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Biomedical subjects

H M Jansen

Publications and source records attributed to H M Jansen.

At least 163 records · Page 9Linked to original sources

Primary cell-mediated immune response in bronchial asthma. Relationship between primary in vitro and in vivo cell-mediated and antibody responses in patients with asthma and healthy controls.

Eleven patients with asthma and ten sex and age matched healthy controls were immunized with the primary immunogen Helix pomatia Haemocyanin (HPH). The amplitude and the kinetics of in vitro cell-mediated immune response were measured by HPH-induced lymphocyte proliferation. Lymphocytes were also challenged in vitro with mitogens and recall antigens. In vivo cell-mediated immunity was determined by inducing delayed type hypersensitivity reactions with HPH. Anti-HPH antibody responses in the IgE, IgG and IgM classes were measured to gain an insight into the relation between cell-mediated and humoral immune responses in patients with asthma and healthy controls. The in vitro and in vivo cell-mediated response and the IgM antibody response did not differ between patients with asthma and controls. The IgE and IgG antibody responses, however, were increased in the patients. IgM antibody response correlated with both the in vitro and in vivo cell-mediated response (R = 0.45, P less than 0.05). IgE and IgG antibody responses however were not correlated with cell-mediated responses. These data suggest that the primary abnormality in immune regulation in patients with asthma concerns the control of the IgE and IgG class antibody responses.

Adult↗

The primary immune response in bronchial asthma. I. A kinetic study of Helix pomatia hemocyanin-specific IgE, IgG, IgA, and IgM antibody responses in patients with asthma and in matched controls.

Eleven asthmatic patients with allergy and 10 age- and sex-matched controls were immunized subcutaneously with 1 mg of the primary test immunogen Helix pomatia hemocyanin (HPH). The HPH-specific IgE, IgG, IgA, and IgM antibody response was measured by ELISA. After immunization, not only the IgE but also the IgG antibody response of the patients exceeded that of the controls (p less than 0.01). IgA antibody response also tended to be higher in the asthmatic group (NS). Except for an earlier rise after immunization in the asthmatic group (p less than 0.05), IgM peak responses did not differ significantly between the two groups. There was a high correlation (r = 0.9) between the magnitude of the IgE and the IgG antibody responses. IgM antibody response did not correlate with the response in any of the other antibody classes measured. The total serum immunoglobulin concentration was determined before immunization. Only the IgE level was significantly higher in the asthmatic group (p less than 0.01). No correlation was found between serum immunoglobulin concentrations and the magnitude of the HPH-specific antibody response in the same class. We conclude that the increased humoral responsiveness of asthmatic patients with allergy is not restricted to the IgE class nor to a limited number of commonly encountered antigens (allergens).

Adult↗

Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions.

In order to obtain information about the nature of the local inflammatory process during late asthmatic reactions after house dust mite inhalation, bronchoalveolar lavage (BAL) was performed in 19 asthmatic patients and in 5 control subjects. In 16 of the patients and in all of the control subjects, BAL was performed 6 to 7 h after allergen inhalation. Six of the patients showed early and late asthmatic reactions (LAR), 5 showed early reactions, and 5 showed no reactions. Bronchoalveolar lavage was also performed shortly after the early reaction in 5 patients with documented combined early and late reactions. In the BAL fluid of the patients with LAR, a significant eosinophilia (0.01 less than p less than 0.05) was found compared with that in all other patient groups and with that in the control subjects. This bronchoalveolar eosinophilia was accompanied by elevated eosinophil cationic protein/albumin ratio in the BAL fluid (0.01 less than p less than 0.05). These observations suggest that eosinophils and their mediators might be involved in the development of LAR after allergen inhalation.

Adult↗

Lung allograft rejection in the rat. V. Inhaled stimuli aggravate the rejection response.

Responses to inhaled stimuli in lung allografts might intensify the rejection response against the grafts. Therefore, we investigated the rejection of lung allografts in rats exposed to various degrees of stimuli via the airways. A group of these rats was selectively decontaminated to eliminate infection of the graft. Stimuli provided were intrabronchially injected purified protein derivative in sensitized rats and dust inhaled from sawdust used as bedding in the cages. Both intrabronchially injected purified protein derivative and stimuli inhaled from sawdust were found to aggravate lung allograft rejection, thus shortening mean graft survival from 32 to 11 days. Selective decontamination did prolong lung graft survival (p less than 0.05) because it lowered the overall immune reactivity of the recipient rats. For clinical lung transplantation, these observations suggest that patients should be selectively decontaminated and protected against inhalation of exogenous stimuli during a rejection episode.

Adjuvants, Immunologic↗

Amiodarone pneumonitis: three further cases with a review of published reports.

Three further patients are presented who developed evidence of a parenchymal pulmonary disturbance in the course of treatment with amiodarone. In one case the progress of the condition was rapid and ended fatally. Histological examination of the lungs showed evidence of diffuse alveolar damage. The concentration of amiodarone was from four to seven times higher in the lungs than in other organs studied. The concentration of the metabolite desethylamiodarone in the lungs was even higher in relation to other organs studied. The remaining two patients showed a more insidious onset and improvement after withdrawal of amiodarone and treatment with corticosteroids. Gallium 67 scintigraphy appeared to be a sensitive indicator of this adverse effect. Review of published reports revealed 35 cases of amiodarone pneumonitis, including the cases reported in this study. In 11 instances the dose of amiodarone was 400 mg or less. The onset was either insidious or rapidly progressive. Exertional dyspnoea was always present and a nonproductive cough, hypoxaemia, a raised erythrocyte sedimentation rate and diminished carbon monoxide diffusing capacity (transfer factor) were usually noted. Chest radiographs showed either a reticular pattern or diffuse patchy alveolar infiltrates. Discontinuation of amiodarone and an institution of corticosteroid treatment was usually followed by improvement or resolution.

Adult↗

Steroid-responsive interstitial pulmonary disease in systemic sclerosis. Monitoring by bronchoalveolar lavage.

We describe a 38-year-old woman with systemic sclerosis of recent onset and progressive dyspnea. Studies of pulmonary function revealed a restrictive ventilatory disorder with decreased diffusing capacity. Interstitial fibrosis and infiltration with lymphocytes and plasma cells with formation of follicles were observed in the lung biopsy. Analysis of fluid from bronchoalveolar lavage showed an increase in the total number of cells, with a relative increase in neutrophils. Also, the relative amount of the immunoglobulins, IgG and IgM, was increased. During corticosteroid treatment, rapid improvement of pulmonary volumes occurred, together with disappearance of neutrophils and an increase in the percentage of lymphocytes in the lavage fluid. Later on, the total number of cells in the fluid from bronchoalveolar lavage and the percentage of lymphocytes reached normal values. Bronchoalveolar lavage may be of value in assessing and monitoring pulmonary disease in patients with systemic sclerosis.

Adult↗

Local immune complexes and inflammatory response in patients with chronic interstitial pulmonary disorders associated with collagen vascular diseases.

Evidence is accumulating that the lung injury in collagen vascular diseases (CVD) is triggered by immune complexes (IC). These reactions are neutrophil- and complement-dependent. The direct, in vivo phagocytosis of IC by bronchoalveolar lavage polymorphonuclear leucocytes (BAL-PMN), was studied in 15 patients with CVD and chronic interstitial pulmonary disorders. A control group (NC) consisted of nine healthy, non-smoking volunteers. Concentrations of soluble IC were measured using a solid phase Clq ELISA assay, and an indirect, in vitro phagocytosis assay performed using healthy donor PMN. Local Ig and C3 concentrations were determined using laser nephelometry and Mancini techniques, respectively. In the patient group the total cell counts/ml recovered lavage fluid and the proportions of BAL-PMN were significantly increased (P less than 0.05 and P less than 0.001, respectively). The influxed PMN showed high scores of direct IC phagocytosis. Soluble IC concentrations were significantly increased compared with controls (all comparisons P less than 0.01), and in the BAL relatively higher than in the serum of the same patients. Concomitantly high local IgG concentrations were observed. Corticosteroid treatment gave rise to significantly decreased total cell counts (P less than 0.05), and proportions of BAL-PMN (P less than 0.001), a decrease in the in vivo IC phagocytosis (P less than 0.05), in the indirect, in vitro IC phagocytosis, in the Clq ELISA and in the local IgG concentrations (all comparisons P less than 0.001). We concluded that locally formed IC may induce an inflammatory response in the lungs of patients with CVD.

Adult↗

Simultaneous occurrence of pulmonary interstitial fibrosis and alveolar cell carcinoma in one family.

The coexistence of interstitial pulmonary fibrosis and alveolar cell carcinoma is well known. The familial occurrence of a combination of these two entities, however, is very rare. We present a family of which five members had diffuse interstitial pulmonary fibrosis. Three of them had in addition alveolar cell carcinoma. In a sixth family member, evidence of alveolar cell carcinoma was present without proven interstitial fibrosis. An autosomal dominant trait is suggested as the mode of inheritance of both interstitial fibrosis and alveolar cell carcinoma in this family.

Adenocarcinoma, Bronchiolo-Alveolar↗

[Arsenic poisoning through the roof. A case of arsenic poisoning in cattle].

A case of arsenic poisoning in cattle is reported, in which six out of fifteen animals died. The source of poisoning was traced to a substance in the loft of the hay-barn, which probably consisted of the remains of a pesticide which had been there for several years. This had become liquefied as the result of a leak in the roof and had found its way into the hay. The arsenic content of the substance ranged from 17 to 37 per cent, that of the hay being up to 0.3 per cent. The concentration of arsenic in the organs, blood, faeces and urine of the animals were indicative of poisoning. The main clinical findings consisted in profuse diarrhoea, loss of appetite, muscular weakness and an ataxic gait. Dehydration set in later and the animals became deeply soporous. Symptomatic treatment was mainly directed against dehydration, hypoglycaemia and hypocalcaemia. The greater part of the animals gradually recovered. Marked hyperaemia of the abomasal mucosa and, to a less extent, hyperaemia of the small and large intestines was observed on post-mortem examination.

Animal Feed↗

Adjuvant immunotherapy with BCG in squamous cell bronchial carcinoma.

Fifty-four patients with evidence of locally advanced primary squamous cell bronchial carcinoma (SCC), and three patients with adenocarcinoma (AC) had lung resection to remove all the visible tumour. After operation an randomly chosen group of 20 SCC patients received adjuvant BCG immunostimulation by scarifications (BCG-A). An additional group of 14 SCC patients, and three AC patients received initially intrapleural BCG treatment and subsequently scarifications (BCG-B). A control group of 20 SCC patients received no adjuvant treatment. Follow-up studies were done from three to 51 months. Immune reactivity was monitored in vivo with PPD skin tests in 33 treated and in 18 untreated patients. In both the BCG-treated SCC groups recurrence rates decreased statistically significant during follow-up (BCG-A; six to 51 months, p less than 0.001; BCG: 6-9 months, p less than 0.01 and nine to 24 months, p less than 0.001). However, no difference could be demonstrated between systemic and combined systemic and intrapleural treatment. The three BCG-treated AC patients all relapsed within nine months of follow-up. A pronounced increase in skin reactivity to PPD was seen six months after surgery in the BCG-treated patients (BCG-A, p less than 0.001; BCG-B, p less than 0.01), whereas the control patients remained anergic after surgery. This improved immune reactivity went in parallel with a more favourable outcome of the individual patients (BCG-A, p less than 0.02; BCG-B, p less than 0.05). It is concluded that adjuvant BCG immunotherapy used in strongly selected patients with minimal residual squamous cell bronchial carcinoma improves the prognosis. Intrapleural treatment did not improve the prognosis further. A favourable clinical outcome was mirrored by an increase in cellular immune reactivity.

Adenocarcinoma↗

The primary immune response of patients with different stages of squamous-cell bronchial carcinoma.

Using the indirect ELISA technique, the IgM, IgG, and IgA antibody response to the primary test immunogen Helix pomatia haemocyanin (HPH) was studied in 30 patients with various clinical stages of primary squamous-cell bronchial carcinoma and compared with values obtained in 15 controls matched for sex, age, smoking habit, and presence of chronic bronchitis. Patients with disseminated disease (stage III) showed a significant decrease in IgG and IgA antibody response (P less than 0.001), but IgM antibodies were relatively high and not different from the controls. Although normal IgG and IgA antibody titres were found at the peak response two weeks after immunisation in patients with localised disease (stage I), these antibody titres showed a significantly more rapid decline after serial investigations at eight and 14 weeks after immunisation compared with the controls (P less than 0.001) despite total removal of the tumour burden at c four weeks after immunisation. In-vitro HPH-induced lymphocyte transformation was considerably decreased in state I patients (P less than 0.01) as well as in stage III patients (P less than 0.001). The results suggest that patients with squamous-cell bronchial carcinoma develop impaired T-cell function, which gives rise to a defective antibody response and in-vitro lymphocyte reactivity to the T-cell dependent primary immunogen HPH.

Aged↗