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The effect of processing on inflammatory markers in induced sputum.

The effects of the mucolytic agent, dithioerythritol (DTE), and the temperature at which sputum processing is conducted on cellular and biochemical markers in induced sputum was assessed. Samples from healthy and atopic asthmatic subjects were treated with either DTE or phosphate-buffered saline (PBS) at 22 or 37 degrees C and compared for cell counts and concentrations of histamine, tryptase, eosinophil cationic protein (ECP), free interleukin (IL)-8, immunoglobulin (Ig)A, IL-8/IgA complexes and secretory component (SC). In addition, the influence of DTE on in vitro mediator release from blood eosinophils, basophils and bronchoalveolar lavage (BAL) mast cells was studied. Processing with DTE improved cytospin quality and increased the cell yield and measurable ECP, tryptase, IgA and SC, but reduced levels of histamine in PBS-treated samples and had no effect on IL-8. Cell counts or mediator levels were similar when sputum was processed at 22 or 37 degrees C, even though DTE induced blood basophils and BAL mast cells to release histamine at 37 degrees C. In spiking experiments, recovery of added ECP, tryptase, total IL-8 and histamine from sputum was similar in DTE- and PBS-processed sputum, but reduced for free IL-8 in PBS-treated samples. In conclusion, dithioerythritol improves cell and mediator recovery without causing cell activation when sputum processing is conducted at room temperature. The extent of recovery depends on the mediator studied.

Asthma↗

Development of intestinal mucosal immunity in fetal life and the first postnatal months.

Nine premature infants who were either stillborn or who died shortly after delivery (gestational age, 24-32 wk), eight full-term infants who died during the first 3 postnatal wk, and four infants who died in the postneonatal period were studied by immunohistochemistry for duodenal expression of secretory component (SC) and epithelial HLA class I and II determinants and for the presence of IgA-, IgM-, and IgG-producing immunocytes. Only small amounts of SC appeared before the 29th gestational wk, but thereafter it increased rapidly; 1 wk after birth, SC showed an adult distribution pattern. Epithelial class I was expressed throughout the period investigated, whereas class II (HLA-DR) determinants were absent on the duodenal villi until 1 wk after birth. HLA-DP and -DQ were not expressed by the epithelium. No IgA immunocytes were seen before 1 wk after birth, whereas a few IgM- and IgG-producing cells were present throughout the period studied. The intense epithelial HLA-DR expression from the 2nd postnatal wk, along with SC and the appearance of IgA immunocytes, suggests that the intestinal immune system is modulated in response to environmental factors shortly after birth.

Antibody-Producing Cells↗

Comparison of pulmonary inflammatory mediators in preterm infants treated with intermittent positive pressure ventilation or high frequency oscillatory ventilation.

Ventilated preterm infants prone to the development of bronchopulmonary dysplasia have been shown to have increased inflammatory mediators in their tracheal aspirates. High frequency oscillatory ventilation (HFOV) is thought to be less traumatic than intermittent positive pressure ventilation (IPPV) in premature infants with surfactant deficiency, and therefore may reduce the inflammatory response in tracheobronchial aspirates. We randomized 76 premature infants requiring mechanical ventilation (birth weight 420-1830 g, median 840 g, gestational age 23 3/7 to 29 2/7 wk, median 26 4/7 to receive either an IPPV with a high rate (60-80/min) and low peak pressures, or an HFOV aiming at an optimization of lung volume, within 1 h of intubation. Tracheal aspirates were systematically collected during the first 10 d of life and analyzed for albumin, IL-8, leukotriene B4 (LTB4), and the secretory component (SC) for IgA as a reference protein. Bacterially colonized samples were excluded. On the treatment d 1, 3, 5, 7, and 10, the resulting median values of albumin (milligrams/mg of SC) were 28, 23, 24, 18, and 10, in IPPV-ventilated infants, and 33, 28, 18, 25, and 39 in HFOV-ventilated infants, respectively. Median IL-8 values (nanograms/mg of SC) were 671, 736, 705, 1362, and 1879 (IPPV) and 874, 1713, 1029, 1426, and 1823 (HFOV), respectively, and median LTB4 values (nanograms/mg of SC) were 26, 13, 27, 22, and 11 (IPPV) and 15, 12, 7, 12, and 16 (HFOV), respectively. Values were similar in IPPV- and HFOV-ventilated infants, and no significant differences were noted. We conclude that HFOV, when compared with a high rate low pressure IPPV, does not reduce concentrations of albumin, IL-8, and LTB4 in tracheal aspirates of preterm infants requiring mechanical ventilation.

Albumins↗

Localized amyloidosis in canine mammary tumors.

Histopathologic and immunohistochemical examinations were performed on localized amyloidosis associated with mammary tumors in two dogs. These tumors were identified as adenoma and adenocarcinoma. An acellular, amorphous pale eosinophilic material (amyloid) was observed in the lumina of acini lined by neoplastic cells and in the stroma of the tumors. Concentrically laminated pale eosinophilic bodies (corpora amylacea) were also found in the lumina of the acini. Amyloid and corpora amylacea stained positively with Congo red with and without 5% potassium permanganate pretreatment and revealed a green birefringence under polarized light. Corpora amylacea showed an occasional Maltese-cross pattern. Immunohistochemically, amyloid and corpora amylacea usually stained positively with anti-bovine alpha-casein antibody but negatively with anti-human amyloid AA, anti-bovine kappa-light and lambda-light chains, anti-human lactoferrin, anti-human transferrin, anti-human secretory component, and anti-human polyglucosan antibodies. These findings suggested that the amyloid deposition in these canine mammary tumors was related to lactating casein.

Adenocarcinoma, Papillary↗

Early postnatal dexamethasone decreases hepatocyte growth factor in tracheal aspirate fluid from premature infants.

OBJECTIVE: To evaluate in preterm infants the effect of dexamethasone on hepatocyte growth factor (HGF), an epithelial cell mitogen, and on vascular endothelial growth factor (VEGF), an endothelial cell mitogen, in tracheal aspirate fluid (TAF). METHODS: Thirty preterm infants (birth weight: 1000-1500 g) with respiratory distress syndrome were randomized to receive dexamethasone or to serve as control subjects. Dexamethasone was started at the age of 12 to 24 hours at a dose of 0.5 mg/kg/d for 2 days and 0.25 mg/kg/d for the subsequent 2 days. HGF and VEGF levels were examined from TAF samples during the first postnatal week. For eliminating the effect of dilution, the concentration of the secretory component of immunoglobulin A was determined. Student t test, 1-way analysis of variance, chi2, and simple regression analysis were used for statistical analysis. RESULTS: Mean HGF concentrations were similar in the dexamethasone and control groups on days 1 to 2, but the dexamethasone group had a lower mean HGF concentration on days 3 to 4 and 5 to 7. In contrast, no differences existed in mean VEGF levels between the dexamethasone and control groups. CONCLUSIONS: In preterm infants who received early postnatal dexamethasone, reduced levels of HGF were seen in tracheal aspirates. This reduction may participate in the suppressive effects of dexamethasone on lung development.

Bronchoalveolar Lavage Fluid↗

Low levels of tissue inhibitors of metalloproteinases with a high matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio are present in tracheal aspirate fluids of infants who develop chronic lung disease.

OBJECTIVE: The pathogenesis of chronic lung disease (CLD) involves inflammation with proteolytic damage to lung extracellular matrix. Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that, acting in concert with their tissue inhibitors, tightly orchestrate extracellular matrix morphogenesis and repair after injury. Imbalances in their levels relative to that of their inhibitors have been implicated in diseases characterized by matrix disruption and remodeling. We investigated the possibility that imbalances in MMP-9 and MMP-2 relative to their tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2, respectively, in tracheal aspirates of preterm infants may be involved in the development of CLD. METHODS: Serial tracheal aspirates collected from birth until extubation in 49 ventilated preterm infants (24-32 weeks' gestations) were analyzed for MMP-2, MMP-9, TIMP-1, and TIMP-2. Data normalized by TA values of free secretory component of immunoglobulin A were compared for CLD (n = 22) versus no CLD (n = 27). Also, known clinical predictors of CLD (gestational age, birth weight, and sex) were assessed for both groups. Association of predictors with the outcome CLD was assessed by logistic regression. RESULTS: Mean gestational age was lower in CLD infants, but birth weight and gender were comparable for both groups. CLD infants had significantly lower TIMP-1 level with higher MMP-9/TIMP-1 ratio during the first 2 weeks of life and low TIMP-2 and MMP-2 levels during the first 3 days of life compared with no-CLD infants. Logistic regression analysis indicated that the findings are predictive of CLD. CONCLUSIONS: We conclude that low tracheal aspirate levels of TIMPs, with a high MMP-9/TIMP-1 ratio early in life, are associated with subsequent development of CLD.

Bronchopulmonary Dysplasia↗

Effects of modifying gonadotrophin-releasing hormone input before and after the oestrogen-induced LH surge in ovariectomized ewes with hypothalamo-pituitary disconnection.

The patterns of gonadotrophin-releasing hormone (GnRH) input to the pituitary gland that affect the expression of a positive-feedback event by oestrogen on LH secretion were investigated in ovariectomized ewes with hypothalamo-pituitary disconnection (HPD). In experiment 1, ovariectomized HPD ewes were given hourly i.v. pulses of 250 ng GnRH and an i.m. injection of 50 micrograms oestradiol benzoate (OB). The ewes were given a bolus pulse of 2.25 micrograms GnRH 16 h after injection of OB, followed by half-hourly pulses of 250 ng GnRH for 14 h (treatment A). The LH surge response was significantly (P less than 0.05) greater in these ewes compared with that in ewes given a continuous infusion of GnRH (250 ng/h) after the OB injection, followed by a continuous infusion of 500 ng GnRH/h after the bolus pulse of GnRH (treatment B). When no GnRH was administered after the OB injection, except for the bolus pulse of GnRH (treatment C), the surge response was significantly (P less than 0.05) reduced compared with that in treatment A, and was reduced compared with treatment B. These data suggest that GnRH pulses are important in the generation of the OB-induced LH surge, but that a baseline secretory component can prime the pituitary to some extent. In experiment 2, a doubling of the continuous infusion dose of GnRH used in treatment B to 500 ng/h before the bolus pulse of GnRH and to 1 micrograms/h afterwards (treatment D) gave a similar response compared with treatment A, suggesting that if the baseline input of GnRH is of sufficient magnitude, it can overcome the lack of pulsatile input. In experiment 3, halving the GnRH pulse amplitude used in treatment A from 250 to 125 ng (treatment E) did not reduce the LH surge response, implying that when the GnRH input is in a pulsatile mode, the amplitude of GnRH pulses is less important than the pulsatile nature per se. In experiment 4, removal of GnRH input after the bolus pulse of GnRH (treatment F) significantly (P less than 0.05) reduced the surge response compared with when pulses were maintained (treatment A), indicating that GnRH input is still required once the LH surge has been initiated. Collectively, these experiments show that several forms of GnRH delivery, both pulsatile and baseline, can result in the full expression of a positive-feedback response in ovariectomized ewes treated with oestrogen.

Animals↗

Altered instantaneous and calcium-modulated oscillatory PTH secretion patterns in patients with secondary hyperparathyroidism.

The relative contributions of increased parathyroid cell mass and altered control mechanisms of parathyroid hormone (PTH) secretion in secondary hyperparathyroidism are still controversial. In this study, endogenous pulsatile PTH secretion was analyzed by the multiparameter deconvolution technique to differentiate alterations in cell mass-dependent (PTH burst mass) and regulation-dependent (frequency, synchrony, calcium responsiveness) PTH release in uremic patients. PTH concentration versus time profiles were obtained in 13 uremic and 16 healthy adults under baseline conditions and during acute hypo- and hypercalcemia. Plasma PTH half-life was increased in patients compared with control subjects (4.7+/-1.9 versus 2.6+/-0.1 min, P < 0.005). The baseline PTH secretion rate was elevated eightfold in the patients as a result of an increased PTH mass secreted per burst (17.1+/-4.7 versus 2.0+/-0.4 pM, P = 0.0001), higher burst frequency (8.0+/-0.3 versus 6.8+/-0.3 h(-1), P < 0.01), and a higher tonic secretion rate (343+/-99 versus 30+/-4 pM/h, P = 0.0001). Acute hypocalcemia elicited an immediate, frequency- and amplitude-mediated selective increase in the pulsatile secretory component, which was fractionally weaker in patients (+595%) than control subjects (+1755%, P < 0.001). The acceleration and the amplification of PTH bursts were 35 and 60% lower in the patient group. Acute hypercalcemia suppressed total PTH secretion by 79% in control subjects but only by 63% in patients (P < 0.002). PTH burst frequency was reduced during hypercalcemia by 30% in control subjects, but remained unchanged in patients. In conclusion, uremic hyperparathyroidism is mediated by a marked increase in glandular secretion, but also by reduced PTH elimination. The increased spontaneous PTH burst frequency and the blunted responsiveness to changes in Ca2+ indicate partial uncoupling of hyperplastic parathyroid glands from the physiologic regulatory mechanisms that direct pulsatile PTH release.

Adolescent↗

Poult enteritis complex.

Poult enteritis complex (PEC) is a general term that encompasses the infectious intestinal diseases of young turkeys. Some diseases, such as coronaviral enteritis and stunting syndrome, are relatively well characterised, while others, such as transmissible viral enteritis, poult growth depression and poult enteritis mortality syndrome, remain ill-defined. All forms of PEC are multifactorial, transmissible and infectious. Salient clinical features include stunting and poor feed utilisation that result from enteritis. In the more severe forms, runting, immune dysfunction and mortality are reported. Gross and microscopic lesions of enteritis are present in all forms but tend to be non-specific. Other lesions may be present, depending on the agents involved. The basic pathogenesis involves the following: a) alteration of the intestinal mucosa, generally by one or more viruses infecting enterocytes; b) inflammation; c) proliferation of secondary agents, usually bacteria. Non-infectious factors interplay with infectious agents to modulate the course and severity of disease. Diarrhoea is believed to be primarily osmotic because of maldigestion and malabsorption, but may also have a secretory component. Transmission is primarily faecal-oral. No public health significance is recognised or suspected. Prevention is based on eliminating the infectious agents from contaminated premises and preventing introduction into flocks. This is accomplished by an effective cleaning, disinfection and biosecurity programme. All-in/all-out production or separate brooding and finishing units are helpful. Control may require regional co-ordination among all companies producing turkeys, especially if the production is highly concentrated, and a quarantine programme for more severe forms of PEC. No vaccines or specific measures for controlling the organisms involved in PEC are available. Treatment is supportive for the viral component, while antibiotics, especially those with efficacy against Gram positive bacteria, may help to reduce the impact to bacterial infections. Evidence suggests that PEC occurs wherever turkeys are raised commercially, but this is not well documented and distribution of the various organisms that have been associated with PEC is largely unknown. The disease causes enormous economic loss, mostly from failure of the turkey to reach its genetic potential.

Animals↗

Ultrastructure of murine dermis following topical application of the vitamin D3 analogue KH-1060.

The aim of this study, was to observe the effects of KH-1060, a new vitamin D3 analogue, on the dermis of hairless mice by electron microscopy. KH-1060 (0.2 micrograms/ml in isopropanol) or KH-1060 following betamethasone 17-valerate (2 mg/ml in isopropanol) was applied topically to the backs of hairless mice for 4 weeks. KH-1060 increased the number of dermal fibroblasts, the cytoplasm of which was dominated by secretory components. Mast cells contained normal mature granules and degranulated after disintegration. No extrusion of non-disintegrated granules was seen. Collagen fibrils were thickened and increased in number; however the content of type I collagen in the fibrils did not increase. Glycosaminoglycan figures appeared distinct. KH-1060 prevents betamethasone-induced changes in collagen fibrils and glycosaminoglycans, while no prevention was seen for mast cells.

Animals↗

Inflammation in the bovine female reproductive tract.

Inflammation of the reproductive tract of a cow occurs when the physical and functional barriers to contamination are breached or specific infection occurs. Commonly, contamination occurs at parturition and to a lesser extent at estrus. Uterine contamination following calving is common, but most healthy cows are able to clear the uterus of bacteria in the first 2 to 3 wk after calving. Persistent infections are more likely to be caused by Actinomyces pyogenes. Specific venereal infections tend to be more host-adapted and produce a lower grade inflammation. Nonspecific bacterial contamination of the endometrium generally induces a neutrophilic influx into the stratum compactum and uterine lumen. Neutrophils phagocytize bacteria with the aid of opsonins in the uterine fluid. Mast cells and eosinophils may also contribute to the inflammatory reaction, which may damage the surface epithelium and release vasoactive substances that allow leakage of serum antibodies into the uterine secretions. Specific antibodies of immunoglobulin (Ig) isotype A, M, G1, and G2 in uterine secretions have been described. In model species, the immune capability of the uterus is influenced by steroid hormones, especially estradiol, which increases secretory component and both IgA and IgG content in uterine secretions and increases the activity of antigen-presenting cells in the uterus. Similar cyclic fluctuations in immune components have been described for cows, including changes in the population of subsurface cytotoxic and helper T cells and changes in the expression of major histocompatibility II antigen on surface cells.

Actinomycosis↗

Evidence of serum antibodies against inner ear tissues in the blood of patients with certain sensorineural hearing disorders.

In healthy human temporal bones, immunoglobulins (IgG, IgA) and the secretory component are demonstrated by two immunohistochemical methods in epithelial cells and in the lumen of the endolymphatic sac. The normal human inner ear does not otherwise show any localization of immunoglobulins. By means of indirect immunofluorescence, antibodies against healthy inner ear tissue were found in the serum of 15 out of 21 patients with double-sided progressive or fluctuating sensorineural hearing loss of undefined etiology. In 2 cases of Cogan's syndrome, it was also possible to demonstrate serum antibodies against epithelial structures of the cornea. The lymphocyte mitogen stimulation test performed with the fresh blood of 5 patients with positive detection of serum antibodies against healthy inner ear tissue was negative.

Autoantibodies↗

Antibodies to pneumolysin and pneumococcal capsular polysaccharides in middle ear fluid of children with acute otitis media.

Antibodies to pneumococcal pneumolysin and capsular polysaccharides were measured by enzyme immunoassay in 169 acute phase middle ear fluid samples of 116 children with acute otitis media. Antibodies to pneumococcal pneumolysin were detected in 84% and to capsular polysaccharides in 50% of the MEF samples. The Ig class detected most often was IgA to both types of pneumococcal antigens, and it was present in MEF even with non-detectable levels of serum IgA of the same specificity. 59% of the MEF samples positive for IgA to pneumolysin were also positive for secretory component of the same specificity, and 53% of IgA to capsular polysaccharide pool (containing serotypes 6B, 14, 19F, and 23F), respectively. This suggests both leakage of specific IgA from serum to the middle ear and local production of it. In contrast, specific IgG was detected in MEF only with concomitant IgG in serum. Antibodies to pneumolysin occurred in no relation to bacterial findings in MEF. On the contrary, IgG class antibodies to capsular polysaccharides, most likely serum-derived, were detected less often in MEF samples positive for pneumococcus than for other bacteria.

Antibody Formation↗

Immune functions and immunopathology of the mucosa of the upper respiratory pathways.

The specific defence of airway mucosae depends primarily on secretory immunity. The B cells involved are initially stimulated in organized mucosa-associated lymphoid tissue, apparently including the tonsils and adenoid. From these inductive sites, memory cells migrate to secretory effector sites where they differentiate terminally to immunoglobulin (Ig)-producing plasma cells. Locally produced Ig consists mainly of J chain-containing dimers and larger polymers of IgA (pIgA) that are selectively transported through glandular cells by an epithelial receptor called secretory component or the pIg receptor. IgG can participate in immune exclusion because it reaches the secretions by passive diffusion. However, its proinflammatory properties render IgG antibodies of local immunopathological importance when elimination of penetrating antigens is unsuccessful. T helper (Th) cells activated in this process may by a Th2 cytokine profile promote persistent inflammation with extravasation and priming of eosinophils. This development appears to be part of the late-phase allergic reaction, perhaps initially driven by interleukin-4 (IL-4) released from mast cells that are subjected to IgE-mediated activation, and subsequently also by Th2 cell activation. Eosinophils are potentially tissue-damaging, particularly after priming with IL-5. Various cytokines up-regulate adhesion molecules on endothelial and epithelial cells, thereby enhancing migration of eosinophils into the mucosa, and perhaps in addition causing aberrant immune regulation within the epithelium. Soluble antigens bombarding the epithelial surfaces normally seem to induce several immunosuppressive mechanisms, but mucosal homeostasis appears less patent in the airways than oral tolerance to dietary antigens operating in the gut.

B-Lymphocytes↗

The monitoring of inflammation by specific cellular markers.

The use of specific assays for unique secretory components of various inflammatory cells in the clinical evaluation of inflammatory diseases is a new and fascinating possibility, since these assays seem to be more sensitive indicators of inflammatory activity than the conventionally used methods and since these unique cellular markers in addition provide us with useful pathophysiological information. So far the most widely used markers are eosinophil cationic protein (ECP) from the eosinophil and neutrophil markers such as myeloperoxidase and elastase. Serum measurements of the former are used quite extensively in the evaluation of the inflammatory process in the lung of asthmatics whereas the latter predominantly are used in relation to bacterial infections and as compatibility markers in relation to extracorporeal circulation. Recent developments have shown that the serum measurement of a new protein from the neutrophil, human neutrophil lipocalin (HNL), is a superior means to distinguish acute bacterial and viral infections. The future access to a panel of unique cellular markers of inflammatory cells will undoubtedly reveal new exciting possibilities in the diagnosis and therapeutic monitoring of patients with inflammatory diseases.

Eosinophils↗

Characterization and quantification of plasma proteins excreted in faeces from healthy humans.

Faecal plasma protein loss was studied in 38 healthy adults. Using crossed immunoelectrophoresis and single radial immunodiffusion the most frequently found proteins were alpha 1-antitrypsin, IgA, alpha 1-antichymotrypsin (found in 97, 92, and 84% of subjects), prealbumin and IgM (both found in 55%). The major plasma proteins, albumin and IgG, were found in 37 and 13% of subjects, respectively, and in trace amounts only. alpha 2-macroglobulin could not be detected. There was no relation between the presence of proteins in faeces and their plasma concentration. When added to faeces, alpha 1-antitrypsin, alpha 1-antichymotrypsin, and prealbumin were resistant to incubation (37 degrees C, 48 h), whereas albumin, IgG, IgM, and IgA were rapidly degraded (within 8-24 h). Some IgA was bound to secretory component, indicating enteric secretion. alpha 2-macroglobulin was semi-resistant to degradation, but its passage to the intestinal lumen may have been prevented by its molecular size. In conclusion, resistance to degradation, enteric secretion, and low molecular weight are the primary factors which favour the excretion of plasma proteins in faeces. The technique used in this study allows further studies in patients with inflammatory changes and protein-losing enteropathy.

Adult↗

Local immune defence in relation to gastritis in Billroth-II-resected stomachs.

Biopsy specimens from Billroth-II-resected stomachs obtained endoscopically 28-32 years after the operation were subjected to an immunohistochemical study by two-colour immunofluorescence staining. The epithelial distribution of immunoglobulin A (IgA), secretory component (SC), lysozyme (Ly), and lactoferrin (Lf) was evaluated, and IgA-, IgM-, and IgG-producing cells were quantified in the lamina propria. Gastric body mucosa excised from resected stomachs obtained from patients with duodenal ulcer was used as control and showed considerably less extensive gastritis than the stump mucosa. Both specimen categories showed enhanced expression of epithelial IgA, SC, Ly, and Lf associated with severe gastritis, except for areas with intestinal metaplasia, which lacked Ly and Lf. The number of IgA-, IgM-, and IgG-producing cells was significantly increased with increasing degree of gastritis, particularly so for IgG cells on a relative basis. After partial gastrectomy, therefore, the stump mucosa generally responds with activation of local immune mechanisms; this response is principally similar to that seen in simple gastritis of comparable severity.

Adult↗

Expression of prostasome-like granules by the prostate cancer cell lines PC3, Du145 and LnCaP grown in monolayer.

Prostasomes are a granular type of secretory product in the human prostate gland cells. It is not known, whether in vitro grown cells derived from human prostate cancers also express prostate secretory components containing granules with properties similar to the prostasomes. Therefore, we carried out the present investigation and found that cytospins of in vitro grown PC3, DU145 and LNCaP cells generally expressed a granular secretion. DU145 demonstrated the highest ratio of cells with granules (about 90%), while cytospins of PC3 and LNCaP contained less stained cells (50-70%). Purified granules from PC3 cells were immunoreactive with a monoclonal antibody (mAb78) originally raised against human seminal prostasomes. The PC3 granules also shared the property with human seminal prostasomes having an elevated UV260/UV280 absorbance ratio. On the other hand we found a low aminopeptidase activity in PC3 granules contrary to that of human prostasomes. Prostasomes may form a heterogeneous group with different properties due to the source from which they are isolated and perhaps it is justified to recognize them as different members of a prostasome family.

Aminopeptidases↗