Biomedical subjects

P Conti

Publications and source records attributed to P Conti.

At least 73 records · Page 4Linked to original sources

PubMed1997

Infra-red laser irradiation enhances interleukin-1 receptor antagonist, increases 3H-thymidine incorporation and the release of [3H]arachidonic acid in human monocytes.

The effect of infra-red laser irradiation has been experimented on various biological systems and particularly in human tissues, in vitro as well as in vivo. In order to examine the influence of laser irradiation on cells of the monocytic lineage we have irradiated human peripheral blood mononuclear cells with an infra-red laser at a wavelength of 904 nm, at 2000 Hz frequency and 15 mW for 2 min. Here, we report that laser irradiation for 2 min. at different preincubation times (T = 0 and T = 30 min) enhances LPS (10 micrograms/ml or PHA (10 micrograms/ml, suboptimal concentration)-stimulated monocytes by modifying cell proliferation, as judged by [3H] thymidine incorporation. IL-1 receptor antagonist (IL-1ra) along with an increased release of [3H] Arachidonic acid production, is also influenced by laser irradiated monocytes when treated for 2 min after 1 h incubation. IL-1RA production increased 4-5 fold after laser irradiation, while 3H-arachidonic acid incorporated from PMA-stimulated cells increased and the effect was significant at T = 0 and T = 30 min; while at T = 1 h the effect was negligible. These results may provide new information regarding the effect of laser irradiation on the immune system.

Arachidonic Acid↗

PubMed1997

Augmentation of monocyte chemotactic protein-1 and mRNA transcript in chronic inflammatory states induced by potassium permanganate (KMnO4) in vivo.

Monocyte chemotactic protein-1 (MCP-1) is a proinflammatory cytokine that attracts and activates specific types of leucocytes. The purpose of this work was to analyse the generation of MCP-1 and mRNA transcript in a model of chronic inflammation using a granulomatous tissue induced by potassium permanganate (KMnO4; water soluble crystals). The data presented here shows that MCP-1 is generated in granuloma tissue and its level was strongly increased by i.p. injections of lipopolysaccharide (LPS) and inhibited in rats treated with injections of dexamethasone, 18 hr before the animals were killed. In histological studies LPS and dexamethasone increased and decreased, respectively, the recruitment of mononuclear cells in the granuloma tissue compared with the control granulomas from phosphate-buffered saline (PBS)-treated animals. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used for mRNA extraction and cDNA synthesis. mRNA MCP-1 was significantly produced in the granuloma tissue of untreated animals, an effect increased by LPS and inhibited by dexamethasone, compared with the controls. Moreover, MCP-1 protein was found in the supernatant from homogenized granuloma tissues and the levels of MCP-1 were higher in the LPS-treated animals, while they were lower in the dexamethasone group, compared with the granulomas from the PBS-treated groups (control). The generation of MCP-1 was also found in minced granuloma tissue incubated for 18 hr (overnight) from treated (LPS or dexamethasone) and untreated (PBS) rats. When LPS was added in vitro for 18 hr to the controls and treated animals the production of MCP-1 was further increased except in the dexamethasone group (P > 0.05). Analysing blood serum from LPS, dexamethasone or PBS-treated rats, we found that MCP-1 was also present. The level was higher in the LPS group and lower in the dexamethasone group, compared with the control (PBS). In these studies we show for the first time that MCP-1 transcript and translation is generated in chronic experimental inflammatory tissue, an effect inhibited by dexamethasone.

Animals↗

PubMed1997

Monocyte chemotactic protein-1 is a proinflammatory chemokine in rat skin injection sites and chemoattracts basophilic granular cells.

Chemokines may control mast cell infiltrates found in many inflammatory diseases. These cells act through at least two main functions: migration and degranulation. Here we show that human recombinant monocyte chemotactic protein (MCP)-1 (10 ng/50 microliters) induces, after 4 h, an inflammatory vascular permeability and cellular extravasation reaction, determined by Evan's blue dye (1% in saline) injected into the tail vein of the rat, when injected intradermally in the rat skin. The blue color accumulating at the sites of injection provides evidence of vascular permeability and cellular extravasation. The colored areas of the skin were then enucleated and immersed in a fixative solution. Slides were prepared with sections of tissue colored with toluldine blue and analyzed under an optical microscope. A significant number of basophilic cells migrated to the injected area where MCP-1 (10 ng/50 microliters) was used compared to the control PBS treatment. Cell recruitment was slightly less than N-formyl-methionine-leucyl-phenylalanine (used at 10(-6) M/50 microliters). Electron microscopy studies confirmed the presence of basophilic granular cells where MCP-1 was intradermally injected. After preparation of a histidine decarboxylase (HDC) probe, a Northern blot analysis was determined for HDC mRNA in the enucleated tissue injected with MCP-1 (10 ng/50 microliters). Steady-state levels of HDC mRNA levels were induced after 4 h. These results were confirmed by the higher amount of histamine release, compared to the control PBS, in the enucleated tissue from the MCP-1 injection sites. Our results suggest that MCP-1 could play a significant role in diseases characterized by basophilic cell accumulation and migration to sites of tissue damage. Moreover, we show for the first time that MCP-1 is a pro-inflammatory chemokine that induces basophilic cell migration in rat skin injection sites.

Animals↗

PubMed1997

[Malignant tumors of the peripheral nerve sheath (MPNST) after irradiation].

A case of relapsed malignant tumor of the brachial plexus and its nervous roots (MPNST) was observed in a patient treated with radiotherapy for Hodgkin's disease 24 years previously. A known risk of radiation therapy is the induction of secondary neoplasms, less commonly malignant peripheral nerve sheath tumor (MPNST). The clinico-pathological features of this rare tumor are presented and the possible relationship between radiotherapy and MPNST is discussed.

Adolescent↗

PubMed1996

Human recombinant interleukin-1 beta induces thromboxane A2 release in polymorphonuclear leukocytes, macrophages and platelets: effect of IL-1 receptor antagonist.

Prostaglandins and thromboxanes (Txs) are produced by polymorphonuclears (PMNs) and macrophages (Mphis) in response to various stimuli. PMNs were separated from other human blood cells and Mphis were separated from rat peritoneal lavage. In this paper we show that human recombinant interleukin-1 (hrIL-1) can stimulate the release of thromboxane B2 (TxB2) by PMNs and Mphis. In addition, we have shown that aggregation of PMNs may occur when calcium ions (7 mM) and hrIL-1 (100 ng/ml) are added to the cell preparation, but not when Ca2+ alone, hrIL-1 alone, or first hrIL-1 then calcium are added to the cell preparation. The treatment of human platelets with hrIL-1 shows that after 15 min incubation TxB2 is released. In addition, we compared the aggregation of platelets caused by ADP with that caused by hrIL-1. Human recombinant IL-1 at a concentration of 100 ng/ml also causes little aggregation of platelets, in this case the aggregation is reversible. In conclusion, hrIL-1 beta stimulates TxB2 release in PMNs, Mphis and platelets and this effect increases with addition of Ca2+ ions. The mixture of hrIL-1 and Ca2+ causes little aggregation of PMNs. In monocyte suspensions, pretreated with human recombinant IL-1 receptor antagonist (IL-1ra) 500 ng/ml for 10 min and then treated with LPS or hrIL-1 beta 10 micrograms/ml, the release of TxB2 was partially inhibited. IL-1ra may play a significant role in the control of IL-1 and LPS induction in the release of TxB2.

Adenosine Diphosphate↗

PubMed1996

Effect of interleukin-1 receptor antagonist (IL-1RA) on histamine and serotonin release by rat basophilic leukemia cells (RBL-2H3) and peritoneal mast cells.

Recently, it has been appreciated that cultured mast cells are significant sources of cytokines. However, the role of interkeukin-1 (IL-1) on mast cells and/or basophil degranulation is still unclear. In this report we provide evidence that rat basophilic leukemia cells (RBLC) cultured with a natural inhibitor of IL-1, interleukin-1 receptor antagonist (IL-1RA) (500 ng/ml) for 48 h, strongly inhibited the spontaneous release of serotonin (5HT) and histamine (from 22.50 to 43.49%), compared to untreated cells (control). When IL-1RA-treated and untreated RBLC were stimulated with a secretagogue (anti-IgE), no difference was found in the percent of 5HT and histamine release. Moreover, in another set of experiments using rat peritoneal mast cells (RPMC) treated and untreated with IL-1RA, we found that IL-1RA did not affect the release of 5HT or histamine, even when the secretagogue anti-IgE or compound 48/80 (C48/80) were used. The present studies describe an additional biological activity of IL-1RA, inhibiting histamine and 5HT release from RBLC cultures.

Animals↗

PubMed1996

Electrophoretic separation of biopolymers in a matrix of polyacrylamide covalently linked to agarose.

A new type of agarose polyacrylamide mixed-bed gel, obtained by simultaneous gelation of a novel type of allyl-activated agarose and its copolymerization with acrylamide, has pore sizes intermediate between those of polyacrylamide and agarose. The process used to activate the agarose chains enables the substitution to be controlled. As indicated by nuclear magnetic resonance (NMR), only one allyl group was inserted per agarose basic unit. Several formulations of mixed-bed gels, containing different percentages of acrylamide, were compared with conventional polyacrylamide or agarose gels. Resolution, migration distance and band sharpness of different molecular mass fragments were evaluated, with two types of gel run side-by-side in a vertical or horizontal system. The faster electrophoretic mobility of DNA in dilute mix-bed gels and the improved separation of the component of high molecular mass (1 to 6 kbp) of the 1 kbp ladder indicate that these matrices have larger porosity than any dilute polyacrylamide formulations. Sodium dodecyl sulfate (SDS)-protein complexes migrate in the mixed gels faster than in polyacrylamide gels of the same %T.

Biopolymers↗

PubMed1996

Major neurological sequelae of lumbar epidural anesthesia. Report of three cases.

We here report the major permanent neurological complications that developed in three patients after epidural anesthesia. MR clearly showed that paraplegia, which arose one and nine days after anesthesia, was due to epi-subdural haematoma in the first case and epidural abscess in the second. The sudden left lower limb palsy in the third patient was caused by a paracentral ischemic lesion all along the conus-epiconus following a probable trauma of the cord during the insertion of the needle. Despite the fact that this was reported to have been performed at L1-L2, an erroneous introduction into the upper interspace must be postulated since the spinal cord of this patient terminated at mid-L1. Our report is useful insofar as it may remind anesthesiologists and neurologists to pay attention to the unusual complications of spinal anesthesia that may require urgent intervention.

Abscess↗

PubMed1996

Generation of TNF alpha, IFN gamma, IL-6, IL-4 and IL-10 in mouse serum from trichinellosis: effect of the anti-inflammatory compound 4-deoxypyridoxine (4-DPD).

Infections caused by the nematode Trichinella spiralis is characterized in the host by an inflammatory response with cytokine production. In these studies we have detected TNF alpha, IL-6, IFN gamma, IL-4 and IL-10 in the serum of 10 mice infected with T. spiralis. Moreover, we detected, for the first time, these cytokines in the serum of mice treated with 4-DPD, a potent antagonist of vitamin B6 coenzyme which has anti-inflammatory properties. 4-DPD was used at 100, 400, 800 micrograms/bolus for 20 days, starting one day before the infection. After 15 days of T. spiralis infection, TNF alpha reached a maximum level, while IL-6 was maximal after 7 days, IFN gamma at 20 days and IL-4 at 14 days. IL-10 was not affected by the T. spiralis infection. When the animals were treated with 4-DPD at the reported dosages and infected with T. spiralis the inhibition of TNF alpha and IL-6, were dose-dependent in the first 7 days while IL-4 was reduced only at 400-800 micrograms/bolus. 4-DPD-treated mice did not statistically (P > 0.05) affect the generation of IFN gamma. In healthy animals the production of cytokines were not measurable, just as it was in non-infected animals treated with 4-DPD. The increase of cytokines such as, TNF alpha and IL-6 may be related to the severity of the disease, boosting the host's resistance to the pathogen and inhibiting parasite survival. In addition, the augmentation of IL-4 production enhances T and B cells and macrophage responses and may stimulate T-cell antibody-mediated response to the pathogen. 4-DPD, an inhibitor of IL-1 and inflammatory reactions, proved to be most effective on TNF alpha and IL-6, which are mainly produced by macrophages.

Animals↗

PubMed1996

Down-regulation of cyclooxygenase-2 (COX-2) by interleukin-1 receptor antagonist in human monocytes.

Cyclooxygenase (COX) is the key rate-limiting enzyme in the synthesis of prostanoids from arachidonic acid. Two isoforms of COX have been described in mammalian cells, referred to as cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is a constitutively expressed enzyme; COX-2 is an inducible enzyme that appears to be expressed in inflamed tissue and following exposure to growth factors or cytokines, such as interleukin-1 (IL-1). The aim of the present study was to test if the antagonism on the binding of IL-1 to its cell-surface receptor by human recombinant IL-1 receptor antagonist (hrIL-1ra) may control the COX mRNA expression and prostaglandin E2 (PGE2) production by human monocyte cultures. Northern blot studies showed that hrIL-ra (500 ng/ml) had a strong inhibitory effect on inducible COX activity. The effect was evident after 6 hr incubation (2.7-fold decrease of mRNA COX-2 transcripts); and about a threefold decrease at 24hr incubation. A non-significant effect was observed with COX-1 transcripts. Induced PGE2 production by monocyte cultures treated with lipopolysaccharide (LPS) or interleukin-1 beta (IL-1 beta) was strongly inhibited in the presence of hrIL-1ra (500 ng/ml). In addition, a significant inhibition of COX-2 protein expression, as evaluated by Western blotting, was also observed. These data suggest that hrIL-1ra may be the key mediator in the down-regulation of the COX-2 inducible pathway.

Blotting, Northern↗

PubMed1996

Biliary malformation with renal tubular insufficiency in two male infants: third family report.

We report two male sibs, born to non-consanguineous healthy parents, who showed arthrogryposis, cholestatic jaundice and tubular renal insufficiency. The liver biopsy of the first case showed scanty hypoplastic biliary ducts. This association, first reported by Lutz and Richner in 1973, is a distinct syndrome, characterized by intra-extrahepatic biliary hypoplasia, and described in McKusick's catalogue under the number 210550. All reported cases were males and consanguinity was found in two families. For these reasons, the possibility of an autosomal recessive or of an X-linked transmission should be considered. A similar association, in reports by Nezelof, Di Rocco, and Saraiva, without intra-extrahepatic atresia but with a cholestatic pigmentary liver disease was considered as another condition (no. 301820) by McKusick in 1992.

Abnormalities, Multiple↗

PubMed1996

Cysteinyl leukotriene D4 induced vascular smooth muscle cell proliferation: a possible role in myointimal hyperplasia.

Cysteinyl leukotrienes (i.e. LTC4, LTD4), produced by activated leukocytes or by transcellular metabolism may act at different levels on vascular smooth muscle cells (VSMC) during inflammatory process or atherosclerosis. We studied the effect of LTC4, LTD4, and LTE4 on the in vitro proliferation of rat VSMC, measured by [3H]-thymidine incorporation and cell count. LTD4 had a stronger stimulatory effect on [3H]-thymidine incorporation than LTC4, whereas LTE4 was inactive. The effect of LTD4 on [3H]-thymidine incorporation was dose-dependent, with the maximal activity at 10(-6) M. The stimulatory activity of LTD4 was inhibited in a dose-dependent manner by MK-571, a specific LTD4 receptor antagonist. In addition, MK-571 (1 mg/kg/day) given for at least 1 day after injury in a model of balloon catheter injury of rat carotid artery, provided effective inhibition of myointimal VSMC proliferation, with a 58% reduction of 5-bromo-2'-deoxyuridine (BrdU) uptake in the neointima and 69% reduction of neointimal thickening. Our data support the importance of inflammatory mechanisms in the pathogenesis of atherosclerosis and suggest a possible role for cysteinyl leukotrienes, specifically LTD4, in the control of VSMC proliferation.

Animals↗

PubMed1996

Spinal meningiomas in pregnancy: report of two cases and review of the literature.

Although meningiomas of the spinal district are frequently found, first presentation of these growths during pregnancy is extremely rare. Few cases have been reported in the literature up to now. In a series of 122 spinal meningiomas operated-on at our institution over the period 1962-1994, first neurological symptoms and signs became evident during pregnancy in two cases. Considering this noteworthy, the hydrodynamic and hormone-mediated mechanisms regarding meningioma growth during pregnancy and a review of the pertinent literature are discussed.

Adult↗

PubMed1995

The down-regulation of IL-6-stimulated fibrinogen steady state mRNA and protein levels by human recombinant IL-1 is not PGE2-dependent: effects of IL-1 receptor antagonist (IL-1RA).

Infections, trauma and inflammatory processes induce a host response with increases in a large group of structurally and functionally diverse plasma proteins. Parental administration of foreign proteins also induce an increase in plasma fibrinogen. Interleukin-6 (IL-6) is a monocyte-derived mediator and has regulatory effects on acute phase protein genes which result in the induction of fibrinogen synthesis in primary hepatocytes, while the addition of interleukin-1 (IL-1) exerts a negative modulating influence on the IL-6-stimulated fibrinogen. In order to understand the mechanisms by which IL-1 inhibits IL-6-stimulated fibrinogen transcription and translation, and since IL-1 is believed to act through PGE2 stimulation, we have studied the influence of PGE2 in IL-6 or IL-1, alone and in combination, on Fg mRNA expression (by Northern blot analysis) and the influence of PGE2, indomethacin, and arachidonic acid on Fg secretion. Moreover, since human recombinant interleukin-1 receptor antagonist (hrIL-1ra) is a strong inhibitor of IL-1 induced IL-1 transcription and translation and has an inhibitory effect on PGE2, we have studied the effects of IL-1ra on the down-regulation of IL-6 stimulated fibrinogen by IL-1, using an Fg ELISA method.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acid↗

PubMed1995

Modulation of rat vascular smooth muscle cell (VSMC) proliferation by cysteinyl leukotriene D4: a role for mediation of interleukin 1.

Recent studies suggest the involvement of inflammatory mechanisms in the progression of atherosclerosis. Cysteinyl leukotrienes and cytokines could orchestrate this progression by acting on the proliferation of vascular smooth muscle cells (VSMC). In cultures of rat VSMC, proliferation was modulated by cysteinyl leukotriene C4 (LTC4) and LTD4, but not LTE4. Co-culturing LTD4 with VSMC produced an increased cell proliferation as assessed by [3H]thymidine incorporation studies (200%) as well as cell counts (70%), using LTD4 at 10(-6)M compared to controls. LTD4 exerted its effect through an interleukin 1 (IL-1)-dependent autocrine regulatory mechanism. When IL-1 was inhibited by using a receptor antagonist (IL-1ra) and a polyclonal antibody to IL-1, we found an inhibition of VSMC proliferation. The increase of VSMC proliferation was associated with the autocrine production of interleukin-1 (IL-1) concomitant to LTD4 stimulation (55.5 +/- 2.5 pg/ml in controls and 177 +/- 0.5 pg/ml in 10(-6)M LTD4). These results may shed new light on the mechanism of inflammatory involvement during atherogenesis, suggesting that the control of cysteinyl leukotrienes may be important in inflammatory processes involving IL-1.

Animals↗

PubMed1995

Cysteinyl-leukotriene D4 induced IL-1 beta expression and release in rat vascular smooth muscle cells.

Vascular cells, including smooth muscle cells (VSMC), may release interleukin 1 (IL-1) and transcribe its genes for both isoforms. Previous studies have shown that cysteinyl-leukotrienes can modulate cytokine production by monocytes and a cytokine-eicosanoid network has been suggested during atherosclerosis. In this study the effects of cysteinyl-leukotriene D4 (LTD4) on IL-1 beta production and IL-1 beta mRNA expression were tested on rat VSMC. LTD4 showed a significant dose-dependent (from basal production of 55 +/- 15 pg/ml to maximal production of 177 +/- 14 pg/ml) and time-dependent (peaking at 24 h 16 +/- 54 pg/ml) increase of IL-1 beta immunoreactivity in the supernatants of conditioned medium and cell lysates. Furthermore, LTD4 induced an increased mRNA expression which began at 1 h and peaked at 12 h incubation time. The production of IL-1 beta was inhibited by MK-571 (from 145 +/- 12 to 60 +/- 10 pg/ml), a specific receptor antagonist of LTD4 and partially reduced by IL-1 receptor antagonist (IL-1 ra) (from 160 +/- 12 to 85 +/- 5 pg/ml). These experiments suggest that cysteinyl-leukotrienes, potentially produced in the vascular wall by leukocytes or by transcellular metabolism, may be involved in local IL-1 production.

Analysis of Variance↗

PubMed1995

Synergistic activation of serum amyloid A (SAA) by IL-6 and IL-1 in combination on human Hep 3B hepatoma cell line. Role of PGE2 and IL-1 receptor antagonist.

Serum amyloid A (SAA) protein is a major acute phase reactant in human and many other species. Infections and traumatic inflammation are characterized by a rapid increase of SAA; its concentration in the plasma may augment many-fold. Cytokines such as IL-1 and IL-6 are considered mediators of acute phase protein synthesis. The most accredited mechanism of action of IL-1 in inflammatory diseases is the stimulation of PGE2 release, which is highly dependent on the concentration of IL-1. In this study we found that human Hep 3B hepatoma cells treated with the combination of hrIL-6 (10ng/ml) plus hrIL-1 (1ng/ml) produced an augmentation in steady-state levels of SAA mRNA (87%) compared to hrIL-6 (10ng/ml) plus PGE2 (5 microM), which induced an increase of only 33%, compared to IL-6 alone, while cells treated with hrIL-6 plus PGE2 (0.5 microM) had a similar effect as hrIL-6 did alone. Moreover, the addition of exogenous PGE2 (5 microM) to the cell cultures produced no significant increase in concentration of SAA mRNA compared to the control. In addition, according to the data obtained by the blot analysis we also found, by ELISA method, that hrIL-6 acts in synergism with hrIL-1 on SAA protein secretion in human Hep 3B hepatoma cell cultures after 48 h incubation. In fact, the cell cultures treated with hrIL-6 plus hrIL-1 caused a higher release approximately 1.5-4-fold of SAA protein than the cells treated with IL-6 plus PGE2 5 microM or IL-1 + PGE2 5 microM, respectively. The synergistic effect of hrIL-6 plus hrIL-1 beta was inhibited by hrIL-1 receptor antagonist (hrIL-1ra) 50 micrograms/ml, a protein which specifically binds to the IL-1 receptor and is structurally similar to IL-1 beta but with no IL-1-like activity; while indomethacin (5 microM) was ineffective. These results strongly suggest that the synergism between hrIL-6 plus hrIL-1 on the transcription and the protein release of SAA release is not due to a PGE2-dependent process in human Hep 3B hepatoma cells. This finding highlights a specific biological effect of IL-1 not in relation to PGE2, suggesting a specific mechanism of action for IL-1 in regulating acute phase protein synthesis.

Arachidonic Acid↗

PubMed1995

Monocyte chemotactic protein-1 provokes mast cell aggregation and [3H]5HT release.

Monocyte chemotactic protein-1 (MCP-1) and MCP-3, the most active and representative compounds of the CC chemokine family, are proinflammatory cytokines that attract and activate specific types of leucocytes. We have used highly purified isolated rat peritoneal mast cells (RPMC) cultured for different lengths of time with and without MCP-1 (200, 100, 50 and 25 nM). Our data clearly show that MCP-1 (200 nM) causes a marked release of [3H]serotonin ([3H]5HT and histamine, which reach a peak at 40 min of incubation (56.6 +/- 5.3 and 34.7 +/- 6 above the control, respectively). In dose-response experiments, MCP-1 (200, 100, 50, 25, 12.5, 6.25 and 3.12 nM) provoked a dose-dependent release of [3H]5HT and histamine from RPMC, which was maximum at 200 nM. After preparation of the histidine decarboxylase (HDC) probe, a Northern blot analysis was determined for HDC mRNA. After 4 hr, steady-state levels of HDC mRNA were induced in a dose-dependent manner by MCP-1 (200-25 nM), compared to the controls. However, MCP-1 failed to prime RPMC in [3H]5HT and histamine release when C48/80 (0.05 micrograms/ml) or anti-IgE was used. In contrast, murine interleukin-3 (IL-3) in combination with MCP-1 (200 and 100 nM) provoked a greater release of histamine and [3H]5HT than the compounds alone. Moreover, RPMC treated with MCP-1 (200 nM) showed, under light microscopy (20x), greater clump formation, a phenomenon absent in the controls (untreated cells). The electron microscope studies revealed that treatment with MCP-1 (200 nM) promoted binding of RPMC and clearly demonstrated a communication between the cytoplasms of adjacent mast cells. Our report describes additional biological activities for MCP-1, suggesting for the first time that this human monocyte chemoattractant plays a fundamental role in histamine and serotonin release and cell aggregation in rat peritoneal mast cells.

Animals↗