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PubMed1999

Macrophage inflammatory protein-1alpha and RANTES are present in nasal secretions during ongoing upper respiratory tract infection.

Macrophage inflammatory protein-1alpha (MIP-1alpha) and RANTES (regulated upon activation, normal T-cell expressed and secreted) were measured by enzyme-linked immunosorbent assay (ELISA) from virus-infected respiratory cell culture supernatants and from 100 nasal wash samples obtained from patients aged 8 d to 10 yr. The results of the nasal wash samples were analyzed in relation to the etiology of the viral infection. In vitro, respiratory syncytial virus (RSV) induced the production of MIP-1alpha, while both RSV and adenovirus were associated with the production of RANTES. Both MIP-1alpha and RANTES were detected in nasopharyngeal secretions from pediatric patients with acute upper respiratory tract RSV, adenovirus, influenza, and parainfluenza virus infection (p<0.001 by Fisher's exact test). As both of these chemokines have potent effects on the recruitment and degranulation of eosinophils and basophils, further understanding of their role in upper respiratory tract infections may provide valuable insights into the immunopathogenesis of respiratory viral infections.

Adenoviridae↗
PubMedDate not supplied

Evaluation of granulation peripheral blood basophils in people exposed to industrial contaminants.

The effect of industrial contaminants on the cytomorphometry of basophils was studied. A statistically significant difference in the densification of cytoplasmic granules of basophils was observed in people exposed to pollutants compared to people from less contaminated areas. No differences in cell area, nucleus area, or cytoplasm size were found among the tested groups.

Adult↗
PubMed1970

Cutaneous basophil hypersensitivity. II. A light and electron microscopic description.

Delayed onset erythematous skin reactions elicited in guinea pigs early in the course of sensitization with azobenzenearsonate-protein conjugates or with protein antigens in incomplete Freund's adjuvant or in saline were found to have a characteristic morphology which sets them apart from delayed hypersensitivity and the classic antibody mediated reactions. The principle feature was massive dermal infiltration with basophilic leukocytes. Mononuclear cells of several types including activated and small lymphocytes, monocytes, macrophages, and blast cells were also present. Such reactions have in the past been designated Jones-Mote hypersensitivity, but we prefer the descriptive term cutaneous basophil hypersensitivity (CBH) for the reasons given. Occasional basophils extruded their granules, and individual granules, retaining their characteristic ultrastructure, were commonly seen in the interstitium. However, intercellular junctions between endothelial cells were closed except during cell emigration and there was no morphologic evidence of an histamine-like effect. The majority of basophils, moreover, did not degranulate but underwent nuclear pyknosis and cytoplasmic degeneration and were phagocytosed by macrophages. Phagocytosed basophil granules retained their ultrastructure. Skin tests performed at late intervals after sensitization had a different time course and morphology. Animals sensitized with protein antigens in complete Freund's adjuvant developed delayed hypersensitivity; however, reactions elicited in such animals at early (but not late) intervals after sensitization contained a prominent basophil component. We interpret such reactions to be a mixture of delayed hypersensitivity and cutaneous basophil hypersensitivity. The function of the basophil in CBH and its relation to the mononuclear cells which accompany it are unknown, and various possibilities are discussed. We conclude that cutaneous basophil hypersensitivity is a distinct immunologic and morphologic entity, occurring early in the course of sensitization with protein antigens incorporated in any of several vehicles. The mechanism of the reaction is presently unknown, and a general hypothesis to explain its pathogenesis has been proposed.

Animals↗
PubMed1985

Microscopic findings of delayed reactions elicited by the skin test reagent Leprosin A derived from M. leprae.

Punch biopsies taken 12, 24, 48, and 72 hours after skin testing with Leprosin A have been used to prepare ultrathin sections for the identification and enumeration of infiltration cells. The study was performed on small numbers of both healthy persons and leprosy patients with various forms of the disease living in India. Similar cells were found to infiltrate both positive and negative responses to the skin test reagent, although there were quantitative differences. The most striking findings were the absence of the expected basophils and an infiltration of eosinophils which proceeded to degranulate. This was especially noticeable in a healthy leprosy contact and in patients at the tuberculoid end of the leprosy spectrum, whether or not they produced positive skin reactions to Leprosin A. In patients at the lepromatous end of the spectrum, infiltrates were largely neutrophils.

Antigens, Bacterial↗
PubMed2000

[Allergic risk of aprotinin].

OBJECTIVE: To analyse the risk of anaphylactic reaction with the administration of aprotinin, either by i.v. route or as a biological sealant application and to propose updated guidelines in accordance with current data of the literature. DATA SOURCES: Search in the Medline data base of articles in French, English and German, published since 1960, using following key words: aprotinin, allergy, anaphylaxis. STUDY SELECTION: All categories of articles on this topic have been selected. DATA EXTRACTION: Articles have been analysed for history, incidence and mechanisms of anaphylactic reactions, symptomatology, factors of risk, diagnosis and precautions of use. DATA SYNTHESIS: Aprotinin is widely used for decreasing preoperative bleeding, especially in cardiac and orthopaedic surgery. This heterologue protein can cause anaphylactic reactions in 0.5 to 5.8% of patients, depending of the inclusion criteria. They are mediated by IgG and IgE antibodies. Aprotinin has also a direct, non specific, histaminoliberation effect. The clinical presentation includes various degrees of severity, up to cardiac arrest. Documented factors of risk are a previous parotinin administration, 15 days to 6 months before, and intolerance to beef meat, white of egg, cheese and milk. The immediate biological diagnosis is obtained on assessing the degranulation of basophiles (histamine) and mastocytes (tryptase), as well as the concentration of anti-aprotinin antibodies (RAST IgE), with a test of inhibition. The secondary assessment, six weeks later, includes prick-tests and intradermoreactions if the former are negative. The mean precaution consists to search factors of risk at preanaesthetic assessment. The predictive value of systematic prick-tests has not yet been validated. Anti H1 and anti H2 premedication is inefficient. A test dose can trigger a severe reaction. CONCLUSION: Considering a significant anaphylactic risk, aprotinin administration becomes only licit after a careful evaluation of the benefit-risk ratio.

Anaphylaxis↗
PubMed1990

Characterization of model antigens composed of biotinylated haptens bound to avidin.

Model antigens of defined structure and limited valency have been prepared by binding 2,4-dinitrophenyl (DNP)-biotin haptens of different lengths to the biotin binding sites of avidin. These complexes have been characterized structurally by spectroscopic methods and functionally by testing their ability to crosslink cell-bound anti-DNP immunoglobulin E-receptor complexes to stimulate degranulation of rat basophilic leukemia cells. One of these haptens, 1-DNP-amino-12-biotinamido dodecane, is shown to have only two tight binding sites per avidin molecule, and the resulting bivalent (DNP-biotin)-avidin antigen is found to stimulate substantial degranulation. Another DNP-biotin hapten that is approximately 10 A longer has four tight binding sites per avidin and, when bound to avidin, has greater activity similar to a highly DNP-conjugated multivalent antigen. These and other (DNP-biotin)-avidin complexes described here represent a new group of chemically well-defined antigens that are useful for studying the binding to and functional crosslinking of cell-bound immunoglobulins in immunological responses.

Animals↗
PubMed1993

Immediate and delayed (late-phase) dermal contact sensitivity reactions in guinea pigs. Passive transfer by IgG1 antibodies, initiation by mast cell degranulation, and suppression by soybean proteinase inhibitor.

Specific immediate and delayed (24-hour) local dermal reactivity to oxazolone and dinitrochlorobenzene (DNCB) was passively transferred to naive guinea pigs by the intradermal injection of immune guinea pig serum and its IgG1 fraction. In both actively sensitized and passively sensitized animals, neutrophils were the major cells present in the immediate reaction to the specific contactant. Basophils and mononuclear cells were the major cells present in the delayed reaction to the contactant. This late-phase reaction is, therefore, a cutaneous basophil hypersensitivity (CBH) response. The serum factor that passively transferred this CBH response was stable when heated at 56 degrees C for 1-4 h. Since transfer factor, cutaneous basophil hypersensitivity factor and guinea pig IgE are heat-sensitive, these factors probably made little or no contribution to this response. Because proteinase inhibitors are known to inhibit mast-cell degranulation in vitro, we tested the effect of soybean proteinase inhibitor in vivo. This inhibitor suppressed both the immediate and the delayed skin reactivities mediated by intradermal contactant-specific IgG1. These studies support the following concept: IgG1 in guinea pigs (and IgE in human beings) sensitize mast cells to specific antigens. Such antigens degranulate mast cells, releasing histamine and other mediators for the immediate hypersensitivity reaction, and cause mast cells to produce cytokines that recruit basophils, eosinophils and mononuclear cells for the late-phase (CBH) reaction.

Animals↗
PubMed1991

Respiratory viruses induce production of histamine-releasing factor by mononuclear leukocytes: a possible role in the mechanism of virus-induced asthma.

Histamine-releasing factor (HRF) is a cytokine produced by mononuclear leukocytes when stimulated with antigens or mitogens. HRF is capable of inducing degranulation of basophils and release of histamine. To determine if respiratory viruses can induce HRF production, mononuclear leukocytes from healthy adult donors were exposed to influenza or respiratory syncytial virus in vitro. HRF activity was tested by culturing the supernatants with fresh peripheral blood leukocytes and measuring the percentage of histamine released. Significant enhancement in histamine release was found in both virus groups compared with that of media controls. Thus, mononuclear leukocytes from normal individuals produce HRF in response to exposure to respiratory viruses, suggesting that this cytokine, which causes basophil degranulation, may play a role in the mechanism of virus-induced bronchospasm.

Adult↗
PubMed1976

Morphology of delayed-type hypersensitivity reactions in man. II. Ultrastructural alterations affecting the microvasculature and the tissue mast cells.

Profound alterations in the dermal microvasculature and the closely related fixed tissue mast cells were observed in allergic contact dermatitis reactions to dinitrochlorobenzene and urushiol in man. The vascular changes were of two types. The superficial capillary venule, a distinct anatomical and functional vessel system in the dermal papillae, developed interendothelial cell gaps, maximal at 3 days after skin test, which very likely were responsible for locally increased vascular permeability and consequent dermal edema. The products of degranulating tissue mast cells and infiltrating basophils may have been partly responsible for these changes. By contrast, vessels of the superficial venular plexus, oriented parallel to the cutaneous surface at the junction of the papillary and reticular dermis, were the site of diapedesis and perivascular cuffing by lymphocytes and other inflammatory cells. The superficial venular plexus vessels exhibited striking endothelial cell and pericyte hypertrophy, occasional necrosis of endothelial cells, endothelial cell mitoses, and an extensive and progressive laying down of new and abnormally disposed basal lamina. These changes, somewhat slower to develop than those affecting the superficial capillary venule, were present in all biopsies taken at 3 days or later and were accompanied by mast cell mitoses and the appearance of immature dermal mast cells. The basal lamina-alterations persisted and evolved for at least several weeks. The mechanisms initiating these vessel and mast cell changes have not been identified, but circumstantial evidence suggests that lymphocytes or their products or both may have been responsible.

Administration, Topical↗
PubMed2004

Inhibition of allergen-specific IgE reactivity by a human Ig Fcgamma-Fcepsilon bifunctional fusion protein.

BACKGROUND: Coaggregating FcepsilonRI with FcgammaRII receptors holds great potential for treatment of IgE-mediated disease by inhibiting FcepsilonRI signaling. We have previously shown that an Fcgamma-Fcepsilon fusion protein, human IgG-IgE Fc fusion protein (GE2), could inhibit FcepsilonRI-mediated mediator releases in vitro and in vivo. OBJECTIVE: We sought to test whether GE2 was capable of blocking mediator release from FcepsilonRI cells sensitized with IgE in vivo or in vitro before exposure to GE2, a critical feature for GE2 to be clinically applicable. METHODS: GE2 was tested for its ability to inhibit Fel d 1-induced mediator release from human blood basophils from subjects with cat allergy, human lung-derived mast cells, human FcepsilonRIalpha transgenic mice sensitized with human cat allergic serum, and rhesus monkeys naturally allergic to the dust mite Dermatophagoides farinae. RESULTS: Basophils from subjects with cat allergy and lung mast cells degranulate when challenged with Fel d 1 and anti-IgE, respectively. GE2 itself did not induce mediator release but strongly blocked this Fel d 1- and anti-IgE-driven mediator release. GE2 was able to block Fel d 1-driven passive cutaneous anaphylaxis at skin sites sensitized with human serum from subjects with cat allergy in human FcepsilonRIalpha transgenic mice, but by itself, GE2 did not induce a passive cutaneous anaphylaxis reaction. Finally, GE2 markedly inhibited skin test reactivity to D farinae in monkeys naturally allergic to this allergen, with complete inhibition being observed at 125 ng. CONCLUSION: GE2 is able to successfully compete for FcepsilonRs and FcgammaRs on cells presensitized in vitro and in vivo and lead to inhibition of IgE-mediated reactivity through coaggregation of FcepsilonRI with FcgammaRII.

Allergens↗
PubMed1987

[In vitro exploratory methods in immuno-allergology].

The authors discuss different in vitro tests that provide evidence for: involvement of atopy in clinical symptoms (eosinophilia, total IgE titre, histaminemia); the identification of the responsible allergen (specific IgE, basophil degranulation, and release of histamine); following the course of hyposensitization treatment (specific IgG).

Allergens↗
PubMed1990

Mapping the site of interaction between murine IgE and its high affinity receptor with chimeric Ig.

We have investigated the interaction of mouse (m) IgE with its Fc epsilon RI on rat basophilic leukemia cells using a set of chimeric Ig that were constructed by exchanging homologous H chain C domains between human (hu) IgG1 and mIgE. Binding affinities were examined with equilibrium and kinetic measurements, and we found that epsilon/C gamma 3 (mIgE with C epsilon 4 replaced by C gamma 3) was indistinguishable from mIgE. The huIgG1 and the other chimeric Ig, which did not contain both C epsilon 2 and C epsilon 3, did not bind detectably to rat basophilic leukemia cells (Ka less than 10(6) M-1). The ability of these chimeric Ig to stimulate a cellular response (degranulation) in the presence of multivalent Ag was also tested. The epsilon/C gamma 3 was indistinguishable from mIgE in eliciting a high level of degranulation, whereas the other chimeric Ig stimulated no response even when they were preaggregated to enhance their binding avidity. These results demonstrate that C epsilon 4 may be replaced by C gamma 3 without affecting the binding and cell activating properties of mIgE. The lack of binding by the other chimeric Ig indicates that both C epsilon 2 and C epsilon 3 are necessary for the binding interaction.

Animals↗
PubMed1987

Membrane-bound IgE receptor complexes fused with rat basophilic leukemia cells mediate degranulation.

The high affinity receptor for IgE on rat basophilic leukemia (RBL) cells mediates antigen-triggered cellular degranulation. Polyethylene glycol-induced membrane fusion methods were used to introduce exogenous IgE receptors into living RBL cells, and these were tested for normal activities. In cell-cell fusion experiments, RBL cells with fluorescein-labeled rat IgE bound to receptors and containing [5-1,2-3H(N)]hydroxytryptamine binoxalate ([3H]5HT) in their secretory granules were fused to cells with receptors occupied by rhodamine-labeled anti-dinitrophenyl mouse IgE. The fused cells showed a uniform surface distribution of both types of IgE, which could be patched independently by anti-IgE or dinitrophenylated bovine gamma globulin (DNP16BGG). [3H]5HT release could be triggered specifically by DNP16BGG. In vesicle-cell fusion experiments, plasma membrane vesicles, with receptors occupied by fluorescein- and 125I-labeled anti-DNP mouse IgE, were fused to RBL cells containing [3H]5HT. The cells showed substantial associated fluorescein fluorescence and 125I counts, and [3H]5HT release could be triggered specifically by DNP16BGG. These experiments indicate that IgE receptors can be dissociated from their natural cellular interactions and retain the ability to reassociate with another cell's components to deliver the transmembrane signal for degranulation.

Animals↗
PubMed1985

The human adenoidal mast cell. Susceptibility to different secretagogues and secretion inhibitors.

Mast cells from adenoid tissues of man do not form a homogeneous population but differ in size and ultrastructure. They degranulate on stimulation with specific antigen, ionophore A 23187, Concanavalin A and, under certain conditions, antihuman IgE or acetylcholine. Compound 48/80, dextran, purified C3a or C5a are ineffective. Adenosine exerts either an enhancing or inhibiting effect on the stimulated histamine release, depending on the actual conditions of the mast cells. The study of a range of known mast cell degranulation inhibitors revealed important differences between human adenoidal mast cells and human basophils or animal mast cell systems. The efficacies of the drugs or drug combinations so far tested correspond well with the established therapeutic effects in man.

Adenoids↗
PubMed2002

Monitoring of basophil activation using CD63 and CCR3 in allergy to muscle relaxant drugs.

Allergic or pseudoallergic reactions that occur during anesthesia have been increasing for the last few years. To date, the diagnosis of allergy to muscle relaxants remains difficult. In this respect, we developed a flow cytometric method for the study of drug-induced basophil degranulation using CD63 and CCR3. Fifty patients who developed clinical features evocative of allergic reactions immediately after induction of anesthesia were included and classified into two groups. Group 1 (n = 39) comprised true allergic patients, who developed typical signs of shock associated to positive skin testing. Group 2 (n = 11) consisted of patients whose clinical history was not typical and skin testing was negative or nonconclusive. Seventeen control subjects were also studied in this report. We compared data from flow cytometry to skin tests, specific IgE, and histamine release results. Flow cytometry showed a sensitivity of 54%, while that of specific IgE was similar, at 62%. Interestingly, when considering the sensitivity of IgE + CD63 for diagnosis, we reached a sensitivity value of 80%. Of 15 negative results for specific IgE, we found 7 positive CD63 tests, while histamine release gave positive results in only 2 cases. Furthermore, the CD63 protocol showed good specificity (100%). We conclude that our flow cytometry protocol is a promising tool in allergy diagnosis since it is specific and complementary to specific IgE detection.

Anesthesia, General↗