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Notes: The importance of bronchial epithelial shedding in the pathogenesis of asthma has been highlighted by many investigators as a potential mechanism for bronchial hyperresponsiveness. It has been suggested that this disruption is the result of cytotoxic injury leading to shedding of damaged cells. To investigate whether damaged ciliated epithelial cells can be detected within the bronchial mucosa. we used tannic acid which only permeates disrupted cellular membranes, as a marker of cell damage. Bronchial biopsies from seven asthmatic and six normal subjects, were processed in tannic acid prior to preparation and sectioning for electronmicroscopic examination. Ciliated epithelial cells staining darkly with tannic acid were seen to comprise a similar proportion of the intact portion of bronchial epithelium in both normals and asthmatics (medians 31% vs 40%). We suggest that ciliated epithelial cells are not shed from the bronchial mucosa immediately after damage and that mechanisms other than granulocyte-mediated cytotoxicity may account for epithelial disruption in asthma, possibly involving the selective damage or reduced expression of intraepilhelial intercellular adhesion molecules.

Notes: As part of a larger epidemiological study, 114 children with respiratory symptoms, born between 1978 and 1980, were skin-prick tested to Dermatophagoides pteronyssinus (DP), mixed grass pollens (G) and cat dander (C), and to histamine and saline controls (Bencard, U.K.) using 1 mm prick-lancets (Dome/Hollister-Stier), between July and September 1987 and again in October 1989. A weal ≥ 2 mm to one or more allergens was regarded as a positive result. Each child was tested by the same investigator on each occasion, using similar techniques. Three children were excluded from analysis as they had failed to respond to histamine testing on one of the two occasions. In 1987, of the 111 children analysed, 58 (52%) children were skin-test positive, and 53 (48%) skin-test negative, while in 1989 62 (56%) were positive and 49 (44%) negative. Twelve children (11%) changed status from negative to positive, while eight (7%) changed from positive to negative. For the group as a whole the percentage agreement between the results obtained 2 years apart was 82%. In comparison to previous studies a greater number of subjects in this population than expected changed atopic status. We therefore further examined the data from those who had changed status and classified as borderline those subjects with no difference in weal size of greater than 2 mm for any allergen between 1987 and 1989. Only five children then changed status from negative to positive, none from positive to negative and 15 demonstrated only borderline changes. The coefficients of repeatability for the 106 children who did not change status were 3.37 mm, 2.80 mm and 2.33 mm for D. pteronyssinus, mixed grass pollens and cat dander respectively. The good short-term repeatability of the testing method was demonstrated in a group of 29 similar children; the coefficients of repeatability were 0.38 mm for DP and G, and 0.72 mm for C. These data demonstrate that, in a population of children with respiratory symptoms, skin-prick testing within individuals is highly repeatable over the short term, but poorly repeatable over a 2 year period. However, the percentage agreement in skin-prick test status for the group as a whole was high (82%). While no child became unequivocally skin-test negative having been previously positive, a small number of children changed status from negative to unequivocally positive, suggesting a genuine but small (4%) increase in the prevalence of skin-test positivity in this population.

Notes: Abstract. Evidence suggests that atopic individuals may be predisposed to more severe rhinoviral colds coupled to a worsening of existing airway disease than those with asthma. The role of atopy and IgE levels, as well as their relationship to clinical disease expression have not been defined. We hypothesized that an allergic diathesis modulates rhinoviral colds and have initiated studies of normal, atopic and asthmatic subjects employing experimental rhinoviral infection, with measurements of symptom scores, viral shedding and cultures, albumin in nasal washes and serological responses. Twenty-two subjects (11 normal, 5 atopic, 6 atopic and asthmatic) participated and were inoculated with human rhinovirus serotype 16 (HRV 16). Measurements of neutralizing antibody and viral culture were performed at screening, pre-inoculation, during the cold and at 8–10 weeks convalescence. Daily symptoms were noted, nasal washes done, IgE measured and atopy was diagnosed by skin tests. Seventeen volunteers developed clinical colds as assessed by symptom scores, virus shedding was demonstrated (with positive culture) in all subjects and a fourfold or higher seroconversion occurred in 11/22. Neutralizing HRV antibody developed unexpectedly in 10 subjects between screening and inoculation and the presence or absence of this pre-inoculation antibody determined subsequent severity of colds in normal but not in atopic subjects. Atopic antibody positive individuals developed severe clinical colds that were independent of preinoculation antibody in contrast to normal subjects who developed mild colds in the presence of a neutralizing antibody (.P= 0.01). Both atopic and normal antibody negative subjects developed severe colds. This differential response was matched by nasal wash albumin levels which were significantly increased (P= 0–01) during the cold in atopic (but not in normal) volunteers with pre-inoculation antibody. Levels of IgE were not correlated with severity of clinical disease or viral shedding. Our studies of HRV disease in atopic subjects suggest heightened susceptibility to the detrimental effects of colds; additional studies are needed to clarify the relevant mechanisms.