Biomedical subjects

J W Lammers

Publications and source records attributed to J W Lammers.

At least 73 records · Page 4Linked to original sources

PubMed1997

Multiple tyrosine residues in the intracellular domain of the common beta subunit of the interleukin 5 receptor are involved in activation of STAT5.

In contrast to the general model of cytokine-induced JAK/STAT signaling, tyrosine phosphorylation of the IL-5R beta chain seems to be dispensable for STAT activation in cells overexpressing exogenous STAT proteins. In this study we expressed IL-5 receptor mutants in 293 cells and studied IL-5-induced endogenous STAT-dependent transcription. Our results indicate that: (a) tyrosine phosphorylation of the IL-5R beta chain is required for endogenous STAT5 activation, (b) multiple tyrosine residues are phosphorylated upon IL-5 stimulation, including Tyr577, Tyr612, Tyr695, and Tyr750, and (c) Tyr612, Tyr695, and Tyr750 are all capable of inducing activation of STAT5, demonstrating a high level of functional redundancy within the IL-5R beta chain.

3T3 Cells↗

PubMed1997

Neutrophil adhesion to fibrinogen and fibrin under flow conditions is diminished by activation and L-selectin shedding.

The adhesion of neutrophils (polymorphonuclear leukocytes [PMNs]) to immobilized fibrinogen/fibrin is mediated by beta2-integrins. However, the influence of physiologic flow conditions on neutrophil adhesion to these surfaces is poorly defined. In this report, the effect of flow and neutrophil activation on adhesion to immobilized fibrinogen and fibrin was examined. For the evaluation of (the distribution of) neutrophil adhesion, real-time video-assisted microscopy and custom-made software were used. Under flow conditions, adherent neutrophils appeared to support the subsequent margination of other neutrophils, thereby enhancing the adherence of these cells to fibrin. Consequently, neutrophils adhered in clusters, especially at higher shear stresses (eg, cluster index 1.4 at shear 80 mPa). Preactivation of PMNs with fMLP (10(-7) mol/L) or 4beta-phorbol, 12-myristate, 13-acetate (PMA; 100 ng/mL) resulted in approximately 50% inhibition of adhesion to fibrin and a more random distribution (cluster index <0.5). L-selectin antibodies or neuraminidase treatment of PMNs also inhibited adhesion and clustering, indicating a role for L-selectin. Under static conditions, no clustering appeared and PMN activation with fMLP or PMA caused threefold and sevenfold increased adhesion, respectively. Under these conditions, anti-L-selectin antibodies or neuraminidase did not affect adhesion. These results indicate that, under flow conditions, adherent neutrophils support adhesion of flowing neutrophils by L-selectin-mediated cell-cell interactions. Preactivated neutrophils, with lowered L-selectin expression, are less susceptible for this interaction. By this mechanism, adhered leukocytes can modulate the recruitment of leukocytes to the vessel wall at sites of inflammation.

Cell Adhesion↗

PubMed1997

Activation of 12-O-tetradecanoylphorbol-13-acetate response element- and dyad symmetry element-dependent transcription by interleukin-5 is mediated by Jun N-terminal kinase/stress-activated protein kinase kinases.

Interleukin-5 (IL-5) is one of the major regulators of eosinophilic granulocytes in vivo. IL-5 exerts its pleiotropic effects by binding to the IL-5 receptor, which is composed of an IL-5-specific alpha chain and a common betac chain shared with the receptors for IL-3 and granulocyte-macrophage colony-stimulating factor. Previous studies have shown that binding of IL-5 to its receptor triggers the activation of multiple signaling cascades, including the Ras/mitogen-activated protein kinase, the phosphatidyl -3'-kinase, and the Janus kinase/signal transducer and activator of transcription pathways. Here we describe that IL-5 activates the serine/threonine protein kinase Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway. We show that IL-5 activates TPA response element (TRE)-dependent transcription in transfection experiments. TRE activation by IL-5 is mediated by a region of the betac (577-581) that is also responsible for activation of JNK/SAPK and for activation of dyad symmetry element (DSE)-dependent transcription. Dominant-negative SAPK or ERK kinase-1 was used to demonstrate that JNK/SAPK activation is necessary for induction of DSE- and TRE-dependent transcription by IL-5, whereas extracellular signal-regulated kinase 2 was not essential for TRE- and DSE-dependent transcription. By contrast, IL-5-induced activation of the tyrosine kinase Janus kinase 2 seems to be a prerequisite for TRE- and DSE-dependent transcription. Taken together, we show for the first time that IL-5 activates kinases of the JNK/SAPK family, and that this activation is linked to IL-5-induced TRE- and DSE-dependent transcription.

Animals↗

PubMed1997

Platelet and fibrin deposition at the damaged vessel wall: cooperative substrates for neutrophil adhesion under flow conditions.

At sites of vessel wall damage, the primary hemostatic reaction involves platelet and fibrin deposition. At these sites, circulating leukocytes marginate and become activated. Adhered platelets can support leukocyte localization; however, the role of fibrin in this respect is not known. We studied the adhesion of human neutrophils (polymorphonuclear leukocytes [PMNs]) to endothelial extracellular matrix (ECM)-bound fibrin and platelets under flow conditions. ECM alone did not show PMN adhesion. ECM-coated cover slips were perfused with plasma to form a surface-bound fibrin network, and/or with whole blood to allow platelet adhesion. Unstimulated PMNs adhered to fibrin at moderate shear stress (20 to 200 mPa). ECM-bound platelets induced rolling adhesion and allowed more PMNs to adhere at higher shear (320 mPa). ECM coated with both platelets and fibrin induced more static and shear-resistant PMN adhesion. PMN adhesion to fibrin alone but not to platelet/fibrin surfaces was inhibited by soluble fibrinogen. Adhesion to fibrin alone was inhibited by CD11b and CD18 blocking antibodies. Furthermore, fibrin formed under flow conditions showed up to threefold higher PMN adhesion compared with fibrin formed under static conditions, due to structural differences. These results indicate that circulating PMNs adhere to fibrin in an integrin-dependent manner at moderate shear stresses. However, at higher shear rates (> 200 mPa), additional mechanisms (ie, activated platelets) are necessary for an interaction of PMNs with a fibrin network.

CD18 Antigens↗

PubMed1997

Bronchial and cutaneous responses in atopic dermatitis patients after allergen inhalation challenge.

BACKGROUND: Atopic dermatitis (AD) is often associated with allergic asthma (AA). Inhalation of allergens influences the activity of AA but the effect on the skin in AD is unclear. OBJECTIVES: We evaluated the degree of bronchial hyperresponsiveness to methacholine in eight AD patients with AA (AD+) and eight AD patients without AA (AD-) and studied bronchial and cutaneous responses after allergen inhalation challenge. METHODS: All patients were treated in hospital for their eczema with tar ointment (pix liquida) and orally administered antihistamines (mean hospital stay 37 days). After clearing of the skin lesions allergen inhalation challenge was performed. Cutaneous responses were studied by measuring the 'Costa' score before and 24 h after allergen inhalation challenge. RESULTS: The median value of the provocative concentration of methacholine causing a 20% fall (PC20 Mch) in forced expiratory volume in 1 second (FEV1) was significantly higher in the AD- group compared to the AD+ group with median values of 10.70 and 0.60 mg/mL, respectively. These values did not change significantly in both groups during hospital stay. After challenge all AD+ patients showed early and late asthmatic responses whereas only four AD patients showed early asthmatic responses (mean values of the maximal fall in FEV1 during the EAR 37%/16% and in PEF during the LAR 27%/4% for AD+ and AD-patients, respectively). The 'Costa' score increased in both groups (mean score before 19.1/24.4 and after challenge 26.8/26.9 for AD+ and AD- patients, respectively). The increase in the AD+ group was significantly higher compared with the AD- group (P=0.016). CONCLUSION: We conclude that allergen inhalation challenge causes a flare up of the skin lesions in atopic dermatitis patients. This was more prominent in atopic dermatitis patients who already suffered from an IgE-mediated allergic inflammation in the lung.

Adolescent↗

PubMed1997

Bronchial and skin reactivity in asthmatic patients with and without atopic dermatitis.

It is unclear whether the presence and severity of atopic dermatitis (AD) is predictive for the occurrence and severity of early and late asthmatic responses to inhaled allergens. The aim of this study was to compare the bronchial effects of allergen inhalation challenge in allergic asthma (AA) and atopic dermatitis. We therefore studied these responses in: nine patients with mild-to-moderate AA without AD; eight patients with mild-to-moderate AA and mild AD; eight patients with severe AD and mild AA; and eight patients with severe AD without AA. Allergen challenge was performed by inhaling doubling doses until the dose provoking a 20% fall in forced expiratory volume in one second (PC20) was reached. The late asthmatic reaction (LAR) was defined as a fall of >20% in peak expiratory flow (PEF) between 3 and 8 h after the challenge. All but four of the patients with severe AD without AA developed an early asthmatic response (EAR). A LAR was seen in all patients with severe AD and mild AA, in four patients with mild AD and mild-to-moderate AA, and in three patients with mild-to-moderate AA without AD. The LAR was most pronounced in patients with a combination of mild AA and severe AD. This could be explained, in part, by a decreased skin sensitivity in these patients, which made the Cockcroft formula for prediction of PC20 allergen less accurate in such patients. We conclude that patients with severe atopic dermatitis and mild asthma are at risk for developing pronounced late asthmatic responses after allergen exposure. This suggests that eosinophils activated in atopic dermatitis also predispose to airway inflammation.

Adolescent↗

PubMed1997

Sustained protection against distilled water provocation by a single dose of salmeterol in patients with asthma.

The long-acting beta2-agonist salmeterol inhibits in vitro the release of inflammatory mediators up to 20 h. These mediators are involved in ultrasonically nebulized distilled water (UNDW)-induced bronchoconstriction. We investigated whether salmeterol provides prolonged protection against UNDW provocation and whether this effect was paralleled by its bronchodilator effects. Nineteen asthmatic patients (mean forced expiratory volume in one second (FEV1) 84.8% predicted, mean provocative concentration of histamine producing a 20% decrease in FEV1 0.65 mg x mL(-1)) participated in this randomized, double-blind, placebo-controlled crossover trial. After measuring baseline FEV1, patients inhaled 50 microg salmeterol or placebo by metered-dose inhaler. FEV1 was measured after 20 and 40 min, and UNDW provocations and FEV1 measurements were performed after 10, 20 and 34 h. Compared to placebo, salmeterol caused marked bronchodilatation from 20 min up to 20 h after inhalation. Salmeterol also provided more than 20 h of protection against UNDW provocation (still more than one doubling dose). Protection beyond the period of bronchodilatation did not occur. Eleven subjects had a significant reduction in provocative dose of UNDW causing a 20% fall in FEV1 (PD20,UNDW) values between 10 and 20 h, at a time when there was still persistent bronchodilation. No correlation existed between changes in FEV1 and changes in PD20,UNDW. From the equations of regression lines between FEV1 and corresponding PD20,UNDW values, it was calculated that only approximately 25% of the afforded protection was explained by bronchodilatation. In conclusion, a single dose of salmeterol induces both bronchodilatation and protection independently of this bronchodilation against a physiological bronchoconstrictor stimulus for more than 20 h.

Administration, Inhalation↗

PubMed1997

Transtracheal oxygen therapy: an effective and safe alternative to nasal oxygen administration.

Transtracheal oxygen therapy (TTOT) improves the efficiency of oxygen delivery and overcomes the discomfort associated with nasal oxygen delivery in patients on long-term oxygen therapy (LTOT). In addition, TTOT improves compliance and quality of life, and may reduce morbidity. Experience with TTOT in Europe is, however, scarce and the safety of TTOT has not yet been completely determined. These were reasons for testing the acceptance, efficacy and safety of TTOT. Patients were selected on the basis of the accepted indications and contraindications for TTOT. In 75 patients (48 males and 27 females) the mean follow-up time was 16 (range 0.5-51.5) months. Compared to nasal cannulae, TTOT caused a reduction in the oxygen flow rate of 47 (33-60)% at rest and a significant increase in the number of hours that oxygen was used. All patients on TTOT used oxygen for at least 20 h x day(-1). Most patients saw the procedure as a minor intervention. It was usually performed on an out-patient basis. In 34 patients, 51 mainly minor complications were seen, and most of these occurred in the first 10 patients. After precautions had been taken, complications occurred less frequently. No patient needed to be hospitalized because of a complication. TTOT had to be stopped in two patients; nevertheless, all patients preferred TTOT to the nasal cannulae. We conclude that transtracheal oxygen therapy is an effective and safe alternative to nasal oxygen administration, provided that it is restricted to a well-defined group of patients and applied by a motivated and experienced group of physicians.

Administration, Intranasal↗

PubMed1996

Cloning and characterization of Fc alpha Rb, a novel Fc alpha receptor (CD89) isoform expressed in eosinophils and neutrophils.

The Fc receptor for IgA (Fc alpha R, CD89) is a transmembrane glycoprotein found on monocytes, macrophages, neutrophils, and eosinophils. Here we describe the characterization of a novel isoform of the Fc alpha R cloned from a human eosinophil cDNA library. This clone, Fc alpha Rb, lacks the exon encoding the transmembrane/intracellular region of wild type Fc alpha R, which is replaced by 23 new amino acids. Expression of Fc alpha Rb mRNA could be detected in eosinophils and neutrophils. IIA1.6 murine pro-B cells transfected with Fc alpha Rb cDNA secrete high levels of the protein, but also a substantial amount of Fc alpha Rb is expressed at the cell membrane. Membrane-bound Fc alpha Rb binds IgA-coated beads equally well as wild type Fc alpha R. Surface expression is not affected by phosphatidyl inositol phospholipase C, indicating that glycosyl phosphatidyl inositol-linkage of Fc alpha Rb is not likely. In IIA1.6 cells expressing Fc alpha Rb and FcR gamma, which is necessary for signal transduction by wild type Fc alpha R, no tyrosine phosphorylation or Ca(2+)-mobilization could be observed after receptor cross-linking. These results indicate that Fc alpha Rb is likely to have a different function than wild-type Fc alpha R receptor.

Amino Acid Sequence↗

PubMed1996

[Causative role of infections with viruses or atypical pathogens in acute exacerbations of chronic bronchitis less frequent than expected].

OBJECTIVE: To determine the prevalence of viruses and atypical pathogens as causes of acute severe exacerbations of chronic bronchitis. DESIGN: Retrospective. SETTING: University Hospital Utrecht, the Netherlands. METHODS: In 4 studies with 305 patients with severe type-1 exacerbations (increase of dyspnoea, of sputum volume and of sputum purulence) serological tests for viral and atypical pathogens were performed. RESULTS: Positive serology for viral infections was seen in 18 (5.9%) patients and for the atypical pathogens in 12 (3.9%) patients. CONCLUSIONS: Since viruses and atypical pathogens are the cause of the exacerbation in only few cases, clinical signs can be used in decision-making whether or not to prescribe antibiotics in acute exacerbations of chronic bronchitis.

Anti-Bacterial Agents↗

PubMed1996

STAT3beta, a splice variant of transcription factor STAT3, is a dominant negative regulator of transcription.

The 89-kDa STAT3 protein is a latent transcription factor which is activated in response to cytokines (interleukin (IL)-5 and -6) and growth factors (epidermal growth factor). Binding of IL-5 to its specific receptor activates JAK2 which leads to the tyrosine phosphorylation of STAT3 proteins. Here we report the cloning of a cDNA encoding a variant of the transcription factor STAT3 (named STAT3beta) which was isolated by screening an eosinophil cDNA library. Compared to wild-type STAT3, STAT3beta lacks an internal domain of 50 base pairs located near the C terminus. This splice product is a naturally occurring isoform of STAT3 and encodes a 80-kDa protein. We found by reconstitution of the human IL-5R in COS cells that like STAT3, STAT3beta is phosphorylated on tyrosine and binds to the pIRE from the ICAM-1 promoter after IL-5 stimulation. However, STAT3beta fails to activate a pIRE containing promoter in transient transfection assays. Instead, co-expression of STAT3beta inhibits the transactivation potential of STAT3. These results suggests that STAT3beta functions as a negative regulator of transcription.

Amino Acid Sequence↗

PubMed1996

Platelet-dependent primary hemostasis promotes selectin- and integrin-mediated neutrophil adhesion to damaged endothelium under flow conditions.

Co-localization of blood platelets and granulocytes at sites of hemostasis and inflammation has triggered an intense interest in possible interactions between these cellular processes and induction of vessel wall injury. Leukocyte adhesion to endothelial cells decreases with increasing shear and is dependent on an initial rolling phase mediated by selectins. We hypothesized that flow-dependent platelet adhesion at an injured vessel wall will lead to P-selectin expression by platelets, thus mediating leukocyte co-localization. A perfusion chamber was used in which flowing whole blood induced platelet adhesion to a subendothelial matrix (ECM) of cultured human umbilical vein endothelial cells (HUVEC). We compared neutrophil (polymorphonuclear leukocyte [PMN]) interactions with HUVEC and their ECM with and without adhered platelets. PMNs adhered predominantly to ECM-adhered platelets and not to endothelial cells. ECM alone did not support PMN adhesion under flow conditions. PMN adhesion to unstimulated HUVEC was only substantial at low shear (up to 200 cells/mm2 at shear stress 80 mPa). In marked contrast, PMN adhesion to ECM-adhered platelets was dramatically increased, and adhesion was demonstrated at much higher shear stress (up to 640 mPa). Studies with specific antibodies showed that the platelet-dependent neutrophil adhesion was selectin-mediated. Inhibition of P-selectin caused a marked inhibition of adhesion at high shear stress, whereas the role of leukocyte L-selectin was less pronounced. beta2-Integrin-blocking antibodies inhibited static neutrophil adhesion. fMLP induced L-selectin shedding from leukocytes, resulting in decreased leukocyte adhesion. In conclusion, platelet-dependent hemostasis at the ECM appears to be a powerful intermediate in neutrophil-vessel wall interactions at shear stresses that normally do not allow neutrophil adhesion to intact endothelium.

Antibodies, Monoclonal↗

PubMed1996

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease): new insights in pathogenesis, complications, and treatment.

Hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, is a hereditary disorder leading to easily bleeding telangiectases on skin and mucosal surfaces, and it is associated with the presence of arteriovenous malformations (AVMs) in multiple organ systems. These AVMs may cause serious complications when they are located in the lungs, liver, or brain. The prevalence of AVMs in patients with HHT might be higher than previously estimated. Nowadays, treatment is often possible. In some families, mutations have been shown in the gene encoding for a transforming growth factor receptor, endoglin. Genetic heterogeneity has been demonstrated, suggesting involvement of other transforming growth factor receptors. This might explain the variable clinical expression of the disease. In view of the high prevalence of pulmonary and cerebral AVMs, all patients with HHT should be screened for their presence, and relatives of patients with HHT should be investigated for presence of the disease.

Humans↗

PubMed1996

Mechanisms involved in eosinophil migration. Platelet-activating factor-induced chemotaxis and interleukin-5-induced chemokinesis are mediated by different signals.

Eosinophils play an important role in the pathogenesis of allergic diseases such as allergic asthma. Eosinophil migration in vitro can be divided into directed migration, or chemotaxis, and random migration, or chemokinesis. Here, we studied intracellular signals involved in eosinophil migration in vitro induced by platelet-activating factor (PAF) and interleukin-5 (IL-5), applying a Boyden chamber assay. Migration induced by PAF (10(-11)-10(-6) M) largely consisted of chemotaxis with some chemokinesis, whereas IL-5 (10(-12)-10(-8) M) induced chemokinesis only. Eosinophils were depleted from intracellular and extracellular Ca2+ to study the role of Ca2+ as a second messenger. Ca2+ depletion did not change PAF-induced chemotaxis, however, IL-5-induced chemokinesis was inhibited. Interestingly, PAF, but not IL-5, induced changes in [Ca2+]i. This rise originated mainly from internal stores. Inhibition of protein kinase A by H-89 and protein kinase C by GF 109203X had no effect on both forms of eosinophil migration. Addition of the protein kinase inhibitor staurosporine significantly inhibited IL-5-induced chemokinesis. Inhibition of tyrosine kinases by herbimycin A completely blocked IL-5-induced chemokinesis. PAF and IL-5-induced actin polymerization was studied to compare migratory responses with a migration-associated intracellular response. Ca2+ depletion significantly enhanced PAF-induced (10(-8) M) actin polymerization, whereas IL-5-induced actin polymerization was not influenced. Addition of staurosporine led to an increase in F-actin. Subsequent addition of PAF or IL-5 resulted in an additive increase in F-actin content. In summary, both forms of eosinophil migration are protein kinase A and protein kinase C independent. In contrast to PAF-induced chemotaxis, Il-5-induced chemokinesis was found to be completely Ca2+ and tyrosine kinase dependent.

Actins↗

PubMed1996

Optimal particle size for beta 2 agonist and anticholinergic aerosols in patients with severe airflow obstruction.

BACKGROUND: The optimal particle size of a beta 2 agonist or anticholinergic aerosol in patients with severe airflow obstruction is unknown. METHODS: Seven stable patients with a mean forced expiratory volume in one second (FEV1) of 37.9% of the predicted value inhaled three types of monodisperse salbutamol and ipratropium bromide aerosols with particle sizes of 1.5 microns, 2.8 microns, and 5 microns, respectively, and a placebo aerosol. The volunteers inhaled 20 micrograms salbutamol and 8 micrograms ipratropium bromide, after which lung function changes were determined and analysed with repeated measurements analysis of variance (ANOVA). RESULTS: Greater improvements in FEV1, specific airway conductance (sGaw) and maximum expiratory flow at 75%/50% of the forced vital capacity (MEF75/50) were induced by the 2.8 microns aerosol than by the other particle sizes. CONCLUSIONS: In patients with severe airflow obstruction the particle size of choice for a beta 2 agonist or anticholinergic aerosol should be approximately 3 microns.

Adrenergic beta-Agonists↗

PubMed1996

Altered composition of urinary heparan sulfate in patients with COPD.

In patients with emphysema the integrity of the extracellular matrix (connective tissue skeleton) is compromised. In this study we analyzed glycosaminoglycans, which are main constituents of this matrix, in urines from patients with chronic obstructive pulmonary disease (COPD)/emphysema. Glycosaminoglycans (GAGs) were purified by anion exchange chromatography and quantified using the 1,9-dimethylmethylene blue assay. Heparan sulfate (HS) was assayed using three different chemical methods: digestion with heparitinase or with nitrous acid and by use of an adapted 1,9-dimethylmethylene blue assay. A specific epitope on the HS molecule, defined by the monoclonal antibody JM403, was determined using an inhibition enzyme immunoassay. In patients with COPD total urinary glycosaminoglycan and HS content were not altered. The JM403 epitope of HS, however, was greatly decreased in patients (0.6 versus 4.1 units/mg creatinine for control subjects, p < 0.0001). A similar pattern was observed when patients with bronchial carcinoma with and without emphysema were compared (0.4 versus 2.4 units/mg creatinine respectively, p < 0.0005). Patients with sarcoidosis did not show a decreased epitope content. These results indicate a structural change or an altered processing of the HS molecule in patients with emphysema. Taking into consideration the importance of HS for the stability of the alveolar extracellular matrix, this change may be associated with the pathogenesis of emphysema.

Adult↗

PubMed1996

Association between Wegener's granulomatosis and Staphylococcus aureus infection?

Two patients are presented with Wegener's granulomatosis (WG) and lower respiratory tract infections with Staphyloccus aureus (SA). It is posulated that there is a relationship between the infection and the induction or relapse of the disease. We suggest that bronchoalveolar lavages should be performed in cases of suspected WG to identify SA-infections. The co-existence of WG and SA support the reported beneficial effects of sulfamethoxazole/trimethoprim, but needs further evaluation in patients with and without SA-infection of the airways.

Anti-Bacterial Agents↗

PubMed1996

Eosinophil cationic protein and immunoglobulin levels in bronchoalveolar lavage fluid obtained from patients with chronic eosinophilic pneumonia.

In chronic eosinophilic pneumonia (CEP), histopathological evidence exists for the degranulation of eosinophils and the release of various toxic proteins. In vitro studies have demonstrated the degranulation of eosinophils in response to aggregated and complexed immunoglobulins. The aims of this study were to investigate: 1) whether the eosinophil cationic protein (ECP) and immunoglobulin (Ig) levels in bronchoalveolar lavage (BAL) fluid from patients with CEP are increased compared to those of healthy controls; 2) and whether a relationship is present between immunoglobulin levels and ECP levels in BAL fluid from patients with CEP. The BAL from 12 patients with CEP was selected, retrospectively, from all BAL analyses performed in our centre between 1986 and 1992. ECP levels were measured using a radioimmunoassay in BAL fluid of patients with CEP and 10 healthy controls. ECP levels and immunoglobulin levels in BAL fluid from patients with CEP were found to be elevated compared to controls (p < 0.001). A relationship was found between IgA levels and ECP levels in BAL fluid from patients with CEP (r = 0.72; p = 0.043). In conclusion, eosinophil cationic protein and immunoglobulin levels were found to be increased in bronchoalveolar lavage fluid from patients with chronic eosinophilic pneumonia. The relationship found between immunoglobulin A levels and eosinophil cationic protein levels may suggest that immunoglobulin A could be involved in the degranulation of eosinophils in chronic eosinophilic pneumonia.

Blood Proteins↗