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Biomedical subjects

I Enander

Publications and source records attributed to I Enander.

At least 19 recordsLinked to original sources
PubMed1992

Indirect evidence of nasal inflammation assessed by titration of inflammatory mediators and enumeration of cells in nasal secretions of patients with chronic rhinitis.

Pathophysiologic mechanisms of perennial rhinitis are poorly understood. The characterization of inflammation was studied in nasal lavage of patients with perennial rhinitis by the enumeration of cells involved in the allergic inflammation and the measurement of six mediators released in nasal secretions to determine whether some mediators were relevant for the etiologic diagnosis and the occurrence of symptoms. Ten healthy subjects and 57 patients with perennial rhinitis were placed into four groups according to the symptoms they presented at the time of the study and the origin of the allergy. Allergy was characterized by the history, skin prick tests to standardized allergens, and RAST. Eosinophil protein X (EPX), tryptase, histamine, myeloperoxidase, prostaglandin D2, and leukotriene C4/D4 (LTC4/D4) were measured in nasal lavage by enzyme assay or radioimmunoassay. Eosinophils and neutrophils were enumerated after cytocentrifugation of the lavage fluid and May Grunwald Giemsa staining. Tryptase, myeloperoxidase and EPX but not histamine levels were increased in all four patient groups. Eosinophils, LTC4/D4, and prostaglandin D2 were significantly (p < 0.001, p < 0.03, and p < 0.01) increased in allergic and symptomatic patients. EPX was significantly increased in symptomatic allergic and nonallergic patients. This study suggests the involvement of mast cells, neutrophils, and eosinophils, but the latter cells appear to have a more prominent role. The importance of EPX and LTC4/D4 in the characterization of chronic symptomatic rhinitis was also observed.

Adolescent↗
PubMed1992

Bronchial exudation of bulk plasma at allergen challenge in allergic asthma.

This study examined plasma exudation into the bronchial lumen after allergen challenge. A novel low-trauma technique was developed to challenge and lavage a medium-sized lingular or middle lobe bronchus. Eleven subjects with challenge-assessed pollen-sensitive asthma were allocated to fiberbronchoscopy in the supine position. In the control bronchus 0.5 ml diluent was instilled. The bronchus was occluded proximally 3 min later by inflation of a balloon, and lavage was carried out twice with 25 ml saline. Incremental doses of allergen solution (0.5 ml) were then instilled in the contralateral lung. The challenge continued until a clearly visible bronchial reaction occurred and was immediately followed by the same lavage as on the control side. The lavage liquids were analyzed for the presence of plasma exudation and mast cell activation indices. On the allergen-challenged side, tryptase, reflecting mast cell activation, was increased by 150% (p < 0.01) compared with the control side. Fibrinogen (mol wt 340,000), reflecting large protein exudation, was increased by 840% (p < 0.05), and N-alpha-tosyl-L-arginine-methyl esterase activity, reflecting both large protein exudation and mast cell activation, increased by 480% (p < 0.01). The level of albumin (mol wt 69,000), the major luminal protein under baseline conditions, increased but not significantly. We conclude that activation of mast cells and luminal entry of little sieved plasma exudates occur early after endobronchial allergen provocation in human subjects with allergic asthma.

Albumins↗
PubMed1991

A new radioimmunoassay for human mast cell tryptase using monoclonal antibodies.

A solid phase immunoradiometric assay was developed for the quantitation of tryptase released from activated human mast cells. Tryptase exhibits a linear dose-response curve over the standard range of 2-50 micrograms/l in buffer, serum, and plasma. The dose-response curve approached a plateau at a tryptase concentration of 100 micrograms/l and exhibited partial inhibition at concentrations above 10,000 micrograms/l. The sensitivity of the assay was 0.2-0.4 micrograms/l, and the intra-assay and interassay coefficients of variation were below 4% at 2 micrograms/l or higher tryptase concentrations. The recovery of known amounts of purified tryptase added to serum ranged from 91 to 115%. Detection of tryptase was evaluated with several body fluids and was accurate in sera, plasma, bronchoalveolar lavage fluid, nasal lavage fluid, and saliva. The concentration of tryptase was examined in serum samples from 100 healthy controls; in each case the level was less than 2 micrograms/l. The immunoassay also was utilized to examine serum levels of tryptase after the onset of a hypotensive reaction in one patient receiving general anesthesia. A maximally elevated level of tryptase (25 micrograms/l) was detected at the first time point, 0.5 h, and elevated levels persisted to 6 h before a return to normal levels was documented at 24 h. Thus, the involvement of mast cell activation in hypotensive subjects can be ascertained by this new tryptase radioimmunoassay.

Animals↗
PubMed1991

Evaluation of mast cell activation (tryptase) in two patients suffering from drug-induced hypotensoid reactions.

Tryptase is predominantly found in mast cells, where it resides in secretory granules, and is released with other mediators during mast cell degranulation. By using a newly developed commercial assay for measurements of tryptase levels we have investigated two cases of suspected drug-induced anaphylaxis. Each patient had a similar clinical presentation, consisting of hypotension and cyanosis after administration of thiopentone and suxamethonium. One of the patients showed a highly elevated serum level of tryptase reaching 26 micrograms/l 30 min after the initial reaction. In addition, slightly elevated levels of specific IgE antibodies to thiopentone were detected. The other patient with similar symptoms showed no increase in the level of tryptase, nor any specific IgE to thiopentone or suxamethonium. These data indicate the patient I suffered from true anaphylaxis, whereas the reaction of patient II occurred by a different mechanism.

Anaphylaxis↗
PubMed1991

Indirect evidence of bronchial inflammation assessed by titration of inflammatory mediators in BAL fluid of patients with asthma.

Bronchial inflammation is a characteristic of asthma that may be examined indirectly by bronchoalveolar lavage (BAL). Nine normal individuals were compared with 38 age-matched adults with asthma of variable severity to appreciate the importance of cell activation in the severity of asthma. The severity of asthma was appreciated by the clinical score of Aas and the pulmonary function of the patients. FEV1 ranged between 35% and 130% of predicted. The indirect activation of eosinophils (EOSs), mast cells, fibroblasts, and neutrophils was examined by the titration of eosinophil cationic protein (ECP), tryptase, hyaluronan (HA), and myeloperoxidase (MPO) by radioimmunoassay in BAL fluid (BALF) and cytology of BALF. In the adults with asthma, there was a significantly increased number of EOSs and a significantly increased level of all mediators but MPO. MPO levels were increased in seven patients only; three of these patients were previous smokers. Only ECP and HA levels were significantly correlated with the severity of asthma. These results demonstrate EOSs, mast cells, and fibroblasts are activated in asthma, whereas the involvement of neutrophils is less clear. There was a significant correlation between ECP and HA levels, suggesting a common activation of EOSs and fibroblasts.

Adult↗
PubMed1991

Increased tryptase levels in suction-blister fluid from patients with urticaria.

The levels of tryptase in the suction-blister fluid from patients with chronic urticaria, urticaria pigmentosa, cholinergic urticaria, urticarial dermographism, prurigo of unknown origin, eczema, psoriasis, atopic dermatitis, and from healthy controls were studied. The blister fluid from controls contained up to 15 micrograms/l of tryptase, whereas that from patients with active urticaria contained greater than 50 micrograms/l. This study demonstrates that patients with urticaria have mast cells that readily release tryptase in both the lesional and non-lesional areas of skin.

Adult↗
PubMed1991

Radioimmunoassay of human eosinophil cationic protein (ECP) by an improved method. Establishment of normal levels in serum and turnover in vivo.

A radioimmunoassay was developed allowing measurement of the cytotoxic cationic ECP. The assay, which has a total incubation time of 3.5 hr, is a double antibody assay with radiolabelled ECP, covering the concentration range of 2-200 micrograms/l. Performance data show a detection limit of less than 2 micrograms/l and a cross-reactivity with eosinophil protein X (EPX/EDN) of less than 0.06%. The coefficient of variation (%) within the measuring range was, within assay 4.8-10.4, and total 6.6-12.0. The assay is useful for measurement in various body fluids including serum, nasal secretions and bronchoalveolar lavage fluid, and dilution of samples prior to analysis was generally not required. Sera from 100 apparently healthy individuals revealed a geometric mean of 6.0 micrograms ECP/l and a range (95%) of 2.3-15.9 micrograms/l. The elimination rate of ECP, t1/2, in vivo was estimated to be 65 min when ECP was measured in serum. Comparisons between this assay and a method previously described showed that the new method is superior with regard to precision and assay procedure.

Blood Proteins↗
PubMed1991

Tryptase in nasal lavage fluid after local allergen challenge. Relationship to histamine levels and TAME-esterase activity.

The activation of mast cells is generally considered to be an important trigger mechanism in the immediate allergic response. This study focused on the determination of three markers of mast cell activation after an allergen challenge. Nasal allergen challenges were performed in 25 subjects with seasonal allergic rhinitis using three allergen doses increasing in 10-fold steps in a standardised nasal lavage model for the subsequent recovery of the markers of mast cell activation. The levels of histamine and tryptase in the nasal lavage fluid were determined using radioimmunoassays, while the TAME-esterase activity was determined using a radiochemical technique. The nasal symptoms obtained on challenge were assessed using a scoring technique. The allergen challenge resulted in significant increases in the levels of all three markers, tryptase, histamine and TAME-esterase. In the individual measurements after the challenges there was a highly significant correlation between the TAME-esterase levels and the tryptase levels (r = 0.71; P less than 0.001), while the generation of histamine and tryptase was not significantly correlated. When comparing the cumulative generation of the three markers, significant correlations were found between all three. Allergen challenges in six non-allergic controls using the same technique did not result in any increase in tryptase levels. The findings suggest that the determination of tryptase in nasal lavage fluid may be a valuable indicator of mast cell activation in the upper airways.

Adult↗
PubMed1991

Inflammatory processes in asthma.

Bronchial inflammation is a characteristic of asthma, but, although postmortem and rare bronchoscopic studies had been performed, it is only after 1980 that many experiments were done. Electron microscopy, immunohistochemistry and molecular biology have enhanced our knowledge. As bronchial biopsies and bronchoalveolar lavage present drawbacks, it is favorable to combine both to obtain the best insights into inflammation. The epithelium is rarely intact in asthmatic patients, the cells being both 'fragile' and activated. Eosinophil inflammation is highly important and likely involved in the damage of the epithelium and submucosa. Airway macrophages and monocytes are present in greater amounts and are activated in the bronchi, and they are certainly involved in the pathogenesis of asthma. Mast cells are activated and some emphasis has been put on lymphocytes. Therefore, asthma appears to be a desquamative bronchitis with mixed cell infiltrate.

Acute Disease↗
PubMed1990

Eosinophilic inflammation in asthma.

BACKGROUND AND METHODS: The importance of eosinophils in the pathogenesis of bronchial asthma is not established. In an attempt to evaluate the role of eosinophilic inflammation in asthma, we compared 10 normal subjects with 43 patients with chronic asthma, 19 of whom had severe disease as assessed by a clinical scoring method described by Aas and by pulmonary-function tests. Eosinophils were counted in peripheral blood and bronchoalveolar-lavage fluid, and in biopsy specimens obtained from the patients and post mortem from 8 subjects without asthma, but not from the 10 normal controls. Eosinophil cationic protein was titrated by radioimmunoassay in the bronchoalveolar-lavage fluid from all subjects and studied by immunohistochemistry in the biopsy specimens. RESULTS: There was a significant increase in the number of peripheral-blood eosinophils in the patients that was correlated with the clinical severity of asthma (P less than 0.001) and pulmonary function (P less than 0.03). Levels of eosinophils and eosinophil cationic protein were increased in the bronchoalveolar-lavage fluid from the patients and were also correlated with the severity of asthma (P less than 0.001 and P less than 0.002, respectively). Hematoxylin-eosin staining of bronchial-biopsy specimens showed that intraepithelial eosinophils were present only in patients with asthma. Immunohistochemical analysis of eosinophil cationic protein revealed that normal subjects had only a few nondegranulated eosinophils deep in the submucosa, whereas all the patients had degranulated eosinophils beneath the basement membrane and among epithelial cells. In some patients there was a relation between the presence of degranulated eosinophils and epithelial damage. CONCLUSIONS: Eosinophilic inflammation of the airways is correlated with the severity of asthma. These cells are likely to play a part in the epithelial damage seen in this disease.

Adult↗
PubMed1989

Origin of the autoreactive anti-type II collagen response. II. Specificities, antibody isotypes and usage of V gene families of anti-type II collagen B cells.

Autoantibodies play an important role in the pathogenesis of type II collagen-induced arthritis in mice. We have earlier reported a high frequency of cells producing anti-CII autoantibodies and a low frequency of cells producing multispecific antibodies, in regional lymph nodes 9 to 11 days after primary immunization with CII. It is shown here that anti-CII antibodies produced during primary immune response are IgG-antibodies mainly of IgG2a, IgG1 and IgG2b subclasses while IgM antibodies dominate primary responses elicited by OVA and denatured CII as analyzed with a large panel of hybridomas. Anti-CII antibodies generated during the primary response recognize at least five different epitopes on the CII molecule. The specificities of these antibodies for various epitopes result from combinational association of products encoded by genes derived from various VH and VK families and/or by the occurrence of somatic mutations. It is suggested that the primary anti-CII autoantibody response involves activation of memory B cells and is in this aspect different from the origin of "natural" autoantibodies.

Animals↗
PubMed1988

Immunological suppression of delayed hypersensitivity responses in mouse lungs as reflected by numbers of mononuclear cells, mast cells and mucus-producing cells.

The suppression of delayed hypersensitivity (DH) in the lung as reflected by the appearance of mononuclear cells, mast cells and mucus-producing cells was studied in Balb/c mice. Immunosuppression was induced by intravenous and peroral administration of picrylsulfonic acid (PSA) in mice subsequently sensitized with picrylchloride (PiCl). The animals exhibited a decreased DH reactivity as assessed by ear thickness increase compared with mice sensitized but not exposed to PSA pretreatment. In mice exposed to PSA intravenously (suppressed) and sensitized with PiCl there was a decrease in the number of mononuclear cells in the lung after challenge, compared to mice sensitized and challenged only. Similarly, the mast cell and mucus-producing cell numbers were slightly lower in animals immunosuppressed intravenously with PSA compared with sensitized mice. Such a decrease in the numbers of mononuclear cells, mast cells and mucus-producing cells in the lung was not seen in animals treated with PSA perorally, although these animals exhibited suppressed DH reaction in the ears. The present results indicate that induction of mononuclear cells and to some extent mast cells and mucus-producing cells in the lung relates to the DH reaction and its regulation.

Animals↗
PubMed1988

Regulation by T cells of delayed hypersensitivity reaction in mouse lung as reflected by mononuclear cells, mast cells and mucus-producing cells.

The appearance of mononuclear cells, mast cells and mucus-producing cells in the lung and their linkage to the development of delayed hypersensitivity (DH) reactions were studied. Adoptive transfer of immune lymph node cells, spleen cells and serum and in vivo treatment with monoclonal antibodies to L3T4-positive T cells in Balb/c mice were performed to investigate the cellular regulation of the number of mononuclear cells, mast cells and mucus-producing cells in the lung. Immune lymph node cells and, to a lesser extent, immune spleen cells from mice sensitized epicutaneously with picrylchloride transferred DH reactions to the recipients as assessed by ear thickness increase after challenge. Serum from sensitized mice was not able to transfer a DH reaction. Cyclophosphamide treatment of donor mice increased the DH reaction in the recipient mice. Adoptive transfer of immune lymph node cells and spleen cells gave a slight increase in the number of mononuclear cells in the lung of recipient mice compared with controls. This weak accumulation of mononuclear cells in the lungs of recipient mice, however, was not accompanied by a consistent increase in the number of mucus-producing cells and mast cells. The number of spleen cells expressing the L3T4 antigen decreased after in vivo treatment with the monoclonal GK1.5 (anti-L3T4) antibody as assessed by immunohistochemistry. This antibody treatment also resulted in an inhibition of the DH reaction and a decrease in the number of mononuclear cells and mucus-producing cells, but not in mast cells in the lung of sensitized and challenged mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Immune regulation of goblet cell development.

In rats, goblet cells were found in the bronchiole epithelium surrounding enlarged lymphoid noduli. The goblet cell number increased with age. Old rats had goblet cells in the columnar epithelium. Immunization with aerosolized antigen increased goblet cell hyperplasia in bronchioli with a luminal diameter of 0.5-1.0 mm. In mice, goblet cell differentiation in the respiratory epithelium was caused by local delayed-type hypersensitivity reactions. Manipulations of the delayed hypersensitivity reactions with immune suppression and depletion of helper T cells eliminated the increase in goblet cell number.

Animals↗
PubMed1987

Regulation of the delayed hypersensitivity reaction in the lung reflected as mononuclear, mast cell and mucus cell appearance after T helper cell depletion and adoptive transfer.

Epicutaneous sensitization with picrylchloride (PiCl) induced a strongly delayed hypersensitivity (DH) reaction in mice. Local challenge in the airways of these mice resulted in increased numbers of mononuclear cells, mast cells and mucus cells. Depletion of T helper cells in vivo by treatment with monoclonal antibody (GK 1.5) inhibited the DH reaction. This treatment also resulted in a decrease in the number of mononuclear and mucus cells in the lung after intranasal challenge. The DH reaction was transferred to recipients with immune lymph node cells and spleen cells from mice sensitized epicutaneously with PiCl. The recipient mice also showed a slight increase in the number of mononuclear cells in the lung after intranasal challenge. These results indicate that T cells are not only involved in the DH reaction but also in the accompanying lung reaction.

Animals↗