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Biomedical subjects

A B Kay

Publications and source records attributed to A B Kay.

At least 181 records · Page 10Linked to original sources
PubMed1992

The effect of a single oral dose of prednisolone or cetirizine on inflammatory cells infiltrating allergen-induced cutaneous late-phase reactions in atopic subjects.

The effect of a single dose of prednisolone (20 mg) or cetirizine (10 mg) on the immunohistology of the cutaneous late-phase reaction was determined in a double-blind, placebo-controlled, cross-over study in 12 atopic allergic individuals. The subjects were challenged with intradermal allergen (30 BU) 2 hr after ingestion of the drugs or placebo. The magnitude of the cutaneous reactions were determined at 15 min, 6 and 24 hr, and skin biopsies performed at 24 hr. Cetirizine produced a 50% average inhibition of the immediate weal and flare response (P = 0.001) and a 27% average inhibition of the 6 hr late-phase induration (NS). Prednisolone reduced the immediate (27%, P = 0.03) and significantly inhibited the late-phase reaction (53%, P = 0.02). Prednisolone significantly inhibited infiltration of CD45+ (total leucocytes), neutrophil elastase+, EG2+ (activated eosinophils) and CD25+ (IL-2R) cells (P = 0.017, 0.005, 0.005 and 0.032 respectively). CD3, CD4, CD8 and HLA-DR expression was also inhibited but this was not significant. Cetirizine also reduced the numbers of EG2+ cells, particularly those with high counts before treatment but the overall results were not significant. No other changes in the cellular infiltrate were demonstrated when cetirizine was compared with placebo. These findings indicate a single dose of prednisolone significantly reduces leucocyte infiltration and activation as well as the magnitude of the cutaneous late-phase reaction.

Administration, Oral↗
PubMed1992

Application of monoclonal antibodies against major basic protein (BMK-13) and eosinophil cationic protein (EG1 and EG2) for quantifying eosinophils in bronchial biopsies from atopic asthma.

A monoclonal antibody prepared against the eosinophil major basis protein (MBP) was compared with the anti-eosinophil cationic protein (ECP) antibodies (EG1 and EG2) in immunostaining of bronchial biopsies from atopic asthma and controls. Anti-MBP (designated BMK-13) did not cross-react with other eosinophil basic proteins (i.e. ECP, eosinophil peroxidase [EPO] or eosinophil-derived neurotoxin [EDN]) and stained more than 98% of peripheral blood eosinophils irrespective of their degree of activation. EG2 stained 15% of resting and 75% of activated eosinophils; EG1 recognized 74% and 78% of resting and activated cells, respectively. The numbers of BMK-13, EG1 or EG2-positive staining cells in bronchial biopsies from asthma were significantly greater than atopic non-asthmatics (P less than 0.02, P less than 0.01 and P less than 0.05, respectively) and normal non-atopic controls (P less than 0.001). For each of the various groups studied, the rank order for the number of eosinophils stained was BMK-13 greater than EG1 greater than EG2. BMK-13 stained significantly more cells from bronchial biopsies of atopic asthma and atopic non asthma when compared to EG2 (P less than 0.001 and P less than 0.05, respectively). Since only a proportion of BMK-13+ cells were EG2+, these results suggest that not all tissue eosinophils are actively secreting. Thus, BMK-13 can serve as a useful pan-eosinophil marker in tissue sections since it appears to stain most eosinophils.

Antibodies, Monoclonal↗
PubMed1992

Allergy. Conventional and alternative concepts. A report of the Royal College of Physicians Committee on Clinical Immunology and Allergy.

Allergy is an exaggerated response of the immune system to external substances. It plays a role in a wide range of diseases. In some, such as summer hayfever, the symptoms are due entirely to allergy. In other conditions, particularly asthma, eczema and urticaria, allergy plays a part in some patients but not all. In these situations, allergy may have either a major role or provide just one of many triggers. In an individual patient's illness, the importance of allergy may change with time. The most common allergens (substances causing allergy) are grass and tree pollens, the house dust mite, products from pets and other animals, agents encountered in industry, wasp and bee venom, drugs, and certain foods. Food allergy presents a particularly difficult problem. Some individuals who react to food suffer from food allergy in its strict sense but in others there is no evidence of an alteration in the immune system. Here the term 'food intolerance' is preferable. Conventional doctors treat allergy by allergen avoidance--where this is possible--and drugs that relieve symptoms. In a few selected cases, in which other methods have failed, immunotherapy (desensitisation or hyposensitisation) is recommended. Although patients who consult practitioners of alternative allergy may do so by preference, it is often also because they are dissatisfied with the conventional approach to diagnosis and treatment, or because they have conditions which conventional doctors do not accept as having an allergic basis. There is a very wide range of alternative approaches to allergy, including the methods used by clinical ecologists and other treatments such as acupuncture and homoeopathy. Hypnosis may have a small role to play in helping the asthmatic and similar effects have been suggested for acupuncture. Furthermore, it is likely that there are still many active ingredients in medicinal plants used by herbalists but these need to be clearly identified and purified before their usefulness can be evaluated properly. Apart from these situations, we have yet to be convinced by substantial evidence that any of the other alternative methods of diagnosing or treating allergic disease are of proven value. There have, however, been many false and misleading claims and serious harm may be caused by misdiagnosis or delays in appropriate treatment. The public should be warned against costly methods of diagnosis and treatment which have not been validated.(ABSTRACT TRUNCATED AT 400 WORDS)

Allergens↗
PubMed1992

T lymphocytes and activated eosinophils in airway mucosa in fatal asthma and cystic fibrosis.

With the use of monoclonal antibodies (mAb) and immunohistology, the numbers of phenotypically distinct cells infiltrating lung tissue from 15 postmortem (PM) cases of fatal asthma were quantified and compared with 6 cases of cystic fibrosis (CF) (three postmortem, three transplant) and 10 nonasthmatic cases of sudden death matched for age and sex. Tissue eosinophilia was significantly greater (p less than 0.001) in the fatal asthma group than in the CF or sudden death controls. In asthma, approximately 40% of the eosinophilic infiltrate was EG2 positive (an indication of eosinophil activation and secretion of eosinophil cationic protein). The numbers of eosinophils and EG2 positive cells were significantly elevated in the subjects with acute severe asthma who had had a duration of terminal illness exceeding, as compared with less than, 24 h (p less than 0.05). When compared with the sudden death controls, there were increases in the numbers of Dako L C positive cells (i.e., CD45 positive "total leukocytes") in both fatal asthma and CF (p less than 0.01 and 0.05, respectively). The mean number of MT-1 positive (T) cells in the asthma and CF groups was approximately twice that of the control (p less than 0.05 and 0.01, respectively). The mean number of MB2 positive (B) cells was similar for both the asthma and sudden death control groups but was significantly increased in CF (p less than 0.05). The average T:B cell ratios were 6:1, 1:1, and 2:1 in the fatal asthma, CF, and control groups, respectively. The results support a role for the T lymphocyte in the pathogenesis of fatal asthma and CF.(ABSTRACT TRUNCATED AT 250 WORDS)

B-Lymphocytes↗
PubMed1992

Immunohistology of the nasal mucosa following allergen-induced rhinitis. Identification of activated T lymphocytes, eosinophils, and neutrophils.

We have studied the immunohistology of the nasal mucosa in allergen-induced rhinitis. Sixteen grass pollen-sensitive patients were challenged twice by randomly allocated allergen or control solutions applied on filter paper disks to the inferior turbinate. All had immediate nasal responses, but late-phase responses were equivocal and only evident as nostril blockage. When cell counts in the nasal submucosa were compared with control values 24 h after allergen, there were no changes in CD45+ (total leukocytes), CD3+, or CD8+ cells. Significant increases were found in the numbers of CD4+ T-helper cells (p less than 0.05) and CD25+ [interleukin-2 receptor (IL-2R+)] cells (p less than 0.02). Increases in eosinophils (anti-major basic protein, p less than 0.01) and neutrophils (antineutrophil elastase, p less than 0.01) were also observed. There were increases in tissue macrophages and HLA-DR-positive immunostaining and a reduction in mast cells (tryptase positive), but none of these changes was statistically significant. No significant changes in epithelial thickness, cross-sectional area, or integrity were observed. There was a significant correlation between CD4+ and CD25+ cells (r = 0.61, p less than 0.01) but not between macrophages and CD25+ cells (r = 0.18). The changes in the nasal submucosa were not merely a reflection of alterations in circulating cell populations since it was shown that a significant increase in the lymphocyte CD4/CD8 ratio (p less than 0.05) was observed in nasal biopsies but not in peripheral blood after allergen challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Identification of T lymphocytes, macrophages, and activated eosinophils in the bronchial mucosa in intrinsic asthma. Relationship to symptoms and bronchial responsiveness.

Using immunohistochemistry and a panel of monoclonal antibodies, we have compared T-lymphocyte, eosinophil, macrophage, and neutrophil infiltration in bronchial biopsies from 10 intrinsic (nonallergic) asthmatics (IA) and seven extrinsic (allergic) asthmatic (EA), with similar degrees of disease severity. The results were compared with 12 normal healthy nonatopic controls (NC). All subjects were nonsmokers and were not taking oral or inhaled corticosteroids. An intense mononuclear cell infiltrate was identified in IA with an increase in the number of CD45+ cells (total leukocytes), CD3+ and CD4+ lymphocytes, and CD68+ macrophages (p < 0.03, p < 0.01, p < 0.03, and p < 0.03, respectively), compared with NC. Increases were also found in CD4+ (p < 0.05) and CD68+ (p < 0.05) cell numbers between IA and EA. IL-2 receptor-bearing cells (CD25+) and the number of total (MBP+) and actively secreting (EG2+) eosinophils, were also increased in IA compared with NC (p < 0.01, p < 0.01, and p < 0.01, respectively). Similar increases in EG2+ eosinophils and CD25+ (IL-2 receptor-positive) cells were observed in EA (p < 0.01 and p < 0.02, respectively). No differences were detected in the three groups for the number of elastase-positive cells (neutrophils). EG2+ numbers in IA correlated with the Aas asthma symptoms score (r = 0.65, p < 0.05), whereas EG2+ cell numbers in all asthmatics (IA + EA) correlated with airway methacholine responsiveness (r = -0.55, p < 0.03) and with the Aas asthma symptom score (r = 0.54, p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Identification on receptors for leukotriene B4 expressed on guinea-pig peritoneal eosinophils.

We have recently reported that guinea-pig eosinophil chemotactic factor of anaphylaxis (ECF-A), an activity present in diffusates from antigen-challenged sensitized lung, is largely accounted for by leukotriene B4 (LTB4) and to a lesser extent 8(S)15(S)-dihydroxy 5,9,11,13 (Z,E,Z,E) eicosatetraenoic acid. We characterized cell surface receptors for LTB4 on guinea-pig eosinophils in order to demonstrate an association between receptor occupancy and eosinophiliotactic activity of guinea-pig ECF-A. Equilibrium binding studies showed that peritoneal eosinophils bound [3H]LTB4 in a cell concentration and time-dependent fashion. The binding was saturable and specific for LTB4 as other eosinophil chemoattractants, i.e. platelet-activating factor (PAF) and 8(S)15(S)-diHETE, were unable to displace significant amounts of [3H]LTB4. In addition the binding was readily reversed by the LTB4 receptor antagonist LY 255283 (Ki 4.30 nM). Scatchard plot analysis revealed two discrete populations of binding sites, high affinity (Kd1 = 0.30 nM; Bmax = 900 sites/cell) and low-affinity sites (Kd2 = 140 nM; Bmax = 60,000 sites/cell). The major migratory component of LTB4-stimulated eosinophil locomotion was chemotaxis, optimal at 1 x 10(-7) M (P < 0.01) with EC50 value of 3 x 10(-9) M. A comparison of the profile of arachidonic acid metabolism by RP-HPLC analysis showed that following stimulation with calcium ionophore (A23187) guinea-pig eosinophils preferentially synthesized LTB4 (10 ng/10(6) cells) while in contrast human eosinophils synthesized LTC4 (10 ng/10(6) cells). Therefore our data show that guinea-pig eosinophils express both high- and low-affinity receptors for LTB4 and that the chemotactic response to this mediator may be mediated by ligation of the high-affinity binding site. Furthermore guinea-pig peritoneal eosinophils can synthesize LTB4, a mediator which constitutes > 60% of guinea-pig ECF-A.

Animals↗
PubMed1992

Expression and generation of interleukin-8, IL-6 and granulocyte-macrophage colony-stimulating factor by bronchial epithelial cells and enhancement by IL-1 beta and tumour necrosis factor-alpha.

We have tested the hypothesis that the bronchial epithelium has the capacity to generate and release cytokines that could contribute to inflammatory events associated with inflammatory lung diseases. Messenger RNA (mRNA) for interleukin-6 (IL-6), IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) was identified in human bronchial epithelial cell primary cultures, characterized on the basis of staining for cytokeratin, using both in situ hybridization and Northern blotting. Using in situ hybridization we have shown that the majority of the cells expressed mRNA for IL-6 and IL-8, whereas fewer than 20% of cells expressed message for GM-CSF. The numbers of cells expressing message were increased by culture with tumour necrosis factor-alpha (TNF-alpha) (20 ng/ml, 24 hr). These observations were substantiated by Northern blotting, which showed that both TNF-alpha and IL-1 beta were able to induce a dose-dependent increase in IL-8-specific mRNA. Immunoreactive IL-6 and GM-CSF were detected and quantified in the culture supernatants by ELISA, and IL-8 by radioimmunoassay. The levels of immunoreactivity were increased by incubation of epithelial cells with either IL-1 beta or TNF-alpha for 24 hr. A transformed tracheal epithelial cell line (9HTEo-) expressed mRNA for IL-6, IL-8 and GM-CSF but, whereas levels of immunoreactive IL-6 in culture supernatants were comparable with those in primary cell cultures, levels of IL-8 were low and GM-CSF trivial. These observations indicate that the bronchial epithelium has the potential to be a major source of IL-8 and a number of other cytokines, and that production can be amplified substantially by IL-1 beta and TNF-alpha. The bronchial epithelium is ideally situated to modulate inflammatory and immunological events in and around the airways, and these observations suggest that it could contribute to promote and sustain inflammatory and immunological processes in inflammatory lung diseases such asthma.

Blotting, Northern↗
PubMed1992

Interleukin-3-induced up-regulation of CR3 expression on human eosinophils is inhibited by dexamethasone.

Eosinophil function is regulated by several cytokines, including interleukin-3 (IL-3), IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF). Culture of human eosinophils with IL-3 produced a marked, dose-dependent up-regulation of CR3 expression. This was maximal after 1 day in culture and dependent on protein and RNA synthesis, as demonstrated by inhibition with cycloheximide and actinomycin D, respectively. IL-5 and GM-CSF had a similar effect on eosinophil complement receptor type 3 (CR3) expression, but the maximal response to IL-5 was always less than to IL-3 or GM-CSF. Dexamethasone inhibited the Il-3-induced up-regulation of CR3 expression in a dose-dependent manner, with an IC50 of 5 x 10(-8) M. This study demonstrates the effect of IL-3, IL-5 and GM-CSF on eosinophil CR3 expression and confirms the capacity of eosinophils to modify their phenotype through de novo protein synthesis. This process could be inhibited by physiological concentrations of glucocorticoids, thus providing an additional mechanism for their mode of action in allergic disease.

Blood Proteins↗
PubMed1992

Co-expression of CD25 and CD3 in atopic allergy and asthma.

In an attempt to identify the phenotype of the CD25+ cells previously demonstrated in late-phase allergic reactions in skin and nasal mucosa, and in the bronchial mucosa in atopic asthma we have investigated the co-expression of CD3 and CD25 using double immunofluorescent staining. Fluorescein isothiocyanate (FITC) conjugated anti-CD3 monoclonal antibody and a biotinylated anti-CD25 monoclonal antibody (which was later developed with Texas Red streptavidin) were applied simultaneously to cryostat sections or cytospins of freshly prepared samples. Skin and nasal biopsies were from antigen-induced late-phase reactions, and bronchial biopsies and cytospins of bronchoalveolar lavage cells were from subjects with moderate atopic asthma. Four to 14% of CD3+ cells in these tissues were CD25+ and 61-100% of CD25+ cells also expressed CD3. However, CD25 was also expressed on non-CD3+ cells, assumed to be non-T cells. These results were comparable to that observed with a positive control of a tuberculin-challenged skin biopsy. Thus the majority of cells expressing CD25 in various types of atopic allergic inflammation in man were T lymphocytes.

Antigens, CD↗
PubMed1991

Identification of guinea pig eosinophil chemotactic factor of anaphylaxis as leukotriene B4 and 8(S),15(S)-dihydroxy-5,9,11,13(Z,E,Z,E)-eicosatetraenoic acid.

We have purified and characterized the guinea pig eosinophil chemotactic factor of anaphylaxis (ECF-A), an activity previously described in diffusates from sensitized lung challenged with specific Ag that appeared to selectively attract eosinophils from mixed leukocyte populations. Time course studies showed that the release of ECF-A from challenged presensitized guinea pig lung fragments closely paralleled the release of immunoreactive leukotriene B4 (iLTB4) and histamine. However, the majority of ECF-A (greater than 80%) and iLTB4 (greater than 79%) was extractable with the lipid fraction from the methanol wash of Sep-Pak-extracted diffusate, whereas histamine remained in the aqueous phase. A comparable neutrophil chemotactic activity was also found in the methanol extracts of the anaphylactic diffusates. By using a combination of HPLC and specific RIA, greater than 60% of ECF-A was attributable to LTB4. A second eosinophil chemotactic activity was also identified and coeluted (on both reverse phase and straight phase HPLC) with the synthetic standard 8(S),15(S)-dihydroxy-5,9,11,13(Z,E,Z,E)eicosatetraenoic acid (8(S),15(S)-diHETE). This was confirmed as 8(S),15(S)-diHETE by gas chromatography-mass spectrometry. Platelet-activating factor and histamine had negligible activity for guinea pig eosinophils, compared with synthetic LTB4 (p less than 0.05, 10(-9) and 10(-8) M; p less than 0.01, 10(-7) to 5 x 10(-6) M). In addition, synthetic 8(S),15(S)-diHETE had 3 times less activity than LTB4 at optimal chemotactic concentrations (10(-6) and 10(-7) M, respectively). Thus, guinea pig ECF-A appears to be largely attributable to lipoxygenase products of arachidonic acid, namely LTB4 and 8(S),15(S)-diHETE. Because guinea pig ECF-A was equally active on neutrophils (greater than 96% purity), it can no longer be considered a selective eosinophil chemoattractant.

Anaphylaxis↗
PubMed1991

Mechanisms of granule enzyme secretion from permeabilized guinea pig eosinophils. Dependence on Ca2+ and guanine nucleotides.

The mechanisms of granule protein secretion have been studied in streptolysin-O-permeabilized guinea pig eosinophils. Secretion of the granule-associated enzyme N-acetyl-beta-D-glucosaminidase was dependent on both Ca2+ and a nonhydrolyzable GTP analogue, guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S), suggesting roles for both calcium and GTP binding proteins. Secretion was maximal by 7 min, and varied between 35 and 60% of the total enzyme activity. Other GTP analogues also elicited secretion, with rank order GTP-gamma-S greater than guanylyl-imidophosphate greater than guanylyl (beta-gamma-methylene-diphosphate). Unrelated nucleotide triphosphates showed little or no effect confirming the specificity of the G protein. Transmission electronmicroscopy confirmed that permeabilization alone did not result in loss of granules and that exocytosis was dependent on the addition of the effectors, Ca2+ and GTP-gamma-S. ATP enhanced the magnitude of the secretory response and also enhanced the effective affinities for both Ca2+ and GTP-gamma-S. In the presence of 10(-5) M GTP-gamma-S the ED50 (Ca2+) was pCa 5.57 +/- 0.04 (2.69 microM) in the absence of ATP and declined to pCa 6.16 +/- 0.03 (0.69 microM) in the presence of ATP (p less than 0.0001). Furthermore, ATP served to restore responsiveness in cells that had been rendered refractory by delaying stimulation after permeabilization. Pretreatment with PMA (an activator of PKC) inhibited the induction of a refractory state, whereas inhibition of PKC partially countered the ability of ATP to restore responsiveness, both observations pointing to a requirement for a specific component of the secretory mechanism to be in a phosphorylated state in order to condone the secretion process. These observations show that secretory mechanisms in eosinophils are similar to those in other myeloid cells, in particular neutrophils and mast cells, although the time course of secretion is more protracted.

Acetylglucosaminidase↗
PubMed1991

Expression of mRNA and immunoreactivity for the granulocyte/macrophage colony-stimulating factor in activated human eosinophils.

Using in situ hybridization, we have shown that activated human peripheral blood eosinophils express mRNA for granulocyte/macrophage colony-stimulating factor (GM-CSF). Between 15 and 27% of eosinophils gave positive hybridization signals for GM-CSF mRNA after stimulation with the calcium ionophore A23187 or interferon gamma, and 4 and 6% after incubation with interleukin 3 (IL-3) or IL-5. Activated eosinophils also gave specific immunoreactivity with an anti-GM-CSF polyclonal antibody, suggesting translation of the mRNA. These data indicate that eosinophils may be an important source of GM-CSF at sites of allergic inflammation. Furthermore, the identification of GM-CSF production by human eosinophils suggests that the pro-inflammatory potential of this cell type may be substantially greater than hitherto recognized.

Calcimycin↗
PubMed1991

Eosinophil activation and T lymphocyte infiltration in allergen-induced late phase skin reactions and classical delayed-type hypersensitivity.

T lymphocyte infiltration is a well documented feature of classical delayed-type hypersensitivity (DTH) reactions. Recently, we have shown that T lymphocytes and activated (EG2+) eosinophils accumulate in the allergen-induced late phase skin reaction (LPR). To compare the kinetics and phenotypic composition of these T lymphocyte responses, LPR and DTH reactions of comparable induration size were induced in atopic subjects. In addition, DTH and LPR were compared between atopic and nonatopic subjects. In atopic individuals, allergen challenge elicited a perivascular influx of T lymphocytes that was predominantly CD4+. Eosinophil accumulation and activation were also prominent. There was no cellular response to allergen challenge in the nonatropic group. In both groups, DTH responses showed an intense T cell infiltrate which was more dense and dispersed than in the LPR. CD4+ T cells predominated but at 48 h CD8+ numbers were also significantly increased. In DTH, total leukocyte numbers (CD45+) were increasing at 48 h, whereas in the LPR, cell numbers reached a plateau between 24 and 48 h. T cell activation (shown by expression of IL-2R) was more prominent in DTH. Endothelial expression of HLA-DR was increased in both LPR and DTH, implying the local release of inflammatory cytokines in both reactions. Small but significant numbers of activated eosinophils (EG2+) were detected in atopics and non-atopics at 24 h in DTH but not at 48 h. These findings suggest that the allergen-induced LPR induced in atopic subjects is, at least in part, a form of cell-mediated hypersensitivity but with T cell kinetics that differ from classical DTH.

Adolescent↗
PubMed1991

Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is alpha 4 beta 1 (very late antigen-4) dependent.

Eosinophils, through their ability to generate an array of potent mediators, are thought to be the major effector cells in a number of conditions, including parasitic infection, asthma, and other allergic diseases. The mechanism(s) by which eosinophils, as opposed to neutrophils, accumulate at inflammatory sites is unknown. One possible mechanism would be an eosinophil-specific pathway of adhesion to vascular endothelium. In this study we have demonstrated that human eosinophils, but not neutrophils, constitutively express alpha 4 beta 1 (CD49d/CD29). Expression was not increased on low density eosinophils or normal density cells stimulated with platelet-activating factor. Eosinophils, but not neutrophils, specifically adhered to COS cells transfected with vascular adhesion molecule-1 in a alpha 4 beta 1-dependent manner. Eosinophil, but not neutrophil, adhesion to IL-1 stimulated human umbilical vascular endothelial cells was significantly inhibited by alpha 4 beta 1 mAb at both 5 h (p less than 0.05) and 20 h (p less than 0.001). Inhibition of both resting and platelet-activating factor-(10(-7) M) stimulated eosinophil adhesion was observed. We conclude that the alpha 4 beta 1/vascular adhesion molecule-1 adhesion pathway may be involved in specific eosinophil, as opposed to neutrophil, migration into sites of eosinophilic inflammation.

Antigens, CD↗
PubMed1991

Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects.

Cryostat sections from skin biopsies from 24-h allergen-induced late-phase cutaneous reactions (LPR) in 14 human atopic subjects were hybridized with 35S-labeled RNA probes for a number of cytokines. mRNA was detected for interleukin 3 (IL-3) (8/14), IL-4 (10/14), IL-5 (11/14), and granulocyte/macrophage colony-stimulating factor (GM-CSF) (13/14). Only 5 of 14 gave hybridization signals for IL-2, and 0 of 14 for interferon gamma. Biopsies from diluent controls gave only occasional weak signals. These results suggest that cells infiltrating the site of the 24-h LPR transcribe mRNA for the IL-3, IL-4, IL-5, and GM-CSF gene cluster and support the hypothesis that atopy is associated with preferential activation of cells having a similar cytokine profile to the murine T helper type 2 subset.

Adolescent↗