Selective regulation of expression of surface adhesion molecules Mac-1, L-selectin, and VLA-4 on human eosinophils and neutrophils.

We studied the differential expression of cellular adhesion molecules on the surface of purified human eosinophils and neutrophils caused by ex vivo activation with platelet-activating factor (PAF), formylmethionylleucylphenylalanine (FMLP), or recombinant human interleukin-5 (IL-5). PAF (10(-7) M) caused a 42.8 +/- 5.7% (mean +/- SEM) increase in Mac-1 expression in eosinophils (P < 0.01) and a 34.6 +/- 9.2% increase in Mac-1 expression in neutrophils (P < 0.05). PAF also caused a decrease in L-selectin expression in eosinophils (-37.0 +/- 8.1%, P < 0.001) and neutrophils (-14.1 +/- 3.2%, P < 0.05). FMLP (10(-6) M) caused a similar increase in Mac-1 expression in both eosinophils (P < 0.001 versus controls) and neutrophils (P < 0.01) and a comparable decrease in L-selectin expression in both eosinophils and neutrophils (P < 0.01). In contrast to the effects of PAF and FMLP, IL-5 affected selectively the surface expression of adhesion molecules in eosinophils but not neutrophils. Expression of Mac-1 increased by 44.3 +/- 7.5% in eosinophils (P < 0.001 versus controls) and by 0.7 +/- 1.2% in neutrophils (P = NS versus controls) after exposure to 10(-9) M IL-5. IL-5 also caused a 49.5 +/- 4.2% decrease in eosinophil L-selectin expression (P < 0.001) but had no effect on L-selectin expression in neutrophils. Eosinophil VLA-4 expression was not altered by any stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of human eosinophil degranulation and activation by endogenous phospholipase A2.

The unique granular proteins of eosinophils may have a pathogenetic role in asthma and in the defense against parasitic infestations. However, the mechanisms regulating eosinophil degranulation are largely unknown. We examined the hypothesis that release of these proteins is regulated by endogenous activation of phospholipase A2. Human eosinophils (HE) were isolated from the peripheral blood of 42 subjects either by Percoll density separation or by negative-selection immunomagnetic fractionation. Eosinophil activation was initiated in vitro with 10(-6) M FMLP and 5 micrograms/ml cytochalasin B and was assessed by measurement of eosinophil peroxidase (EPO), leukotriene C4 (LTC4) and superoxide radical (.O2-) secretion. Treatment of HE with 100 microM mepacrine before activation blocked EPO release (2.0 +/- 0.2 vs 10.2 +/- 2.1% cell content for activated HE, P < 0.004, n = 9), .O2- generation (2.6 +/- 0.9 vs 44.2 +/- 10.8 nmol/ml per 10(6) HE, P < 0.002, n = 5), and LTC4 secretion (68.2 +/- 32.2 vs 1,125.2 +/- 526.8 pg/ml per 10(6) HE, P < 0.04, n = 8). Pretreatment of HE with 100 microM 4-bromophenacyl bromide before activation similarly blocked EPO release, .O2- generation and LTC4 secretion. Addition of AA to HE after treatment with 100 microM mepacrine and before subsequent activation reversed the inhibition of both EPO (10.4 +/- 2.2% with 1 microM AA vs 2.0 +/- 0.2% for mepacrine, n = 5, P < 0.02) and LTC4 secretion (695.1 +/- 412.9 with 10 microM AA vs 68.2 +/- 32.2 pg/ml per 10(6) HE for mepacrine, n = 8, P < 0.04), but did not reverse inhibition of .O2- generation by mepacrine. We demonstrate that secretion of preformed cytotoxic proteins and .O2- by eosinophils is regulated endogenously by phospholipase A2.

Localization and guided removal of soft-tissue foreign bodies with sonography.

Sonography was used to detect, localize, and guide removal of foreign bodies in the soft tissues of the extremities and neck. Twenty localization procedures were performed in 19 patients (12 children and seven adults) with 21 foreign bodies including wood, glass, stone, metal, and lead pencil. Localization was accomplished by using anatomic landmarks, ink marks on the skin, and needle and hemostat markers. Localization was facilitated by the use of small standoff pads that were cut for use on small surfaces. The foreign bodies were visualized as hyperechoic foci with acoustic shadows that were partial or complete depending on the angle of insonation and foreign body composition. Hyperechoic comet-tail artifacts (reverberation artifacts) were seen with six metallic foreign bodies and one glass fragment. Nine foreign bodies were surrounded by hypoechoic halos caused by edema, abscess, or granulation tissue. A slow meticulous scanning technique and high-frequency transducer helped in detection of small foreign bodies. Sonographically guided removal of the foreign body was successful in all four patients in whom it was attempted. Scanning with the ultrasound beam parallel to the long axis of the hemostat and the foreign body was the fastest way to guide the hemostat to the tip of a foreign body. The procedure was accomplished most easily and quickly when one physician performed sonography and hemostat removal of the foreign body simultaneously. Our experience with these cases indicates that sonography is a useful tool in the localization and removal of soft-tissue foreign bodies.