Granulocyte kinetics and methods of evaluating cell performance

Am, Peters

doi:10.1097/00006231-198810000-00003

Cited by 6 publications

(2 citation statements)

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“…Further, evidence to support the hypothesis that inadvertent cell stimulation ⁄ damage results in a prolongation of pulmonary transit time can be gleaned from the measurement of labelled neutrophil recovery in the freely circulating pool. Hence, it has been shown consistently that 35-40% of 111 In-or 99m Tc-labelled neutrophils (prepared in the presence of autologous plasma) are recoverable from the circulation 40 min post-injection [44][45][46][47][48][49][50][51], whereas in many of the studies reporting prolonged neutrophil pulmonary transit times 40 min recovery values have been considerably lower [32,33].…”

Section: Accumulation Of Neutrophils Within the Lungsmentioning

confidence: 99%

Acute lung injury results from failure of neutrophil de‐priming: a new hypothesis

Singh

Johnson

Peters

et al. 2012

Eur J Clin Investigation

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Neutrophils are the most abundant circulating white cell in humans and play a crucial role in the innate immune response. Accumulation and activation of neutrophils, together with delayed clearance, have been shown to be a key event in the pathogenesis of acute lung injury. Previously, it has been proposed that there is substantial pooling of neutrophils within the pulmonary vasculature, even under physiological conditions, making the lung especially vulnerable to neutrophil-mediated tissue injury. However, more recent evidence suggests that only primed neutrophils accumulate in the pulmonary vasculature. This article examines the evidence for these two opposing views and proposes a new two-step model for the recruitment of neutrophils into the lung. Firstly, neutrophils that become primed, by exposure to a range of inflammatory mediators or physicochemical perturbations, become shape changed and stiff because of alterations in their cytoskeleton, and as a result, accumulate within the pulmonary circulation. In the absence of further stimuli, the healthy pulmonary vasculature is able to selectively retained these primed cells, allow them to 'de-prime' and be released back into the circulation in a quiescent, state. If this pulmonary 'de-priming' mechanism fails, or a second insult occurs, such as ventilatorassociated barotrauma, which causes loss of alveolar integrity, primed neutrophils migrate from the pulmonary vasculature into the interstitial space with resultant lung injury. This canonical 'two step' model highlights the importance of neutrophil priming in the genesis of lung injury and the importance of adopting strategies to minimise alveolar injury.Keywords De-priming, lung injury, neutrophils. Eur J Clin Invest 2012; 42 (12): 1342-1349Acute De-priming, lung injury Acute lung injury (ALI) and its more severe form acute respiratory distress syndrome (ARDS) comprise a spectrum of diseases characterised by refractory hypoxaemia, diffuse alveolar damage, neutrophilic lung inflammation and protein-rich pulmonary oedema. The incidence of ARDS ⁄ ALI has been reported to be approximately 80 cases per 100 000 person-years in the United States [1] and, despite being first described more than 40 years ago [2], the mortality rate remains unchanged at 30-50% [1,[3][4][5].Clinically, ALI is defined as a condition of acute onset and characterised by bilateral pulmonary infiltrates consistent with pulmonary oedema (see Fig. 1) and impaired gas exchange, with a PaO 2 ⁄ FiO 2 ratio of < 40 KPa, both occurring in the absence of signs of left atrial hypertension [6]. ALI ⁄ ARDS can result from a wide range of either direct pulmonary insults (e.g. pneumonia and lung contusions) or extra-pulmonary conditions (e.g. sepsis, pancreatitis, major trauma, massive blood transfusion and shock from any cause). One of the unifying features of the many seemingly disparate causes of ALI ⁄ ARDS is the occurrence of systemic neutrophil priming and activation.

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Section: Accumulation Of Neutrophils Within the Lungsmentioning

confidence: 99%

Acute lung injury results from failure of neutrophil de‐priming: a new hypothesis

Singh

Johnson

Peters

et al. 2012

Eur J Clin Investigation

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“…Labelling of DC was performed according to the methods described for leucocyte radiolabelling [24-26]. A part of both iDC and mDC destined for vaccination (about 9.10 6 ) were resuspended in platelet-poor autologous plasma (CFP1) and incubated for 15 min at room temperature with 99m Tc-HMPAO (20 mCi) (Nycomed Amersham plc, Little Chalfont, UK) 111 In-Oxine (1 mCi) (Altana Pharma, Milan, Italy).…”

Section: Methodsmentioning

confidence: 99%

Untitled

et al. 2004

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BackgroundDendritic Cell (DC) vaccination is a very promising therapeutic strategy in cancer patients. The immunizing ability of DC is critically influenced by their migration activity to lymphatic tissues, where they have the task of priming naïve T-cells. In the present study in vivo DC migration was investigated within the context of a clinical trial of antitumor vaccination. In particular, we compared the migration activity of mature Dendritic Cells (mDC) with that of immature Dendritic Cells (iDC) and also assessed intradermal versus subcutaneous administration.MethodsDC were labelled with 99mTc-HMPAO or 111In-Oxine, and the presence of labelled DC in regional lymph nodes was evaluated at pre-set times up to a maximum of 72 h after inoculation. Determinations were carried out in 8 patients (7 melanoma and 1 renal cell carcinoma).ResultsIt was verified that intradermal administration resulted in about a threefold higher migration to lymph nodes than subcutaneous administration, while mDC showed, on average, a six-to eightfold higher migration than iDC. The first DC were detected in lymph nodes 20–60 min after inoculation and the maximum concentration was reached after 48–72 h.ConclusionsThese data obtained in vivo provide preliminary basic information on DC with respect to their antitumor immunization activity. Further research is needed to optimize the therapeutic potential of vaccination with DC.

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Indium-111 labelled white blood cell scintigraphy in cranial and spinal septic lesions

Medina

Viglietti²,

Gozzoli³

et al. 2000

Eur J Nucl Med

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Cranial and spinal infections are severe events that require timely diagnosis and treatment. Physical and neurological examination, laboratory tests and radiological imaging may be insufficient for assessing cranial and spinal septic lesions. This study aimed to evaluate the accuracy of indium-111 white blood cell (WBC) scan in assessing the presence of leucocytes in intracranial and spinal lesions, and in the diagnosis, management and follow-up of primary, post-traumatic and post-surgical infections. One hundred and twenty-four subjects were included in the study (48 with post-traumatic or post-surgical lesions, 73 with primary cerebral lesions, and 3 with spinal lesions). All patients underwent a diagnostic work-up including planar scans with 111In-labelled WBCs, at 4 and 24 h post tracer injection. All subjects underwent surgical treatment. Patients who did not recover from the infection as suggested by clinical evolution underwent further treatment (up to three times) and further WBC scans (up to four times). WBC scintigraphy correctly identified all the areas of leucocyte accumulation, as confirmed after surgery. WBC scintigraphy also correctly excluded the presence of leucocytes in all other lesions, as demonstrated at surgery. The results of this study confirm the accuracy of WBC scan for the assessment of patients with cranial and spinal lesions, in whom the demonstration of leucocyte accumulation can ease the diagnosis of infection, and indicate that the method is also accurate for the follow-up and management of neurosurgical patients.

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Granulocyte kinetics and methods of evaluating cell performance

Cited by 6 publications

References 0 publications

Acute lung injury results from failure of neutrophil de‐priming: a new hypothesis

Acute lung injury results from failure of neutrophil de‐priming: a new hypothesis

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Indium-111 labelled white blood cell scintigraphy in cranial and spinal septic lesions

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