Inflammatory changes in proximal and peripheral airways of asthmatic patients.
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Asthma↗
Biomedical subjects
S Oddera
Publications and source records attributed to S Oddera.
Frequency and specific sensitization to inhalant allergens within nuclear families of children with asthma and/or rhinitis.
OBJECTIVE: The purpose of this study was to investigate the frequency of allergy in 85 families of pediatric patients with asthma and/or rhinitis. METHODS: Families enrolled were drawn according to a table of randomization, from those whose children were referred the outpatient clinic of the Pulmonology Department of Gaslini Institute (Genoa, Italy). In patients and in both their mothers and fathers, allergic sensitization to the three most common classes of inhalant allergens (house dust mites, pollens, and animal danders) was evaluated by skin prick test. RESULTS: As compared with their parents, children showed a similar prevalence of positive skin prick test (50.0% and 58.8%, respectively; chi 2 = 1.4; P > .1), but a significantly higher frequency of specific sensitization to house dust mites, pollens, or pets (P < .05, each chi 2). These differences were at least partially related to the higher frequency of polysensitization (i.e., sensitization to more than one class of allergens) in children than in their parents [chi 2 = 4.2, odds ratio (OR) = 2.3, 95% confidence interval (CI95%) = 1.0 to 5.1; P < .05). In addition, both in children (chi 2 = 5.8, OR = 11.3, CI95% = 1.4 to 81.5; P < .05] and in their parents (chi 2 = 7.4, OR = 4.8, CI95% = 1.5 to 16.7; P < .01), allergy to pollens was less frequent in monosensitized than in polysensitized families, while the prevalence of sensitization to house dust mites was similar in monosensitized and in polysensitized families. The analysis of the role of parental sensitization in the development of allergy in the offspring demonstrated that the prevalence of allergic children: (1) seemed to be higher, without reaching statistical significance, in families with sensitized parents than in those with non-sensitized parents (chi 2 = 0.41, P > .1) and (2) was higher in families with one or both polysensitized parents than in those with one or both monosensitized parents (chi 2 = 4.5, OR = 4.0, CI95% = 1.1 to 15.6; P < .05). In addition, within each family, the coincidence of sensitization to house dust mites was more frequent than that to pollens (60.0% and 36.0%, respectively; chi 2 = 7.6, OR = 4.5, CI95% = 1.5 to 14.3; P < .01), and it was not influenced by the number of parents sensitized to same allergen. CONCLUSION: These data support the concept that, in addition to genetic predisposition, other factors (i.e., environmental exposure) may influence the development of specific sensitization in children with respiratory symptoms. The different sensitization found in this study between children and their parents occurred in a generation span, so as it is more likely to be related to environmental changes than to genetic factors.
Administration, Inhalation↗
Sensitization to airborne allergens in children with respiratory symptoms.
BACKGROUND: Allergy is one of the most common causes of respiratory symptoms in children and youth. OBJECTIVE: Evaluate the presence and the type of allergic sensitization in a paediatric population with respiratory symptoms. METHODS: We studied 564 consecutive children, 5 months to 17 years of age, with a male to female ratio (M/F) = 1.4, referred to our outpatient clinic in a 12-month period retrospectively. Patients were arbitrarily divided into four groups (grs) according to their age: gr1 = 5 months to 4 years old (181 patients), gr2 = 4 to 7 years (201 patients), gr3 = 7 to 10 years (96 patients), and gr4 = 10 to 17 years (86 patients). Sensitization to house dust mites, pollens, animal dander, and molds was determined by skin prick testing. RESULTS: Sensitization to at least one class of allergen occurred in 304 of the 564 patients (53.9%, M/F ratio = 2.0); the percentage of allergic patients increased with age as follows: 29.8% (54 patients) of the patients in gr1, 55.2% (111 patients) in gr2, 68.8% (66 patients) in gr3 and 84.9% (73 patients) in gr4 (chi(2) = 84.1, P < .01). In the entire allergic population and in gr1 to gr3, the most common positive allergic reaction was to house dust mites (P < .01, chi(2) test each comparison). In contrast, gr4 patients showed a nearly equal percentage of sensitization to pollens and to house dust mites (79.5% and 78.1% respectively) (chi(2) = 0.0, P = >.1). Sensitization to only one class of allergen occurred in 51.3% of the allergic patients and the percentage of these monosensitized patients tended to decrease from gr1 to gr4 (chi(2) = 15.2, P < .1). In the monosensitized group, sensitization to house dust mites was the most frequent in gr1 to gr3 (age <10 years) as in the whole sample. In gr4, the frequency of sensitization to house dust mites was similar to that of sensitization to pollens. On the contrary, within the patient group sensitized to two or more allergens (polysensitized patients), sensitization to house dust mites was as frequent as sensitization to pollens already in gr2 as compared with monosensitized patients. CONCLUSIONS: In children with respiratory symptoms, the percentage of allergic individuals was high and increased with the age of the patients. This phenomenon was associated with an age-related enhancement in the ratio of polysensitized to monosensitized patients and with an age-related increase in the frequency of sensitization to seasonal allergens (ie, pollens).
Adolescent↗
Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild-moderate, stable asthma.
Allergic asthma is characterized by chronic recruitment of eosinophils in the airways. Once activated, eosinophils release toxic products, including eosinophil cationic protein (ECP), able to damage airway epithelial cells. To test the hypothesis that also in mild-moderate stable asthma, a significant eosinophil activation could occur, we studied 25 asthmatic patients (34 +/- 19 years old), of whom 18 were allergic (27 +/- 12 years) and seven nonallergic (42 +/- 10 years), with FEV1 values > or = 70% of predicted, and eight normal volunteers (controls, 33 +/- 11 years). All subjects underwent methacholine (MCh) challenge on the first visit, and bronchoalveolar lavage (BAL) on the second visit (approximately 3-4 days later). BAL cells were counted and albumin (Alb) (as index of protein dilution in BAL fluid) and ECP levels (as index of eosinophil activation) in BAL fluid were measured. As compared to controls, a significant increase in BAL eosinophil and in BAL epithelial cell numbers was observed in asthmatic patients (P > 0.05, each comparison), with no differences between the two asthmatic patient subgroups. Detectable ECP levels (> 2 micrograms/1) were found in BAL of 18 asthmatic patients (14 allergic and four nonallergic asthmatic patients), while Alb levels were measurable in 25 BAL fluids and found to be similar in controls and asthmatic patients, and in the two asthmatic patient subgroups (P > 0.05, each comparison). In BAL of asthmatic patients, positive correlations were found between eosinophil numbers and 1) ECP/Alb levels (r = 0.50, P = 0.020); 2) epithelial cell numbers (r = 0.50, P = 0.014). In asthmatic patients, a significant negative correlation was found between bronchial reactivity to MCh (log Pd15) and ECP/Alb levels in BAL fluid (r = -0.6, P = 0.005), whereas no correlation was found between log Pd15 MCh and BAL eosinophil or epithelial cell number (P > 0.1, each correlation). These data suggest that bronchial eosinophil recruitment and activation may occur also in mild-moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.
Adolescent↗
BAL neutrophilia in asthmatic patients. A by-product of eosinophil recruitment?
Although neutrophil number may be increased in the airways of patients with asthma, its pathogenetic role in this disorder remains unclear. We evaluated BAL of 8 normal control subjects, 30 +/- 2 years of age, and 24 patients with mild asthma: 17 patients with allergic asthma, 24 +/- 1 years of age, and 7 patients with nonallergic asthma, 30 +/- 1 years of age. The BAL of asthmatic patients showed increased numbers of neutrophils (p < 0.01), eosinophils (p < 0.01), and ciliated epithelial cells (p < 0.05) and increased concentrations of myeloperoxidase (MPO) (p < 0.01) compared with control subjects. Positive correlations were observed between the number of BAL neutrophils and eosinophils (Rs = 0.780, p < 0.0001) and between BAL neutrophil numbers and BAL MPO levels (Rs = 0.40, p < 0.05). No correlations were found between the following: (1) BAL eosinophils or neutrophils and BAL epithelial cells (p > 0.05, each comparison); (2) BAL neutrophils or eosinophils and log Pd15 methacholine (MCh) (p > 0.05, each comparison); or (3) BAL epithelial cells or log Pd15 MCh and BAL MPO (p > 0.05, each comparison). Dividing the patient population into two groups, allergic asthmatics and nonallergic asthmatics, similar BAL neutrophil, eosinophil, and epithelial cell numbers and similar MPO levels were found (p > 0.05, each comparison). In addition, the correlations between BAL neutrophils and eosinophils showed similar significance in the two patient subgroups (p > 0.05, each comparison). These results suggest that, both in allergic and nonallergic asthma, airway recruitment and activation of neutrophils occur as does parallel eosinophil migration. However, airway neutrophils do not seem to contribute significantly to epithelial cell injury or to airway hyperresponsiveness in the steady state.
Adolescent↗
Azithromycin induces in vitro a time-dependent increase in the intracellular killing of Staphylococcus aureus by human polymorphonuclear leucocytes without damaging phagocytes.
Despite its clinical efficacy on intracellular pathogens, the in-vitro intracellular antimicrobial activity of azithromycin, has been shown to be absent or lower than expected from the intracellular concentrations reached. To test the possibility that the high intracellular concentrations of the drug could damage phagocytes, the present study evaluated the effects of azithromycin on (a) the intracellular killing of Staphylococcus aureus by human blood neutrophils (PMNs) and (b) the viability and the respiratory burst of PMNs. Using a fluorochrome assay, we assessed the phagocytosis and intracellular killing of S. aureus by PMNs preloaded with azithromycin, or by PMNs unloaded but with the drug in the culture medium. In addition, possible drug-induced damage to PMNs was evaluated measuring: (a) hydrogen peroxide (H2O2) production and (b) the percentages of PMNs dead at the end of the phagocytosis process. Compared to control PMNs without drug, a time-dependent enhancement in the intracellular killing was observed which was statistically significant after 60 min incubation. The increased intracellular killing was higher in suspensions of unloaded PMNs and azithromycin (P < 0.01) that in suspensions of preloaded PMNs (P < 0.05). This increased intracellular killing was not associated with increased proportions of dead phagocytes, either in preloaded or unloaded PMNs (P < 0.05, each comparison). Similarly no changes in the production of H2O2 by PMNs were observed in the presence of azithromycin. Thus, azithromycin induces a time-dependent increase in the bactericidal activity of human PMNs, without increasing the phagocyte self-killing or modifying H2O2 production.
Adolescent↗
Effects of "systemic" budesonide concentrations on in vitro allergen-induced activation of blood mononuclear cells isolated from asthmatic patients.
Blood levels of inhaled corticosteroids are significantly lower than those measured in the lung, but their concentration could still have anti-inflammatory effects. To determine whether budesonide, at concentrations similar to those obtained in blood after drug inhalation (10(-9) M), could downregulate the allergen-induced activation of mononuclear cells, we studied 21 atopic patients, sensitized to Dermatophagoides pteronyssinus (Der p). On blood mononuclear cells, isolated from these patients, incubated with Der p allergen extract and with or without budesonide, we evaluated: 1) the proliferative response of T cells; 2) the expression of two surface activation markers, the HLA-DR antigens and the interleukin (IL)-2 receptors; and 3) the release of cytokines known to modulate the allergic processes. Allergen-induced T-cell proliferation was associated with increased HLA-DR antigen and IL-2 receptor expression (P < 0.001), and with increased release of IL-2, interferon-gamma (IFN-gamma), IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), and granulocyte/macrophage colony-stimulating factor (GM-CSF). The addition of budesonide at the beginning of the cell cultures induced a dose-dependent inhibition of T-cell proliferation, still significant (P < 0.05) at the lowest concentrations tested (10(-9) and 10(-10) M). A significant inhibitory effect on T-cell proliferation was also present when budesonide (10(-9) M) was added to the cell cultures 3 or 5 days after the beginning of the cell cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Evaluation of the inhibitory effects of budesonide on the mitogen-induced or the allergen-induced activation of blood mononuclear cells isolated from asthmatic patients.
BACKGROUND: Corticosteroids are thought to be effective in the treatment of allergic reactions including bronchial asthma because they not only have anti-inflammatory effects, but also downregulate the processes of T-cell activation. OBJECTIVE: To evaluate in vitro the inhibitory activity of budesonide, a widely used inhaled corticosteroid, on allergen-induced mononuclear cell activation. METHODS: Thirty-one atopic asthmatic patients, sensitized to Dermatophagoides pteronyssinus (Der p) were studied. Peripheral blood mononuclear cells isolated from these patients were used to determine the ability of budesonide to inhibit (1) the proliferative response of blood T-lymphocytes to Der p allergen extract and to phytohemoagglutinin (PHA) and (2) the release of different cytokines known to modulate the interaction between T-lymphocytes and monocytes in the allergic processes. RESULTS: A significant T-cell proliferation was observed both in the presence of PHA (P < .001) and that of Der p allergen extract (P < .05), and was associated with increased release of interleukin-2 [IL-2 (respectively P < .001 and P < .01)], gamma-interferon [gamma-IFN (respectively P < .001 and P < .01)], granulocyte-macrophage colony-stimulating factor [GM-CSF (respectively P < .01 and P < .001)], interleukin-1 beta [IL-1 beta (respectively P < .05 and P < .01)], and tumor necrosis factor-alpha [TNF-alpha (P < .05 each comparison)]. The addition at the beginning of the cell cultures of different concentrations (from 10(-10) M to 10(-7) M) of budesonide, and as control of dexamethasone, induced a dose-dependent inhibition of T-cell proliferation, in response to PHA and Der p. Budesonide at the lowest concentrations tested (10(-10) M and 10(-9) M) was more effective than dexamethasone. Budesonide was also more active than dexamethasone in inhibiting the release of IL-2, gamma-IFN, IL-1 beta and GM-CSF (in both PHA-stimulated and Der p-stimulated blood mononuclear cell cultures) and TNF-alpha (in Der p-stimulated blood mononuclear cell cultures). CONCLUSIONS: Budesonide is equally or more effective than dexamethasone in inhibiting the allergen-induced T-cell proliferation and in reducing the release of cytokines by allergen-stimulated blood mononuclear cells.
Adult↗
Lower respiratory tract inflammation in chronic bronchitis. Evaluation by bronchoalveolar lavage and changes associated with treatment with Immucytal, a biological response modifier.
Chronic bronchitis (CB) is characterized by inflammatory changes in the bronchial tissue and by recurrent bronchitis exacerbations. In addition, defective systemic and local immune mechanisms have been demonstrated and biologic response modifiers (BRMs) have been recently introduced for clinical use in patients with CB. We studied 24 patients with CB by bronchoalveolar lavage (BAL), before and after a 4-week treatment protocol with inhaled Immucytal (Pierre-Fabre Pharma Srl, Milan, Italy), a BRM composed of bacterial ribosomal fractions and membrane proteoglycans. Compared with normal controls (NC), before treatment BAL in patients with CB contained increased proportions of neutrophils (NC, 0.8 +/- 0.2 percent; CB, 3 +/- 1 percent), of eosinophils (NC, 0.1 +/- 0.02 percent; CB, 0.6 +/- 0.2 percent); and of lymphocytes (NC, 6 +/- 1 percent; CB, 13 +/- 2 percent; p < 0.01 each comparison) with higher percentages of CD3+ and CD8+ lymphocytes (p < 0.01 each comparison). In BAL from patients with CB there were also higher levels of albumin and of the ratio IgG/albumin (p < 0.01 and p < 0.05, respectively, compared with NC). After Immucytal treatment, the proportions of lymphocytes in BAL in patients with CB were decreased (13 +/- 2 percent before, 6 +/- 1 percent after; p < 0.01). In addition, the posttreatment BAL samples contained significantly fewer neutrophils per milliliter of BAL (3.7 +/- 0.8 x 10(3) neutrophils per milliliter of BAL before, 1.5 +/- 0.5 x 10(3) neutrophils per milliliter after; p < 0.05). No differences were seen for the proportions of lymphocyte subpopulations and for the protein levels between the BAL obtained before and after Immucytal treatment. These data demonstrate the presence of a lower respiratory tract inflammation in patients with CB and suggest that treatment of patients with CB with a BRM may change the proportions of inflammatory cells present in BAL.
Aerosols↗
N-acetylcysteine enhances in vitro the intracellular killing of Staphylococcus aureus by human alveolar macrophages and blood polymorphonuclear leukocytes and partially protects phagocytes from self-killing.
The processes of phagocytosis and intracellular killing of bacteria by alveolar macrophages (AMs) and polymorphonuclear leukocytes (PMNs) result in the production of reactive oxygen species that can induce self-damage to the phagocytic cells. N-Acetylcysteine (NAC), a mucolytic agent used to treat chronic respiratory inflammatory disorders, possesses antioxidant properties and has therefore been used for the prevention of damage induced by oxygen radicals. This study was designed to evaluate whether NAC can interfere with the processes of phagocytosis and intracellular killing of bacteria and protect the phagocytic cells from self-killing. Human AM, obtained by bronchoalveolar lavage, and peripheral blood PMNs were cultured with Staphylococcus aureus (American Type Culture Collection 25923 strain) in the presence of different concentrations of NAC (1, 10, and 100 mg/L) and two chromophores (4',6'-diamidino-2-phenylindole dihydrochloride and propidium iodide), which identify live or dead bacteria and dead phagocytes. As compared with PMNs, AMs were more effective in ingesting bacteria (p < 0.05) and were equally effective as intracellular killers (p > 0.05), but were susceptible to a significantly higher rate of self-killing (p < 0.01). The presence of NAC in the cell cultures at the highest dose tested (100 mg/L) induced a significant enhancement of the bactericidal activity of both AMs (p < 0.05) and PMNs (p < 0.05). This increased intracellular killing was not associated with increased proportions of dead phagocytes either in AMs or PMNs cultures (p > 0.05, each comparison), suggesting a protective effect of NAC on damage induced by toxic products generated during phagocytosis.
Acetylcysteine↗
Clinical application of bronchoscopy and bronchoalveolar lavage in the immunocompromised host.
Pulmonary complications are the most frequent cause of morbidity and mortality in immunocompromised patients. The speed of clinical assessment and the initiation of appropriate therapy is critically related to survival. Fibreoptic bronchoscopy and bronchoalveolar lavage (BAL) had proved useful in making the diagnosis of pulmonary complications in a high proportion of immunocompromised patients, where less invasive techniques, such as blood cultures or sputum induction, have failed to establish a diagnosis. Bronchoscopy and BAL cause little discomfort and low morbidity, and should be performed as early in the disease course as possible, preferably before the onset of respiratory failure.
Bronchoalveolar Lavage Fluid↗
T-lymphocytes with gamma delta+ V delta 2+ antigen receptors are present in increased proportions in a fraction of patients with tuberculosis or with sarcoidosis.
T-lymphocytes with T-cell antigen receptor (TCR) comprising a gamma chain and a delta chain (gamma delta+ T cells) are believed to be involved in the immune reaction to mycobacterial antigens, and they have been found in increased proportions in sarcoid patients. We evaluated the proportions of gamma delta+ T-lymphocytes and of two major gamma delta+ subpopulations, the V delta 1+ and the V delta 2+ T-cell subsets, in 10 normal blood donors, in 15 patients with tuberculosis (TB), seven of whom had pleural effusion (PE), and in 12 patients with pulmonary sarcoidosis (PS), nine of whom underwent bronchoalveolar lavage (BAL). T-cell subsets were evaluated in peripheral blood (PBL) of all subjects and in PE from patients with TB and in BAL from patients with PS. Compared with normal blood donors, patients with TB had increased proportions of PBL CD3+ gamma delta+ T cells (6 +/- 1% versus 14 +/- 3% of CD3+ T cells, p < 0.05) because of the presence of four patients who had an increase (respectively, 18.3, 22.0, 24.2, and 35.4% of CD3+ T cells) of gamma delta+ T cells. In patients with TB and PE, gamma delta+ T cells were 7.9 +/- 2.7%, a value not different from that in the tubercular PBL and in normal PBL. Although patients with PS had proportions of PBL gamma delta+ T cells (9.2 +/- 3.4%) similar to those in normal PBL, two patients had increased (35 and 31%) PBL gamma delta+ T-lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The T-cell antigen receptor repertoire of alpha beta+ T-lymphocytes in patients with tuberculosis.
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AIDS-Related Opportunistic Infections↗
Thymomodulin increases HLA-DR expression by macrophages but not T-lymphocyte proliferation in autologous mixed leucocyte reaction.
Thymomodulin (TMD), a thymic biological response modifier, stimulates the release of tumour necrosis factor (TNF) and granulocyte-macrophage-colony stimulating factor (GM-CSF) in macrophage-lymphocyte cultures. We investigated the effects of the cytokines released in cultures with TMD, on the expression of human leucocyte antigen-DR (HLA-DR) antigens by alveolar macrophages (AM) and the T-cell proliferation induced in autologous mixed leucocyte reaction (AMLR) cultures or by T-cell mitogens. Among freshly isolated AM, 84 +/- 4% were HLA-DR positive, and this proportion was significantly reduced after 24 h cultures (60 +/- 3%, p < 0.05). In cultures without peripheral blood (PBL) lymphocytes, TMD did not change HLA-DR expression by AM CHLA-DR+AM); whilst in the presence of autologous PBL lymphocytes, TMD induced an increase in the proportions of HLA-DR+AM (TMD 100 micrograms.ml-1 79 + 3%, p < 0.04 vs control cultures). However, TMD did not change the ability of AM to induce T-cell proliferation in AMLR between AM and PBL lymphocytes. In contrast, in PBL mononuclear cell cultures, TMD induced a further increase of the cell proliferation due to the T-cell mitogens interleukin-2 (IL-2) or phytohaemagglutinin (PHA) (p < 0.05 vs each control culture with mitogens) or anti-CD3 antibodies (p < 0.03 vs control cultures). Thus, the cytokines released in cultures with TMD enhance macrophage HLA-DR expression. Whilst this phenomenon is not associated with changes in the ability of AM to stimulate T-cell proliferation, TMD is able to increase the mitogen-induced T-cell proliferation.
Adult↗
Thymomodulin enhances phagocytic and intracellular killing activities of polymorphonuclear leucocytes without increasing release of chemotactic factors.
Thymomodulin, a calf thymus derivative, is able to stimulate T-lymphocytes and monocytes, and to activate phagocytes and their precursors. However, it is not fully understood whether the effect of thymomodulin on phagocytic cells is a direct stimulation, or a phenomenon mediated by cytokines released by mononuclear cells. To answer this question, we first evaluated the effects of thymomodulin on the phagocytosis and intracellular killing of Staphylococcus aureus by blood polymorphonuclear cells (PMNs), cultured with or without autologous mononuclear cells. Secondly, during the processes of phagocytosis and intracellular killing, we evaluated the release by PMNs of chemotactic factors for PMNs, lymphocytes and monocytes. No difference was found in the phagocytosis and killing processes when PMNs were incubated alone or with autologous mononuclear cells (p > 0.05, each comparison). Thymomodulin was able to increase the phagocytosis process when PMNs were incubated with lymphocytes and monocytes (p = 0.05), and to enhance the killing by PMNs cultured alone (p = 0.05), or cultured with autologous mononuclear cells (p < 0.05). The release of chemotactic factors for PMNs, lymphocytes and monocytes in the supernatants of the phagocytosis experiments, was higher when PMNs were incubated with mononuclear cells, compared to cultures of PMNs alone (p < 0.05, each comparison); and thymomodulin did not increase their release without the presence of autologous mononuclear cells in the cultures (p > 0.05 each comparison). These data suggest that thymomodulin acts upon PMNs, inducing mononuclear cells to release factors able to stimulate the phagocytosis and the intracellular killing of exogenous organisms, but does not amplify the immune reaction enhancing further leucocytes recruitment.
Cell Separation↗
[Effect of pidotimod on phagocytosis and intracellular killing of Staphylococcus aureus by human circulating polymorphonuclear neutrophils and alveolar macrophages].
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Adjuvants, Immunologic↗
Long-term prednisone and azathioprine treatment of a patient with idiopathic pulmonary hemosiderosis.
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Azathioprine↗
Bronchial and bronchoalveolar lavage after allergen challenge in atopic patients.
Twenty patients with allergic rhinitis and/or asthma sensitised to Dermatophagoides pteronyssinus were studied. On two consecutive days they underwent methacholine challenge and allergen bronchial challenge. 72 h after allergen challenge, fibreoptic bronchoscopy with bronchial (BL) and bronchoalveolar (BAL) lavage was performed. Specific IgE antibodies were measured both in serum and in BL from 14 patients. Both BAL and BL cell differentials were similar in patients with isolated early response to allergen and in patients with dual response. Patients with dual response to allergen showed higher levels of antigen specific IgE antibodies in BL than patients with isolated early response, while IgE levels in serum were similar in the two groups.
Adolescent↗