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Measuring whole-body neutrophil redistribution using a dedicated whole-body counter and ultra-low doses of 111Indium

Authors


Professor A. M. Peters, Brighton Sussex Medical School, Audrey Emerton Building, Eastern Road, Brighton BN2 5BE, UK. Tel.: +1273 523360; fax: +1273 523366; e-mail: a.m.peters@bsms.ac.uk

Abstract

Eur J Clin Invest 2010; 41 (1): 77–83

Abstract

Background  There is increasing interest in the ‘homing’ of neutrophils to bone marrow. The aim of this study was to measure the whole-body redistribution of 111In using a whole-body counter following the administration of ultra-small activities of 111In-labelled neutrophils.

Methods  The detectors of a dedicated whole-body counter were fitted with lead collimators. Whole-body 111In distribution was recorded at 45 min, 24 h, and 2, 4, 7 and 10 days after administration of 111In-labelled neutrophils (0·29–0·74 MBq) in eight healthy non-smokers, five healthy smokers, eight patients with inactive bronchiectasis, three with asthma and nine with chronic obstructive pulmonary disease (COPD).

Results  Intravascular 45-min 111In-labelled neutrophil recovery was not significantly different between groups, ranging from 33 (SD 8%) in healthy smokers to 45 (14%) in healthy non-smokers (P > 0·05). Peaks were identified on the whole body count profile corresponding to the chest, upper abdomen (liver/spleen) and pelvis (bone marrow). 111In distribution changed between 45 min and 24 h and then remained stable thereafter. Peak chest counts increased ∼1·5-fold between 45 min and 24 h, whereas upper abdominal peak counts decreased by ∼25% with no significant inter-group differences. The increment in pelvic counts (∼2·7-fold) was similar between groups, except COPD patients, in whom it was 2·04 (0·35; P < 0·02 vs. healthy participants).

Conclusions  Assuming neutrophils are distributed only between blood, liver, spleen and bone marrow, the data suggest that marrow pools 25% and destroys 67% of circulating neutrophils, rising in COPD to 40% and 80%, respectively, possibly as a result of the effects on marrow of chronic hypoxaemia.

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