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S Lorimer

Publications and source records attributed to S Lorimer.

5 recordsLinked to original sources
PubMed1998

Adhesion molecule expression in the lung: a comparison between normal and diffuse interstitial lung disease.

Cellular adhesion molecules are crucial determinants of the migration of immune effector cells to the tissues. In chronic inflammatory diseases, upregulation of the expression of these molecules may contribute to the persistent inflammatory process. The aim of this study was to determine whether there is evidence of adhesion molecule expression in chronically inflamed lung. Soluble adhesion molecules in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunoassay in 54 patients with chronic interstitial lung diseases and 16 normal controls. Adhesion molecule expression in fibrosing alveolitis (FA) lung and in control lung was assessed using immunohistology and reverse transcription-polymerase chain reaction (RT-PCR) amplification. Soluble intercellular adhesion molecule-1 (ICAM-1) was detected in all but two subjects. There was no difference in ICAM-1 concentration between disease groups and normal subjects. In contrast, soluble E-selectin was detected in 17 of the 70 subjects and was significantly associated with the presence of lung disease (p=0.0173). Furthermore, the presence of soluble E-selectin was associated with a raised lymphocyte percentage in BALF (p=0.0069). Soluble VCAM was only detected in five of the 70 subjects (two normals, three patients). There was no difference in adhesion molecule expression in lung parenchyma between FA and controls assessed by immunohistology and RT-PCR. The most striking finding of our study was the universal expression of intercellular adhesion molecule-1 in both normal and diseased lung, emphasizing the important role of the lung in immune function. Upregulation of E-selectin may contribute to inflammatory cell accumulation in chronic interstitial lung diseases.

Adolescent↗
PubMed1995

Fibrosing alveolitis in systemic sclerosis: increase in memory T-cells in lung interstitium.

Despite the large numbers of T-cells present in the lungs in fibrosing alveolitis, their pathogenetic role is poorly understood. If these cells are involved in pathogenesis, they are more likely to express the CD45RO+ memory phenotype. To test this hypothesis, open lung biopsies from patients with fibrosing alveolitis associated with systemic sclerosis (FASSc) were compared with grossly normal lung taken from the periphery of lobes resected for lung cancer. Biopsies from eight patients with FASSc were compared with tissue from seven cancer controls. Paraffin sections were stained with a polyclonal anti-CD3 antibody for T-lymphocytes, monoclonal anti-CD45 antibody for leucocyte common antigen, and monoclonal anti-CD45RO antibody for primed T-lymphocytes. Staining was assessed quantitatively by computerized image analysis: in each case, the number of immunopositive cells was related to alveolar wall area and alveolar wall length. Mean alveolar wall thickness was increased in patients with FASSc (60.7 +/- 24.0 microns) compared with cancer controls (15.7 +/- 5.3 microns). Patients with FASSc had greater numbers of CD45+, CD3+ and CD45RO+ cells.mm-1 alveolar wall length compared with the controls. CD45RO+ cells made up 77% (median) of the CD3+ cells in FASSc, and their numbers per unit alveolar wall length were positively associated with alveolar wall thickness (r = 0.61). In conclusion, in fibrosing alveolitis of systemic sclerosis, most interstitial T-lymphocytes express the phenotype of memory cells; these cells are likely to be involved in the persistent inflammatory process.

Adult↗
PubMed1995

Airway and lung elastic fibre is not reduced in asthma nor in asthmatics following corticosteroid treatment.

By morphometric investigation of the relative content of elastic and collagen fibres, we have tested the hypothesis that loss of elastic fibres in the conducting airways and lung parenchyma may reduce tissue elastic recoil, resulting in increased airway maximal closure and apparent increased responsiveness. The study groups comprised: Group A (n = 11) with relatively mild atopic asthma using inhaled bronchodilators prn (i.e. short-term corticosteroids users); Group B (n = 9) with more severe asthma requiring inhaled bronchodilators regularly, and daily inhaled glucocorticosteroids (i.e. longterm corticosteroid users); Group C (n = 12) normal healthy workers. Bronchial biopsy samples were taken from three sites from the left lung. Group A biopsy samples were taken before and after a 4 wk treatment period with inhaled corticosteroids (200 micrograms b.i.d.) and the relative elastic and collagen fibre content of a subepithelial zone was determined from electron micrographs. In a parallel study, the relative proportion of elastic fibre in post mortem lung tissue samples (inner aspect of the bronchial wall, alveolar wall, and points of attachment of surrounding alveoli to intrapulmonary bronchi) from subjects suffering a fatal asthma attack (n = 11), and non-asthmatic suffering sudden death (n = 9), were determined using Miller's elastic and eosin counterstain for light microscopy. In bronchial biopsies of normal subjects, 4.6 (SEM 1.1)% of subepithelial connective tissue was elastic fibre, similar to mild asthmatic subjects, 1.9 (SEM 0.48)%. Neither short-term (4 weeks) inhaled corticosteroid (200 micrograms b.i.d.) nor long-term (< 6 months) treatment with variable doses of inhaled steroids (100-1000 micrograms b.i.d.) significantly altered the elastic or collagen content of the tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

The relationship between pulmonary interstitial emphysema and clinical features in fatal asthma.

Using retrospective histological material and clinical data from the New Zealand National Asthma Mortality Study, we investigated whether there was a relationship between the presence of pulmonary interstitial emphysema (PIE) and different clinical features in fatal asthma, in particular precipitous asthma death. Histological evidence of PIE was determined in sections from 12 of the 60 patients who had died from asthma who fulfilled the pathological criteria for inclusion in the study. No significant correlation was found between the presence of PIE and the different clinical features examined. For example, of the 13 cases with precipitous fatal asthma (i.e., death occurred within 10 min of the onset of the attack), only two had PIE. This suggests that PIE is not an uncommon histological feature of fatal asthma and may, in fact, significantly contribute to an asthma death, but its presence does not appear to be associated with the specific clinical subgroups studied here.

Asthma↗