of interleukin-8 (IL-8) reduces staphylococcal enterotoxin-A (SEA) induced neutrophil trafficking to the lung

1996

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Staphylococcal enterotoxin A (SEA) is a superantigen, produced by some strains of Staphylococcus aureus (S. aureus), which can cause a variety of clinical manifestations ranging from food poisoning to shock. SEA can also stimulate human alveolar macrophages to produce interleukin-8 (IL-8), a member of the alpha-chemokine subfamily that activates and is chemotactic for neutrophils. In these studies we showed that in rabbits, intravenous SEA significantly decreased the circulating white blood cell population from a baseline value of 6409 +/- 2027 x 10(3) cells/ml to 1943 +/- 862 x 10(3) cells/ml in 7 h. There was a concommitent increase in IL-8 in the circulating plasma (baseline: 60 +/- 34 pg/ml, 7 h post SEA: 109 +/- 64 pg/ml). The increase in circulating IL-8 was accompanied by a much greater increase in the IL-8 concentration of the epithelial lining fluid (ELF) where the IL-8 increased from 0.05 +/- 0.08 ng/ml (control) to 13.8 +/- 9.3 ng/ml (SEA treated). The increase in IL-8 concentration in the alveolar spaces was paralleled by an increase in both the percentage of neutrophils (1.4 +/- 0.9% (control) to 26.0 +/- 10.8% (SEA treated)) and total number of neutrophils (0.04 +/- 0.02 x 10(6)/ml (control) to 4.8 +/- 3.3 10(6)/ml (SEA treated) in the airspaces, and the numbers of neutrophils in the ELF correlated with the IL-8 concentration r = 0.62, p = 0.006). When antileukinate, a hexapeptide which inhibits the binding of IL-8 to neutrophils, was administered to animals receiving SEA, the IL-8 concentration in the ELF (14.8 +/- 10.7 ng/ml) was not significantly different from the concentration of IL-8 in those animals receiving SEA alone). However, both the percentage of neutrophils (9.5 +/- 3.2%), and the total number of neutrophils (1.3 +/- 1.0 x 10(6)/ml) in the ELF following SEA and antileukinate administration was significantly lower than in animals which only received SEA (p < 0.05). The findings suggest that SEA released into the circulation during a Staphylococcal infection can cause an inflammatory reaction in the lung. Since this reaction is at least partially mediated by IL-8, antileukinate may have pharmacologic potential in reducing the inflammatory reaction.

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“…Neutrophil accumulation in the lung has been observed in autopsy patients who have died of ARDS [1][2][3][4]. However, it could not be denied that neutrophil accumulation in the lung is not a cause of the ALI, but a result of an inflammatory reaction following ALI.…”

Section: Introductionmentioning

confidence: 99%

“…In many earlier studies, which have investigated the mechanisms of septic ARDS, either a bolus injection or a continuous infusion of endotoxin [7][8][9] was used in animal models. Although these experiments showed an increased pulmonary permeability, they did not develop severe pulmonary edema which is the most characteristic findings in clinical ARDS [1][2][3][4]. Therefore, it is important to examine the roles of neutrophils and neutrophil elastase in a lung injury model with severe pulmonary edema to elucidate the mechanisms of septic ARDS.…”

Section: Introductionmentioning

confidence: 99%

Neutrophils Mediate Acute Lung Injury in Rabbits: Role of Neutrophil Elastase

Kinoshita¹,

Ono²,

Mochizuki³

2000

Eur Surg Res

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We investigated the roles of neutrophil and neutrophil elastase in acute lung injury (ALI) to elucidate the mechanism of ALI. We designed two protocols. Protocol I: Experimental ALI was induced by endotoxin (0.02 mg/kg) and platelet-activating factor (8 µg/kg/4 h) in untreated rabbits (control group I), in neutropenic rabbits pretreated with nitrogen-N-oxide hydrochloride, and in untreated rabbits infused with a neutrophil elastase inhibitor (ONO-5046; 20 mg/kg/4 h). Protocol II: ALI was induced by smaller doses of endotoxin (0.015 mg/kg) and platelet-activating factor (7 µg/kg/4 h) than those used in protocol I in untreated rabbits (control group II), in neutrophilic rabbits pretreated with human recombinant granulocyte colony-stimulating factor, and in neutrophilic rabbits infused with ONO-5046 (as in protocol I). The severity of ALI was assessed by the protein concentration, the elastase activity in the bronchoalveolar lavage fluid, and the histologic pulmonary edema ratio. The degree of pulmonary neutrophil accumulation was assessed by pulmonary myeloperoxidase activity and histological findings. Both ALI and pulmonary neutrophil accumulation were suppressed by neutropenia (protocol I), while they were exacerbated by neutrophilia (protocol II). The neutrophil elastase inhibitor could suppress ALI, but it could not suppress pulmonary neutrophil accumulation in both untreated and neutrophilic rabbits (protocols I and II). These findings indicate that neutrophils play an important role in the pathogenesis of ALI via neutrophil elastase.

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Pathology of Adult Respiratory Distress Syndrome: Implications Regarding Therapy

Cited by 20 publications

References 7 publications

Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features

Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features

Peptide inhibitor of interleukin-8 (IL-8) reduces staphylococcal enterotoxin-A (SEA) induced neutrophil trafficking to the lung

Neutrophils Mediate Acute Lung Injury in Rabbits: Role of Neutrophil Elastase

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