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PubMed2005

Negative control of basophil expansion by IRF-2 critical for the regulation of Th1/Th2 balance.

Although basophils are known to produce interleukin 4 (IL-4), the roles of these cells have been documented only in mice infected with parasites or in the effector phase of allergic inflammations. Here we show that naive mice lacking the transcription factor, interferon regulatory factor 2 (IRF-2), exhibited signal transducer and activator of transcription 6 (Stat6)-independent expansion of basophils in the periphery. IRF-2 appeared to act autonomously in the cells to negatively regulate the expansion of, but not cytokine production by, basophils. Spontaneous Th2 polarization of CD4+ T cells was observed in these mice and the genetic reduction of basophil numbers by mutating the Kit gene abolished such a polarization in vivo. We also found that both basophils and IL-4 derived from them were indeed essential for Th2 development under neutral conditions in vitro. Furthermore, neutralization of IL-3 abolished IL-4 production by basophils during Th1/Th2 differentiation cultures and subsequent Th2 development. These results indicated that basophils acted as a cellular converter to turn the neutral IL-3 into the Th2-inducing IL-4 during the initiation of Th1/Th2 differentiation. Thus, the negative regulatory role of IRF-2 on the basophil population size is critically important for preventing excess Th2 polarization and the Th1/Th2 balance in naive animals.

Animals↗
PubMed2001

Detection of tryptase in cytoplasmic granules of basophils in patients with chronic myeloid leukemia and other myeloid neoplasms.

Tryptases are serine proteases primarily expressed in mast cells. Normal blood basophils express only trace amounts of the enzyme. However, recent immunohistochemical studies have raised the possibility that neoplastic basophils express significant amounts of tryptase. In this study, tryptase expression was analyzed in normal and neoplastic basophils by immunoelectron microscopy using antitryptase monoclonal antibody G3. Basophils were obtained from patients with chronic myeloid leukemia (CML), idiopathic myelofibrosis (IMF), and myelodysplastic syndrome (MDS), and from healthy donors. Tryptase-immunoreactive material was detected in cytoplasmic granules of basophils in CML, IMF, and MDS. By contrast, normal basophils did not contain significant amounts of tryptase by immunoelectron microscopy. As assessed by reverse transcription-polymerase chain reaction, neoplastic basophils contained messenger RNA (mRNA) for alpha-tryptase, but no beta-tryptase mRNA. In summary, these data provide evidence that neoplastic basophils in CML, IMF, and MDS can express detectable amounts of tryptase. Therefore, tryptase should not be regarded as specific for mast cells when neoplastic myeloid cells are analyzed.

Basophils↗
PubMed1999

Age-dependent increase of IgE-binding and FcepsilonRI expression on circulating basophils in children.

Peripheral blood basophils are sparse in the circulation, but they express high-affinity receptors for IgE (FCepsilonRI) and bind IgE efficiently. The present study was performed to elucidate the role of IgE bound on the basophil surface in the development of allergic responses during infancy and early childhood. IgE-binding and FcepsilonRI expression on basophils were evaluated by two-color flow cytometry. Basophil-bound IgE increased rapidly and reached adult levels during infancy in atopic patients, while it gradually increased with advancing age in parallel with serum IgE in normal controls. IgE-binding and FcepsilonRI expression in atopic children were higher than in normal controls among various age groups. They correlated with serum IgE levels but reached a plateau when serum IgE exceeded 300 ng/mL. A low, but significant level of FcepsilonRI expression was observed on cord blood basophils, although IgE-binding was usually undetectable. Incubation of cord blood with IgE rapidly saturated the preexisting IgE receptors and basophil-bound IgE levels increased. When neonatal basophils were cultured for 48 h with IgE, FcepsilonRI expression was upregulated dose-dependently and IgE-binding increased further. The up-regulation of FcepsilonRI was completely inhibited by cycloheximide, indicating that it was dependent on de novo protein synthesis. These results suggest that IgE-binding on basophils serves as a sensitive indicator of allergic sensitization, and that IgE functions as a positive regulator of FcepsilonRI expression in vivo.

Adolescent↗
PubMed2004

Basophils infiltrate human gastric mucosa at sites of Helicobacter pylori infection, and exhibit chemotaxis in response to H. pylori-derived peptide Hp(2-20).

Basophils, which are normally confined to the circulation, can migrate to sites of allergic inflammation. Using the specific mAb, BB1, we detected basophil infiltration of the gastric mucosa of Helicobacter pylori-infected patients affected by moderate and severe gastritis. Basophils were not found in H. pylori-free individuals or in subjects with mild gastritis. The H. pylori-derived peptide, Hp(2-20), was a potent basophil chemoattractant in vitro, whereas the control peptide, Hp1, was ineffective. Basophils from peripheral blood of healthy volunteers expressed mRNA for the formyl peptide receptors, N-formyl-peptide receptor (FPR), FPR-like (FPRL)1, and FPRL2. Preincubation of basophils with FMLP or Hp(2-20) caused complete desensitization to a subsequent challenge with homologous stimulus. Incubation of basophils with a low concentration of FMLP, which binds with high affinity to FPR, but not to FPRL1 or FPRL2, did not affect the chemotactic response to Hp(2-20). In contrast, a high concentration of FMLP, which binds to FPRL1 and FPRL2, reduced the chemotactic response to Hp(2-20). The FPR antagonist, cyclosporin H, prevented chemotaxis induced by FMLP, but not by Hp(2-20). Hp(2-20) could be responsible, at least in part, for basophil infiltration of the gastric mucosa of H. pylori-infected patients presumably through the interaction with FPRL1 and FPRL2.

Bacterial Proteins↗
PubMed1999

Down-regulation of human basophil IgE and FC epsilon RI alpha surface densities and mediator release by anti-IgE-infusions is reversible in vitro and in vivo.

Previously, infusions of an anti-IgE mAb (rhumAb-E25) in subjects decreased serum IgE levels, basophil IgE and FcepsilonRIalpha surface density, and polyclonal anti-IgE and Ag-induced basophil histamine release responses. We hypothesized that these effects would be reversed in vivo by discontinuation of infusions and in vitro by exposing basophils to IgE. Subjects received rhumAb-E25 biweekly for 46 wk. Blood samples taken 0-52 wk after rhumAb-E25 were analyzed for serum IgE and basophil expression of IgE, FcepsilonRIalpha, and CD32. Basophil numbers were unaffected by infusions. Eight weeks after infusions, free IgE levels rose in vivo but did not reach baseline. Basophil IgE and FcepsilonRIalpha rose in parallel with free IgE while CD32 was stable. FcepsilonRI densities, measured by acid elution, returned to 80% of baseline, whereas histamine release responses returned to baseline. Basophils cultured with or without IgE or IgG were analyzed for expression of IgE, FcepsilonRIalpha, and CD32. By 7 days with IgE, expression of IgE and FcepsilonRIalpha rose significantly, whereas cultures without IgE declined. IgE culture did not effect CD32. IgG culture did not effect expression of any marker. The present results strongly suggest that free IgE levels regulate FcepsilonRIalpha expression on basophils.

Adult↗
PubMedDate not supplied

Detection of activated basophils using flow cytometry for diagnosis in atopic patients.

BACKGROUND: human basophils release mediators of allergy after cross-linking of IgE receptors by allergens. Specific activation of basophils is detectable through flow cytometry (FCM) using an anti-CD63 fluorescein-conjugated monoclonal antibody. OBJECTIVES: this study evaluate the detection of activated basophils by FCM in routine diagnosis of atopic diseases as regard to skin prick tests and specific immunoglobulin E antibodies. METHODS AND RESULTS: whole blood from twenty patients suspected of atopy was preincubated with interleukin-3 (IL-3), then incubated with specific allergens. After staining using anti-CD63 antibodies, activated basophils were detected through FCM. IL-3-preincubation increases the spontaneous expression of CD63 even at low concentrations (0.1 ng/ml) on the basophils of 2 patients out of 20. The sensitivity and specificity of FCM were respectively 0.56 +/- 0.17 (m +/- SD) and 1.0 +/- 0.0 for the detection of dust mite-activated basophils without IL-3 preincubation, and 0.73 +/- 0.13 and 1.0 +/- 0.0 for the detention of grass pollen-activated basophils. IL-3-preincubation increased the sensitivity in a dose-dependent manner but decreased the specificity fo FCM for detecting dust mite hypersensitivity. CONCLUSION: this method allow for rapid and easy detection of activated basophils from whole blood, and could be of interest for detecting allergies to non-conventional allergens such as pharmaceutical drugs.

Allergens↗
PubMed1976

Cutaneous basophil hypersensitivity uncovered in the cell transfer of classical tuberculin hypersensitivity.

Cellular transfer of cutaneous basophil hypersensitivity (CBH) was studied. Guinea pigs immunized for CBH with incomplete Freund's adjuvant (IFA) provided cells which could transfer delayed and basophil-rich reactions in skin tests of recipients. Guinea pigs immunized with complete classical tuberculin-type delayed hypersensitivity reactions (DH), which are characteristically devoid of basophils. However, recipients of cells from donors with DH, surprisingly, were found to have delayed skin reactions containing large basophil infiltrates which were lacking in the donors. Thus, recipients of classical cell transfers of tuberculin-type DH had delayed reactions which resembled CBH. Control experiments verified that the cell transfer of CBH from donors with DH was due to passive transfer with live cells and not transfer of contaminating humoral factors or active sensitization of recipients. It was concluded that cutaneous basophil responses were suppressed in CFA-immunized donors and expressed in cell transfer recipients. Cells from donors immunized with CFA were enriched for nonadherent and nonimmunoglobulin-bearing lymphocytes by passage through nylon wool columns, and these cells transferred conjugate specific CBH reactions. It was concluded that cells mediating these transfers were probably T cells. The finding of basophils in cell transfers of DH and a variety of other findings suggesting complex regulation of basophil numbers in tissue lead to the conclusion that the term CBH be used to simply describe a basophil-containing skin reaction.

Animals↗
PubMed1992

Effects of in vivo administration of interleukin-2 (IL-2) and IL-4, alone and in combination, on ex vivo human basophil histamine release.

Human basophils possess receptors for interleukin-2 (IL-2) and IL-4. The effect of 3 days of intravenous administration of IL-2 and/or IL-4 on basophil histamine release was examined in three groups of patients receiving IL-2, IL-4, or the combination of agents as part of a protocol to treat malignant melanoma or renal cell carcinoma. Because all patients received ranitidine for control of side effects, a control group of patients receiving ranitidine for Zollinger-Ellison's syndrome was also studied. IL-4 significantly inhibited IgE-mediated histamine release, while there was a trend for enhancement of IgE-mediated histamine release by IL-2. Administration of the combination of IL-2 and IL-4 did not alter IgE-mediated basophil histamine release. Both IL-2 and IL-4, alone and in combination, enhanced basophil histamine release induced by histamine releasing factors in human nasal washings. The effect of IL-2 alone was significantly greater than that of IL-4 alone or the combination of IL-2 plus IL-4. Taken together, the data suggest that when coadministered, IL-4 may inhibit the effects of IL-2 on basophils. Neither cytokine exerted any effect on basophil histamine release induced by the calcium ionophore A23187, nor did ranitidine cause any effects on histamine release induced by any of the stimulants. Thus, human basophil reactivity can be affected by IL-2 and by IL-4. The role that these two cytokines play in basophil function in vivo is likely to be complex.

Adult↗
PubMed1992

Preliminary identification and role of phosphodiesterase isozymes in human basophils.

We attempted to identify and establish the role of cyclic nucleotide phosphodiesterase (PDE) isozymes in human basophils by using standard biochemical techniques as well as describing the effects of isozyme-selective and nonselective inhibitors of PDE. The nonselective PDE inhibitors, theophylline and 3-isobutyl-1-methylxanthine, inhibited anti-IgE-induced release of histamine and leukotriene C4 (LTC4) from basophils. This inhibition was accompanied by elevations in cAMP levels. Rolipram, an inhibitor of the low Km cAMP-specific PDE (PDE IV), inhibited the release of both histamine and LTC4 from activated basophils and increased cAMP levels in these cells. In contrast, mediator release from basophils was not inhibited by either siguazodan or SK&F 95654, inhibitors of the cGMP-inhibited PDE (PDE III) or zaprinast, an inhibitor of the cGMP-specific PDE (PDE V). SK&F 95654 failed to elevate basophil cAMP in these experiments whereas zaprinast induced significant increases in cAMP content. The inhibitory effect of rolipram on mediator release was potentiated by siguazodan or SK&F 95654, but not by zaprinast. SK&F 95654 also enhanced the ability of rolipram to increase cAMP content. Forskolin, a direct activator of adenylate cyclase, inhibited IgE-dependent release of mediators from basophils and increased cAMP levels in these cells. These effects were enhanced by rolipram, but not by SK&F 95654 or zaprinast. The cell permeant analog of cAMP, dibutyryl cAMP, inhibited mediator release from these cells, a property not shared by either dibutyryl-cGMP or sodium nitroprusside, an activator of soluble guanylate cyclase. The presence of both PDE III and PDE IV was confirmed by partially purifying and characterizing PDE activity in broken cell preparations. Overall, these data lend support to the hypothesis that cAMP inhibits mediator release from basophils and suggest that the major PDE isozyme responsible for regulating cyclic AMP content in these cells is PDE IV, with a minor contribution from PDE III. However, the finding that zaprinast caused increases in cAMP without inhibiting mediator release indicates that cAMP accumulation is not invariably linked to an inhibition of basophil activation.

Basophils↗
PubMedDate not supplied

[A case of de novo acute basophilic leukaemia: diagnostic criteria and review of the literature].

We report a case of a de novo acute basophilic leukaemia, revealed by an infectious pneumopathy in a 73 year old man. The full blood count revealed an hyperleucocytosis associated with an unregenerative normocytic normochrom anaemia and a thrombocytopenia. The blood and bone marrow smears showed a mixture of undifferentiated blast cells and basophiloblasts (high nucleo-cytoplasmic ratio, coarse basophilic cytoplasmic granules), along with basophilic precursors and basophilic polymorphonuclears. All the blasts were MPO negative but positive for the toluidine blue metachromatic coloration, which is considered as consistent with basophilic lineage. Immunophenotypic studies showed myeloid blasts, without maturity marker, CD 117 negative and CD203 cytoplasmic positive, the latter known to be highly representative of the basophilic lineage. This very clear-cut phenotype, associated with the morphology of cells, were arguments to ascertain the basophilic lineage of the blasts without the need of electron microscopic study. Cytogenetic and RNA analysis revealed the presence of a Philadelphia chromosome and of a BCR-ABL transcript with the unusual junction e6a2. Thus, imatinib was added to the conventional chimiotherapy and the patient is currently in complete remission. This clinical prompted allows us to review the literature on acute basophilic leukaemia and to state on the different diagnostic criteria of this rare disorder.

Aged↗
PubMed1990

Ultrastructure of human basophil leukocytes studied after spray freezing and freeze-substitution.

Normal human blood cells were prepared for transmission electron microscopy by spray freezing, freeze-substitution and embedment in Araldite. Spray freezing was found to damage many cells. Nevertheless, the method developed preserved some leukocytes well and spray frozen, freeze-substituted human basophils showed interesting differences from conventionally prepared cells. Surface vesicles and tubulovesicular structures, extragranular myelin figures, and membranous projections on putative thin membrane-bounded granules were all absent. Preservation of the basophilic granules was clearly improved and their membranes were usually intact. The bulk content of these granules did not look particulate, but showed a very fine texture. Intragranular myelin figure material was well preserved and often enclosed striking lucent areas. Charcot-Leyden crystals were clearly seen in basophils from some donors, always in well preserved granules. A fourth type of material, not seen in conventionally prepared human basophils, was also often observed in the granules. Large lucent vacuoles could be regularly distinguished from basophilic granules. The granules with partly concave outlines, seen in conventionally prepared human basophils to be associated with ill-defined lucent areas and irregularity or projections of the membrane, were absent. In freeze-substituted cells, images suggesting fusion of basophilic granules with each other were seen quite frequently. It is concluded that, while the techniques needed to be improved, rapid freezing and freeze-substitution afford a better understanding of the ultrastructure of human basophil leukocytes.

Adult↗
PubMed1987

Reciprocal regulation of human basophil and eosinophil differentiation by separate T-cell-derived factors.

Basophil and eosinophil progenitors are present in human hemopoietic tissues, including cord blood. In the present studies, cord blood cultures demonstrating differentiation of basophils or eosinophils have been maintained for prolonged periods in the presence of conditioned medium from a human T-cell leukemia line (Mo-CM). Peak basophil counts and histamine levels were followed almost invariably by a second peak of eosinophils in vitro. Morphologic examination revealed the consistent presence of cells with mixed basophil-eosinophil granulation. Both basophil and eosinophil growth-stimulating activities were found in Mo-CM, were heat stable and nondialyzable, and could be partially separated from each other by a multistep procedure that included ion-exchange chromatography on DEAE-cellulose. Mixing experiments using separated basophil- and eosinophil-stimulating activities revealed that suppression of basophil growth was accompanied by reciprocal enhancement of eosinophil growth, a finding that could be confirmed on analysis of morphology of single colonies from cord blood progenitors in methylcellulose. These studies point to the existence of regulatory growth factors in Mo-CM that stimulate and/or inhibit the growth and differentiation of human basophils and eosinophils from a common, committed progenitor cell.

Basophils↗
PubMed1989

Histamine release from basophils in cystic fibrosis.

We determined the histamine release from basophils in patients suffering from cystic fibrosis (CF) (median 17.2 years of age) and compared the data with an age-matched group of healthy donors. No significant differences in the basophil counts were determined between the CF and control groups. However, the absolute histamine content per basophil was elevated in the CF group (2.6 +/- 0.4 pg/basophil versus 1.4 +/- 0.2, mean +/- s.e.m., n = 15/10, P less than 0.004). Stimulation of basophils with the Ca ionophore (7.5 microM) and anti-IgE (10(-2) of a stock preparation) leads to a significantly higher release of histamine per basophil in CF patients as compared to healthy donors (Ca ionophore: 1.6 +/- 0.2 versus 0.9 +/- 0.2, mean +/- s.e.m., P less than 0.008; anti-IgE: 0.45 +/- 0.007 versus 0.28 +/- 0.04, P less than 0.02). These data indicate that basophils in CF may have a greater potential to release mediators although their releasability, expressed as the percentage of histamine release of the total histamine content, does not differ significantly compared to the healthy donors (62.1 +/- 8.3% versus 60.2 +/- 13%, mean +/- s.e.m.). Within the 14-day period of intravenous antibiotic treatment of the pulmonary infection (in 14 out of 15 cases P. aeruginosa was isolated from sputa samples) histamine release per basophil and total histamine content decreased to normal levels (day 1 2.6 +/- 0.3 versus 1.8 +/- 0.3, P less than 0.05). This decline was accompanied by an improvement of the clinical condition of the patient and reduction of P. aeruginosa isolates in sputa (n = 8). In contrast, in three patients with sustained P. aeruginosa colonization of the upper airways and impaired lung function histamine levels remained elevated. Our data demonstrate that the histamine content of basophils, as well as the release of histamine, is increased in patients with cystic fibrosis and correlates with the clinical signs of the chronic infection.

Adolescent↗
PubMed1987

Human blood basophils display a unique phenotype including activation linked membrane structures.

To evaluate the membrane marker profile of human basophils a panel of well-established monoclonal antibodies (MoAbs, n = 60) was used for a combined toluidine/immunofluorescence staining procedure. Myeloid-associated MoAbs (particularly MoAbs against the LFA-1 family (CD11, CDw18), MoAbs directed against lactosylceramide (CDw17), anti-glycoprotein (gp) 150 MoAbs MCS 2 and MY 7 (CDw13), anti-gp 67 MoAb MY 9, anti Fc gamma-receptor (mol wt 40 kd) MoAb CIKM5, anti-CR 1 MoAb E 11, and the antiglycolipid MoAb VIM-2) were reactive with basophils, indicating a close relationship to other mature myeloid cells. Under normal conditions, basophils surprisingly express at least three activation-linked structures not detectable on mature neutrophils, ie, the p45 structure defined by MoAbs OKT-10 and VIP-2b, the p24 structure identified by the CD9 MoAb BA-2, and the receptor for interleukin 2 (IL 2) recognized by three different MoAbs (anti-TAC, IL2RI, anti-IL 2). Moreover, under short-term culture conditions basophils both in mononuclear cell (MNC) suspension and as purified fractions display the HLA-DR and T4 antigens. The neutrophilic/eosinophilic structure 3-fucosyl-N-acetyllactosamine is expressed on basophils only after neuraminidase treatment. Basophils were not stained at all by CD 16 MoAbs directed against the Fc gamma-receptor (mol wt 50 to 70 kd) of neutrophils, by the MoAb 63D3 (CDw12) recognizing the monocyte/granulocyte-associated p 200 antigen, and by the CDw 14 antibodies (VIM-13, Mo 2) defining the monocyte-specific structure p 55. Enriched basophils freshly obtained from chronic granulocytic leukemia (CGL) patients yielded identical results in FACS analyses. In summary, these data indicate that basophils generate a unique combination of surface determinants and possibly represent an activated cell population.

Antibodies, Monoclonal↗
PubMed1982

A rapid simple method of basophil purification by density centrifugation on Percoll.

This study describes simple and relatively rapid methods of purifying basophils from human peripheral blood. Our initial studies defined the densities of basophils in several donors and helped develop strategies for selectively concentrating basophils by isopyknic centrifugation over Percoll. We layered anticoagulated blood over Percoll of appropriate density, centrifuged these for 10 min, and collected the cells held in Percoll separately from the overlying band of mononuclear cells. Most of the basophils were distributed between densities of 1.072 and 1.078 g/ml, with a peak at approximately 1.074 to 1.076 g/ml. Basophil purity of 24.4 +/- 4% (range 5.6 to 50%) was achieved in a Percoll gradient of 1.076 g/ml due to both the increased numbers of basophils and the low numbers of mononuclear cells at this gradient. The cells isolated by this method are viable, appear morphologically normal, and release histamine to various stimuli in a normal manner. A second centrifugation of the cells obtained from this density over appropriate discontinuous gradients of Percoll leads to further enhancement of basophil purity. The main limitation of this technique appears to be the relatively low yield (percent of recovery) of the basophil (less than or equal to 20% for the two-step procedures).

Basophils↗
PubMed1983

[Test of human basophil degranulation. The interpretation and analysis of variability factors in the absence of antigen].

The human basophil degranulation test (TDBH) is performed using a concentrated cell suspension enriched for polymorphonuclear basophils. This preparation is placed in wells on a glass slide with an allergen solution of decreasing concentration. After incubation the cells are fixed in the wells and stained with toluidine blue. Preparations containing fewer metachromatic basophils than in control preparation of the same cell suspension without antigen contain degranulated basophils and in this way a degranulation index can be calculated. By considering the variability in the number of basophils between duplicate control wells from the same cell suspension, it can be shown that the test can be considered to be positive only if the number of degranulated basophils equals or exceeds 50% of the total number of basophils. This variance can be attributed to the subjectivity of the reader, and to differences in the differential cell counts from well to well. On the other hand, the presence of atopic allergy had no effect on the basophil counts.

Adolescent↗
PubMed1994

Monocyte chemotactic protein-2, monocyte chemotactic protein-3, and fibroblast-induced cytokine. Three new chemokines induce chemotaxis and activation of basophils.

Cytokine-dependent mediator release from basophils and mast cells may play an important role in the pathogenesis of allergic and inflammatory conditions. Many C-C chemokines have been found to activate basophils and mast cells. We investigated the effect of three newly identified C-C chemokines, monocyte chemotactic protein-2 and -3 (MCP-2, MCP-3) and fibroblast-induced cytokine (FIC) on basophils and mast cells. We found that all three cytokines induced histamine secretion from basophils in a dose-dependent manner. The secretion of histamine was a Ca(2+)-dependent process. MCP-3 was the most potent activator of basophils. MCP-3 and FIC activated basophils from all study subjects, whereas the histamine release by MCP-2 was donor-dependent. The histamine-releasing activity of MCP-2, MCP-3, and FIC was compared with that of MCP-1, RANTES, and macrophage inflammatory protein-1 alpha using basophils from 10 donors. MCP-1 was the most potent among all the C-C chemokines. However, MCP-3 was nearly as potent. MCP-2, MCP-3, and FIC induced significant chemotaxis of basophils. None of the cytokines activated mouse peritoneal mast cells. The synthesis of mRNA for MCP-3 was investigated by reverse-transcription PCR using allergen-stimulated PBMC and bronchoalveolar lavage cells. Both MNC and bronchoalveolar lavage cells expressed mRNA for MCP-3. The results of this study indicate that MCP-2, MCP-3, and FIC are novel histamine-releasing factors.

Allergens↗
PubMed1994

Interleukin-8 and RANTES induce the adhesion of the human basophilic cell line KU-812 to human endothelial cell monolayers.

Basophils are implicated in the pathogenesis of the late-phase allergic reaction, but the mechanisms by which circulating basophils adhere to vascular endothelium and migrate to lesional sites remain unclear. In order to assess the biological similarity of the basophilic cell line KU-812 to normal human basophils, we have compared the adhesion response of this cell line and normal basophils, following challenge with interleukin-8 (IL-8) and RANTES. We demonstrate here that IL-8 and RANTES are able to stimulate the adherence of the basophilic cell line, KU-812, to cytokine-activated human umbilical vein endothelium (HUVEC). The chemokine-induced increase in adhesion was dose-related and was maximal after prior priming with IL-5. The stimulation of adhesion was partially inhibited by co-incubation with anti-CD18 and anti-CD11c antibodies and antibodies to the beta 1-integrins. In comparison, the chemokine-induced adhesion of normal human basophils was only inhibited by the beta 2-integrins. These chemokines were also able to induce the migration of KU-812 in a dose-dependent manner, but only after prior treatment with phorbol myristate acetate (PMA) or IL-5. In all cases tested, IL-8 was more potent and efficacious than RANTES. We conclude from these studies that these members of the chemokine superfamily may play an important role in the recruitment of reactive leukocytes in allergic inflammation, by stimulating their adhesion and subsequent migration from the vasculature into the inflammatory sites. However, it is apparent that KU-812 is not an adequate substitute for normal human basophils in order to investigate chemokine biology.

Base Sequence↗