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Biomedical subjects

M Humbert

Publications and source records attributed to M Humbert.

At least 127 records · Page 7Linked to original sources
PubMed1998

Pulmonary vascular disorders in portal hypertension.

The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.

Hemodynamics↗
PubMed1998

Inhaled nitric oxide as a screening agent for safely identifying responders to oral calcium-channel blockers in primary pulmonary hypertension.

In a subset of patients with primary pulmonary hypertension (PPH), high doses of oral calcium-channel blockers (CCB) produce a sustained clinical and haemodynamic improvement. However, significant side-effects have been reported during acute testing with CCB. Therefore, to identify accurately patients who may benefit from long-term CCB therapy, there is a need for a safe, potent and short-acting vasodilator. The aim of this study was to compare the acute response to inhaled nitric oxide (NO) and oral high doses of CCB in 33 consecutive patients with PPH. A significant acute vasodilator response was defined by a fall in both mean pulmonary artery pressure and total pulmonary resistance by >20%. Ten patients responded acutely to NO, nine of whom responded acutely to CCB, without any complications. The 23 other patients failed to respond to NO and CCB. In these nonresponders, nine serious adverse events were observed with CCB (38%). There was no clinical or baseline haemodynamic feature predicting acute vasodilator response. Long-term oral treatment with CCB was restricted to the nine acute responders and a sustained clinical and haemodynamic improvement was observed in only six patients. In primary pulmonary hypertension, the acute response rate to high doses of calcium-channel blockers is low (27%). Serious adverse reactions to high doses of calcium-channel blockers during acute testing are frequently observed in nonresponders. It is concluded that nitric oxide may be used as a screening agent for safely identifying patients with primary pulmonary hypertension who respond acutely to calcium-channel blockers and may benefit from long-term treatment with these agents.

Administration, Inhalation↗
PubMed1998

Primary pulmonary hypertension associated with the use of fenfluramine derivatives.

Fenfluramine derivatives (Fds) are a well-established risk factor for primary pulmonary hypertension (PPH). We compared 62 Fd-PPH patients (61 women) evaluated in our center between 1986 and 1997 with 125 sex-matched PPH patients nonexposed to Fd referred during the same period (control PPH). In the Fd-PPH group, 33 patients (53%) used dexfenfluramine alone, 7 patients (11%) used fenfluramine alone, and 5 patients (8%) used both drugs. In 17 cases (27%), Fd use was associated with that of amphetamines. Most of the exposed patients used Fd for at least 3 months (81%). The interval between the onset of dyspnea and that of drug intake was 49+/-68 months (27 days to 23 years). At the time of diagnosis, Fd-PPH and control PPH were similar in terms of New York Heart Association functional class and symptoms. The two groups significantly differed only in terms of age (50+/-12 vs 40+/-14 years) and body mass index (28+/-6 vs 23+/-4). The two groups displayed similar severe baseline hemodynamics (total pulmonary vascular resistance: 32+/-12 vs 31+/-12 IU/m2), but the percentage of responders to acute vasodilator testing was higher in control PPH (27% vs 10%, p < 0.01). As a result, more patients were treated with oral vasodilators in the control PPH group (36% vs 16%, p < 0.01) and long-term epoprostenol infusion was more frequently used in the Fd-PPH group (52% vs 31%, p < 0.01). Overall survival was similar in the two groups with a 3-year survival rate of 50%.

Adult↗
PubMed1998

High-resolution CT of the chest in four patients with pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease.

OBJECTIVE: Clinical differentiation of isolated pulmonary hypertensive arteriopathy from pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease can be difficult on a clinical basis alone. Differentiation is important because misdiagnosis of pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease may lead to severe vasodilator-induced pulmonary edema. The objective of our study was to determine whether high-resolution CT of the chest could distinguish pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease from isolated pulmonary hypertensive arteriopathy. CONCLUSION: Pulmonary hypertension in patients who also have pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease shows characteristics on high-resolution CT that are not seen in patients with isolated pulmonary hypertensive arteriopathy.

Adult↗
PubMed1998

Platelet-derived growth factor expression in primary pulmonary hypertension: comparison of HIV seropositive and HIV seronegative patients.

Primary pulmonary hypertension (PPH) is characterized by intimal fibrosis and cell proliferation (including fibroblasts, smooth muscle and endothelial cells) in the distal pulmonary arterial tree. Considerable interest has been generated by recent reports of PPH in human immunodeficiency virus (HIV)-1-infected individuals. Although the lack of evidence for a pulmonary artery infection has suggested that in such cases HIV may act through mediator release rather than by direct endothelial infection, the mechanisms underlying HIV-associated PPH remain poorly defined. Platelet-derived growth factor (PDGF) has the ability to induce smooth muscle cell and fibroblast proliferation and migration. Given these considerations, we have attempted to document a possible role for PDGF in PPH occurring in HIV seropositive and seronegative patients. Using semiquantitative polymerase chain reaction (PCR), PDGF A-chain messenger ribonucleic acid (mRNA) expression was analysed in surgical lung biopsies from 13 HIV seronegative patients and one HIV seropositive patient, all displaying severe PPH. In parallel, lung samples from two patients with HIV-1-associated PPH were studied by immunohistochemistry and in situ hybridization. Results were compared to those obtained in three HIV-1-infected individuals with no pulmonary complication (as demonstrated by clinical, radiological, bacteriological, and necropsy findings) and five control lung biopsies. As compared to controls, PDGF A-chain mRNA expression is elevated in lung biopsies from patients displaying PPH (p=0.029). In HIV-1-associated PPH, interstitial perivascular cells expressing PDGF A-chain mRNA and protein could be detected by in situ hybridization and immunohistochemistry, respectively. Platelet-derived growth factor expression is elevated in lung biopsies of patients displaying primary pulmonary hypertension. Growth factors such as platelet-derived growth factor may play a part in the initiation and/or progression of primary pulmonary hypertension.

Adult↗
PubMed1998

[Late relapse of sarcoidosis. Report of 3 cases].

We report patients who were treated with corticosteroids for sarcoïdosis and developed recurrent disease after 9 and 28 years of remission. The clinical latency, the type III radiographic aspect different from the initial presentation and the spontaneous course with periods of partial or total remission are characteristic of these late relapses. Clinicians should be aware of this uncommon clinical course and monitor cured cases for prolonged periods.

Adult↗
PubMed1997

Mapmodulin: a possible modulator of the interaction of microtubule-associated proteins with microtubules.

We have purified and characterized a 31-kDa protein named mapmodulin that binds to the microtubule-associated proteins (MAPs) MAP2, MAP4, and tau. Mapmodulin binds free MAPs in strong preference to microtubule-associated MAPs, and appears to do so via the MAP's tubulin-binding domain. Mapmodulin inhibits the initial rate of MAP2 binding to microtubules, a property that may allow mapmodulin to displace MAPs from the path of organelles translocating along microtubules. In support of this possibility, mapmodulin stimulates the microtubule- and dynein-dependent localization of Golgi complexes in semi-intact CHO cells. To our knowledge, mapmodulin represents the first example of a protein that can bind and potentially regulate multiple MAP proteins.

Amino Acid Sequence↗
PubMed1997

Expression of IL-4 and IL-5 mRNA and protein product by CD4+ and CD8+ T cells, eosinophils, and mast cells in bronchial biopsies obtained from atopic and nonatopic (intrinsic) asthmatics.

We recently demonstrated bronchial mucosal expression of IL-4 and IL-5 at the mRNA and protein level in both atopic and nonatopic (intrinsic) asthma. In this report, using double immunohistochemistry (IHC) and in situ hybridization (ISH), we show that 70% of IL-4 and IL-5 mRNA+ signals co-localized to CD3+ T cells, the majority (>70%) of which were CD4+, although CD8+ cells also expressed IL-4 and IL-5 mRNA. The remaining IL-4 and IL-5 mRNA signals co-localized to mast cells and eosinophils. The cellular distribution of these mRNA species did not differ between atopic and nonatopic asthmatics. In contrast, double IHC showed that IL-4 and IL-5 immunoreactivity was predominantly associated with eosinophils and mast cells, with few IL-5 or IL-4 immunoreactive CD3+ T cells detectable. However, total IL-4- or IL-5-positive cells detected by IHC were <40% of the total mRNA+ cells, raising the possibility that insufficient cytokine protein accumulated within T cells to enable detection by IHC. We conclude that: 1) in atopic and nonatopic asthma CD8+ T cells, in addition to CD4+ T cells, mast cells and eosinophils express mRNA for IL-4 and IL-5; 2) whereas IL-4 and IL-5 mRNA expression was associated mainly with T cells, immunoreactivity for the corresponding protein products was detectable predominantly in eosinophils and mast cells; and 3) this discrepancy may be partly attributable to the relative insensitivity of double IHC technique that does not allow detection of cytokine protein in T cells where, unlike eosinophils and mast cells, there is no facility for storage and concentration in granules.

Adult↗
PubMed1997

Allergen-induced recruitment of Fc epsilon RI+ eosinophils in human atopic skin.

We have attempted to identify Fc epsilon RI+ eosinophils in cutaneous late-phase reaction in atopic subjects biopsied at 6, 24 and 48 h after the injection of either allergen or a diluent control. Compared to the diluent sites, allergen-injected sites had significantly increased numbers of eosinophils, peaking between 6 and 24 h, of which approximately 20-30% expressed mRNA for the alpha, beta, and gamma chains of Fc epsilon RI, as shown by in situ hybridization. Using either a monoclonal or a polyclonal anti-alpha chain antibody, the Fc epsilon RI alpha protein also co-localized to approximately 50-80% of eosinophils at all time points studied. We also observed a significant correlation (r = 0.89; p = 0.02) between the numbers of Fc epsilon RI+ (997+)/EG2+ eosinophils and the magnitude of the late-phase reaction. Thus, a significant proportion of eosinophils infiltrating the site of allergen-induced allergic tissue reactions in atopic subjects express Fc epsilon. RI. The findings show that high-affinity IgE receptors may play a role in eosinophil secretory processes in vivo.

Allergens↗
PubMed1997

Elevated expression of messenger ribonucleic acid encoding IL-13 in the bronchial mucosa of atopic and nonatopic subjects with asthma.

Local secretion of cytokines by T cells within the bronchial mucosa, with consequent selective eosinophil influx, has been implicated in the pathogenesis of bronchial asthma. The cytokine IL-13 exhibits activities (selective eosinophil vascular adhesion by very late antigen-4/vascular cell adhesion molecule-1 interaction and promotion of IgE synthesis and "T112-type" T cell responses) that may be relevant to this process. We hypothesized that, compared with conditions in control subjects, elevated expression of messenger ribonucleic acid (mRNA) encoding IL-13 is a feature of the bronchial mucosa of both atopic (positive skin prick test result to at least one of a range of common aeroallergens) and nonatopic (negative skin prick test results and serum total IgE concentrations within the normal range) subjects with asthma. With use of a semiquantitative reverse transcriptase-polymerase chain reaction technique, we measured the quantities (relative to beta-actin) of IL-13 mRNA in bronchial mucosal biopsy specimens from atopic and nonatopic subjects with asthma and atopic and nonatopic control subjects. Biopsy specimens from the subjects with asthma, whether the subjects were atopic or nonatopic, had statistically equivalent quantities of IL-13 mRNA relative to beta-actin, and these quantities were significantly elevated compared with those in specimens from both the atopic and nonatopic control subjects (p < or = 0.02 in each case), in which the quantities of IL-13 mRNA relative to beta-actin were also statistically equivalent. The quantities of IL-13 mRNA reflected the numbers of EG2+ eosinophils per unit area of submucosa in the biopsy specimens as determined by immunohistochemistry, which were statistically equivalent in the atopic and nonatopic subjects with asthma and significantly elevated as compared with those in both the atopic and nonatopic control subjects without asthma (p < or = 0.007 in each case). Taking the subjects with asthma as a group, no correlations were observed between the quantities of IL-13 mRNA (relative to beta-actin) and several measures of disease severity. These data are consistent with the hypothesis that IL-13 plays a role in the pathogenesis of both atopic and nonatopic asthma, at least partly through promoting recruitment of eosinophils to the bronchial mucosa, although other factors may be more important in regulating the severity of the disease.

Adult↗
PubMed1997

Upregulation of alpha GM-CSF-receptor in nonatopic asthma but not in atopic asthma.

BACKGROUND: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa. OBJECTIVE: This study was carried out to investigate the expression of alpha GM-CSF receptor (alpha GM-CSFr) messenger RNA and protein in the bronchial mucosa of patients with intrinsic or atopic asthma and of control subjects and to correlate the expression of alpha GM-CSFr to the number of EG2+ cells (eosinophils) and CD68+ cells (macrophages) and pulmonary function. METHODS: Nineteen patients with stable asthma (9 with atopic and 10 with intrinsic asthma) and 22 normal control subjects (12 atopic and 10 nonatopic subjects) were recruited, and FEV1 (percent predicted) and PC20 were measured before bronchoscopy. Endobronchial biopsy specimens were obtained and examined for membrane-bound alpha GM-CSFr by using in situ hybridization and immunocytochemistry. RESULTS: alpha GM-CSFr mRNA- and protein-positive cells were identified in biopsy specimens from all four groups studied. There was no significant difference in the number of cells expressing alpha GM-CSFr mRNA and protein in patients with atopic asthma compared with atopic and nonatopic control subjects. However, the numbers of alpha GM-CSFr mRNA- and protein-positive cells were significantly higher in nonatopic patients with asthma compared with atopic patients with asthma and atopic and nonatopic control subjects (p < 0.001). In the patients with intrinsic asthma, the number of alpha GM-CSFr mRNA-positive cells per millimeter of basement membrane correlated with numbers of CD68+ cells (r2 = 0.87, p < 0.001) but not with EG2+ cells, and colocalization studies demonstrated that 80% of the cells expressing alpha GMCSFr mRNA were CD68+. The expression of GM-CSF was also significantly increased in patients with intrinsic asthma compared with those with atopic asthma and control subjects (p < 0.05). In addition, in intrinsic asthma, there was a correlation between alpha GM-CSFr mRNA and FEV1 (r2 = 0.61, p < 0.05). CONCLUSION: These results demonstrate that elevated numbers of cells expressing alpha GM-CSFr can be detected in nonatopic asthma but not in atopic asthma and suggest that this increased expression is predominantly macrophage-associated and may play an important pathophysiologic role in intrinsic asthma.

Adult↗
PubMed1997

IL-5 secretion by allergen-stimulated CD4+ T cells in primary culture: relationship to expression of allergic disease.

BACKGROUND: IL-5-producing allergen-specific T cells are thought to play a prominent role in the pathogenesis of allergic inflammation. We hypothesized that T cell allergen-driven IL-5 synthesis is elevated in patients with atopic disease as compared with that in atopic patients free of disease and nonatopic control subjects. OBJECTIVES: The purpose of this study was to compare IL-5 and interferon-gamma (IFN-gamma) secretion and proliferation by peripheral blood T cells from sensitized atopic patients with asthma, rhinitis, and no symptoms and from nonatopic control subjects in response to the allergen Dermatophagoides pteronyssinus (Der p) and the control recall antigen Mycobacterium tuberculosis purified protein derivative (PPD). METHODS: To measure allergen-induced IL-5 production and proliferation, we developed a short-term culture technique that required a single antigenic stimulation of freshly isolated peripheral blood mononuclear cells (PBMC). With this technique, we measured Der p- and PPD-induced IL-5 production and proliferation in PBMC from atopic patients with asthma who were allergic to Der p, atopic patients with rhinitis, atopic patients with no symptoms, and a group of nonatopic normal control subjects. In four experiments, CD4+ or CD8+ T cells were depleted from PBMC to confirm that IL-5 synthesis was T cell dependent. RESULTS: T cell IL-5 production, but not IFN-gamma production, in response to Der p was elevated in atopic patients with asthma and atopic patients with rhinitis compared with findings in atopic patients with no symptoms or nonatopic control subjects. IL-5 production was abrogated by depletion of CD4+, but not CD8+, T cells. In subjects with asthma, allergen-driven IL-5 production correlated with bronchial hyperreactivity. Allergen-induced proliferation was also higher in patients with asthma than in atopic subjects with no symptoms or nonatopic controls. T cell IL-5 and IFN-gamma production and proliferation in response to PPD were similar regardless of atopic status or disease. CONCLUSIONS: Elevated IL-5 production is a characteristic of allergen-specific peripheral blood CD4+ T cells from sensitized patients with atopic disease but not atopy per se.

Allergens↗
PubMed1997

Enhanced expression of high-affinity IgE receptor (Fc epsilon RI) alpha chain in human allergen-induced rhinitis with co-localization to mast cells, macrophages, eosinophils, and dendritic cells.

BACKGROUND: IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (Fc epsilon RI) is involved in the pathogenesis of allergen-induced immediate and late responses. OBJECTIVE: We investigated the expression and cellular distribution of Fc epsilon RI in the nasal mucosa after allergen challenge in patients with summer hay fever. METHODS: Fourteen grass pollen-sensitive patients and seven normal control subjects underwent nasal challenge with grass pollen and allergen diluent in random order separated by 2 weeks. Nasal airway caliber was monitored by acoustic rhinometry, and nasal biopsy was performed at 6 hours. Messenger RNA for Fc epsilon RI was determined by using reverse-transcription polymerase chain reaction, and Fc epsilon RI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the alpha subunit. Co-localization of Fc epsilon RI receptors was performed by using double-immunostaining methods. RESULTS: In atopic subjects, there was a significant early decrease in nasal airway caliber, which extended up to 6 hours after allergen challenge. Fc epsilon RI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing Fc epsilon RI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in Fc epsilon RI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of Fc epsilon RI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% Fc epsilon RI+ cells being unidentified. CONCLUSIONS: Our results demonstrate increased Fc epsilon RI expression during allergen-induced rhinitis and highlight a potential target for treatment.

Adult↗
PubMed1997

Membrane-bound and soluble alpha IL-5 receptor mRNA in the bronchial mucosa of atopic and nonatopic asthmatics.

Eosinophilic inflammation and interleukin-5 (IL-5) expression are characteristic features of the bronchial mucosa in asthma. We have investigated the differential expression of membrane and soluble isoforms of alpha IL-5 receptor (alpha IL-5Rm and alpha IL-5Rs) mRNA in asthmatics and in normal control subjects and examined the correlation between alpha IL-5Rm and alpha IL-5Rs expression and the FEV1 and airway hyperresponsiveness. Nineteen subjects with stable asthma (atopic = 9; intrinsic = 10) and 22 control subjects (atopic = 12; nonatopic = 10) were recruited. Endobronchial biopsies were obtained and processed for in situ hybridization and double-staining techniques. There was a significant increase in the number of cells per millimeter basement membrane expressing mRNA for total, membrane-bound, and soluble alpha IL-5R in asthmatics when compared with that in nonasthmatic control subjects (p < 0.001); 93% of the cells positive for alpha IL-5R mRNA were EG2+ve eosinophils. There was no significant difference in the expression of alpha IL-5Rm and alpha IL-5Rs between the atopic and nonatopic asthmatics. The expression of alpha IL-5Rm and alpha IL-5Rs was also nonsignificantly different between the atopic and nonatopic control subjects. However, in the asthmatic subjects, the number of positive cells expressing mRNA for alpha IL-5Rm inversely correlated with FEV1(r2 = 0.89, p < 0.001), whereas the expression of alpha IL-5Rs mRNA directly correlated with FEV1 (r2 = 0.52, p < 0.001). There were no significant correlations between alpha IL-5R isoforms and the methacholine PC20. These results suggest that alpha IL-5R upregulation and differential regulation of alternatively spliced alpha IL-5R mRNA transcripts may influence the eosinophil response and the accompanying changes in airflow limitation in both atopic and nonatopic variants of chronic asthma.

Adult↗
PubMed1997

Relationship between IL-4 and IL-5 mRNA expression and disease severity in atopic asthma.

Atopic asthma is characterized by chronic inflammation of the bronchial mucosa in which eosinophil- and immunoglobulin E (IgE)-dependent mechanisms are believed to be prominent. Therefore, specific proeosinophilic mediators such as interleukin (IL)-5 and essential cofactors for IgE switching in B-lymphocytes such as IL-4 could play a pivotal role in asthma. However, the exact role that individual inflammatory mediators play in the development of the disease in humans is still unknown. Using semiquantitative reverse transcriptase-polymerase chain reaction amplification in bronchial biopsies from 10 atopic asthmatics, we have tested the hypothesis that IL-4 and IL-5 mRNA expression relative to beta-actin mRNA correlates with validated indicators of disease severity. IL-4 and IL-5 mRNA copies relative to beta-actin mRNA were detected in bronchial biopsies from atopic asthmatics. The numbers of IL-5 mRNA copies relative to beta-actin mRNA correlated with disease severity assessed by the Aas asthma score (r = 0.70, p = 0.01), baseline FEV1 (r = -0.94, p = 0.001), baseline peak expiratory flow rate (r = -0.77, p = 0.01), peak expiratory flow rate variability over 2 wk (r = 0.69, p = 0.028), and the histamine PC20 (r = -0.72, p = 0.018). Conversely, the numbers of IL-4 mRNA copies relative to beta-actin mRNA did not correlate with asthma severity, but they positively correlated with total serum IgE concentrations (r = -0.90, p = 0.001). Our present results support the concept that IL-5 may determine asthma clinical expression and severity, and by inference they support the development of IL-5 targeted therapies.

Asthma↗
PubMed1997

Bronchial mucosal expression of the genes encoding chemokines RANTES and MCP-3 in symptomatic atopic and nonatopic asthmatics: relationship to the eosinophil-active cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor, and IL-3.

Intrinsic (nonatopic) asthma is considered to be a distinct pathogenetic variant of asthma since, unlike extrinsic (atopic) asthma, patients are skin-prick test negative to common aeroallergens and have total serum immunoglobulin E concentrations within the normal range. However both atopic and nonatopic asthma are characterized by chronic inflammation of the bronchial mucosa in which eosinophils are prominent and are believed to be associated with local tissue damage. Therefore, specific eosinophil chemoattractants acting in concert with factors which prolong eosinophil survival may at least partly account for selective eosinophil recruitment to the asthmatic bronchial mucosa. The CC chemokines RANTES and monocyte chemotactic protein 3 (MCP-3) are potent eosinophil chemotactic factors, while the cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor (GM-CSF), and IL-3 prolong eosinophil survival. We have tested the hypothesis that elevated numbers of cells expressing mRNA for RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 are present in bronchial biopsies from atopic and nonatopic asthmatics compared with atopic and nonatopic nonasthmatic controls. The technique of in situ hybridization using 35S-labeled riboprobes was employed to detect mRNA+ bronchial mucosal cells. Compared with controls we observed significant increases in the numbers of cells expressing RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 (all P values < 0.001) in atopic and nonatopic asthmatics. These observations support the view that atopic and nonatopic asthma are associated with combined bronchial mucosal expression of CC chemokines (RANTES and MCP-3), together with eosinophil-active cytokines (IL-5, GM-CSF, and IL-3). These cytokines might contribute to the bronchial mucosal accumulation of activated eosinophils in both atopic and nonatopic variants of asthma.

Asthma↗