Two rat isolates of B. Piliformis are different based on protein banding patterns in acrylamide gels and immunoblots.
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Animals↗
Biomedical subjects
P J Manning
Publications and source records attributed to P J Manning.
The effects of H2-receptor antagonists on exercise refractoriness in asthma.
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Adult↗
Normal bone mineral density following cure of Cushing's syndrome.
OBJECTIVE: Both endogenous and exogenous glucocorticoid excess are well established as causes of osteoporosis. However, there are few data describing bone mineral density in these subjects following the restoration of normal steroid levels. The present study addresses this issue. DESIGN: A cross-sectional assessment of bone mineral density in patients cured of Cushing's syndrome, and comparison of each with four normal subjects matched by age, sex, weight, menopausal status and race, was used. PATIENTS: Seventeen adults cured of Cushing's syndrome 8.6 +/- 1.6 years (mean +/- SEM) took part. MEASUREMENTS: The bone mineral density of the lumbar spine and proximal femur was measured by dual energy X-ray absorptiometry. RESULTS: Bone mineral densities, relative to control, were 100 +/- 16, 98 +/- 14, 97 +/- 19 and 98 +/- 16% (mean +/- SD), in the lumbar spine, femoral neck, Ward's triangle and trochanteric regions, respectively. There was a positive relationship between bone density and time since cure (r = 0.24-0.59, in the four regions). In contrast, bone density was significantly reduced in five subjects with active Cushing's disease when similarly matched (BMD = 87 +/- 4, 83 +/- 4, 75 +/- 6 and 82 +/- 6%, in the respective regions; 0.01 less than P less than 0.05). CONCLUSIONS: Bone density is reduced in subjects with Cushing's syndrome but not in those having undergone cure some years previously. This implies that steroid-induced osteoporosis is substantially reversible, though long-term prospective studies will be necessary to establish this definitively.
Adrenalectomy↗
Clinical relevance of lipid mediators in asthma.
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Animals↗
Colonization of rabbits by Pasteurella multocida: serum IgG responses following intranasal challenge with serologically distinct isolates.
Enzyme-linked immunosorbent assays (ELISAs) and immunoblots were used to measure serum IgG responses in rabbits which were intranasally challenged with Pasteurella multocida. The responses to two serologically distinct isolates (isolate 1, serotype 3:A and isolate 10, serotype 1:D) were compared and then correlated with the ability of the isolates to colonize the nasal passages. Five rabbits were challenged with each isolate (10(5) CFU); nasal washings and sera were collected weekly for 8 weeks. Serum IgG levels were measured by ELISA and immunoblots, using bacterial whole cells and lipopolysaccharides (LPSs) as antigens. The serum IgG response to isolate 1 was evident earlier and was significantly stronger than the response to isolate 10 (P less than 0.025). Immunoblots supported this observation and confirmed that both isolates elicited antibodies which reacted with bacterial protein and LPS antigens, with antibody to protein detectable before antibody to LPS. Results of weekly nasal cultures suggested that the antibody response data could be explained by a difference in the ability of the isolates to colonize the nasal passages: isolate 1 was recovered from four of five rabbits for 8 weeks, whereas isolate 10 was recovered for a maximum of 2 weeks, even when the challenge dose was increased tenfold. The strong response elicited by isolate 1 was therefore probably a result of persistent colonization, whereas the weak response to isolate 10 may have resulted from an inability to persistently colonize the nasal passages. The results of this study demonstrate that isolates of P. multocida elicit antibody responses of differing intensities and vary in their ability to colonize the nasal passages.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Intranasal↗
The acromegalic rosary.
Palpable enlargement of the costochondral junctions on the anterolateral chest wall was detected in 26 of 27 patients with acromegaly. In a further study three doctors wearing eyemasks examined a further 13 acromegalic patients and 12 control subjects; costochondral enlargement was detected with a sensitivity of 77% and specificity of 86%. It was not found in normal subjects in the absence of previous chest injury. The presence and extent of costochondral enlargement was unrelated to the duration of active or cured acromegaly, the initial or present growth hormone concentrations, or other clinical features of growth hormone excess. Costochondral enlargement is a common clinical sign in acromegaly and can serve as a biological marker of previous or current growth hormone excess.
Acromegaly↗
Allergen-induced asthmatic responses. Relationship between increases in airway responsiveness and increases in circulating eosinophils, basophils, and their progenitors.
The inflammatory response during allergen-induced asthma was assessed using serial measures of peripheral blood eosinophils (Eo), basophils (B), and Eo/B progenitor cells (Eo/B-CFU). A group of 14 stable asthmatic individuals (beta 2-agonists only as needed) had inhalation provocation tests with allergen (18 tests in total) and with diluent. Serial blood samples were taken before and 1 and 24 h after the tests; methylcellulose cultures for Eo/B-CFU and granulocyte-macrophage (GM-CFU) were scored at 14 days. Circulating Eo, B, and Eo/B-CFU were increased at 24 h after allergen inhalation when this resulted in increased histamine airway responsiveness (n = 13). In the 5 subjects with isolated early asthmatic responses the Eo, B, and Eo/B-CFU counts did not change. There was no change in the GM-CFU after allergen. The ratio change in circulating Eo/B-CFU was negatively correlated with baseline histamine airway responsiveness (r = -0.8, p less than 0.05). Four subjects who had an isolated early response and no blood changes to one allergen developed an increase in histamine airway responsiveness and an increase in Eo, B, and Eo/B progenitors after inhalation of a second different allergen. The results indicate that in subjects with an allergen-induced increase in histamine airway responsiveness, an inflammatory response occurs that includes an increase in the number of Eo/B progenitors. This response, possibly mediated by Eo/B growth and differentiation factors, could lead to the accumulation of these cells in the airway and contribute to the airways inflammation present in asthma.
Allergens↗
Partial characterization of plasmids from rabbit isolates of Pasteurella multocida.
Plasmids have not been reported for isolates of Pasteurella multocida from rabbits. We assayed 28 isolates of rabbit P. multocida for plasmids and sought to determine whether or not plasmid presence correlated with clinical or pathologic findings, serotype, toxin production, possession of pili, or biochemical characteristics. Fourteen isolates bore a single 1.6 Md (covalently closed circular form in 0.7% agarose gels) plasmid. An additional isolate had two plasmids which migrated as a closely-spaced doublet, centered around 1.6 Md. Eleven isolates appeared to have identical plasmids, according to Hae III and Hinf I digests. The apparent linear size of this common plasmid in 2% agarose gels was 2.1 Md, as calculated from the sums of the sizes of Hae III or Hinf I digestion fragments. Linearization of the common plasmid with Msp I produced an apparent size of 2.5 Md in 0.7% agarose gels. No correlations between presence of the common plasmid and somatic serotype, toxigenicity, presence of pili, antimicrobial resistance, selected biochemical characteristics, anatomic site from which the bacteria were cultured, or disease status of the host were found.
Animals↗
An enzyme-linked immunosorbent assay for detection of chronic subclinical Pasteurella pneumotropica infection in mice.
Serum samples from seventy-five, 3- to 12-week-old and 16 retired breeder male Swiss mice from a conventional colony with enzootic chronic subclinical Pasteurella pneumotropica infection were tested by enzyme-linked immunosorbent assay (ELISA) and Western blots for IgG antibodies to whole cell (WC) and lipooligosaccharide (LOS) antigens of P. pneumotropica. In 3- to 12-week-old mice, serum antibody levels to LOS exceeded those to the WC preparation. Western blots of sera from mice in this age group substantiated that a major component of the early IgG antibody response was directed against LOS antigens. Higher antibody levels to both antigen preparations in 3-week-old mice compared to mice 4 and 6 weeks old were interpreted as reflecting a decline in antibodies acquired from the dam. Active immunity indicative of infection was first detected at 8 weeks of age. Serum samples from retired breeder mice (28 weeks of age) also had substantial antibody titers to LOS but, in contrast to sera from mice in the younger age groups, retired breeders had significantly greater IgG reactivity to WC preparations than to LOS antigens. The superior specificity of the LOS antigen compared to the WC preparation in the ELISA was demonstrated by testing serum samples from retired breeder mice against WC and LOS antigens from P. ureae, P. multocida, and P. hemolytica. The reactivity of IgG against LOS antigens from these organisms was negligible, whereas substantial titers were evident to WC antigens. This ELISA, using LOS preparations as antigen, is a useful serologic assay for the detection of subclinical P. pneumotropica infection in mice.
Age Factors↗
The role of thromboxane in allergen-induced asthmatic responses.
In this study we evaluated the role of thromboxane in causing allergen-induced early and late asthmatic responses and airway hyperresponsiveness in asthmatic subjects. Twelve atopic subjects with stable asthma and documented early and late asthmatic responses to an inhaled allergen were treated with placebo or CGS 13080, a specific thromboxane synthetase inhibitor, given orally (200 mg four times daily) for two days before, the day of, and the day after allergen inhalation. Treatments were administered in a double-blind, placebo-controlled, crossover fashion. The effect of pretreatment with CGS 13080 was examined on serum TxB2 levels and the magnitude of the asthmatic responses after inhaled allergen. Serum TxB2 levels increased significantly from 96 ng.ml-1 (SEM 29) 3 h after diluent to 151 ng.ml-1 (SEM 27) 3 h after allergen (p = 0.008). CGS 13080 pretreatment markedly inhibited the levels of TxB2 at all time points before and after inhaled allergen (p = 0.0001) and had a small but significant effect on the magnitude of the early asthmatic responses after allergen (p = 0.0009). CGS 13080 did not alter either late asthmatic responses, baseline airway responsiveness, or the increase in histamine airway responsiveness after allergen. These results suggest that allergen-induced early asthmatic responses, but not late responses or allergen-induced airway hyperresponsiveness, are partly caused by thromboxane release.
Adult↗
Inhibition of exercise-induced bronchoconstriction by MK-571, a potent leukotriene D4-receptor antagonist.
BACKGROUND: Exercise is a common stimulus of bronchoconstriction in subjects with asthma, who also have bronchoconstriction after inhaling the sulfidopeptide leukotriene D4 (LTD4). The purpose of this study was to investigate the importance of LTD4 as a mediator of exercise-induced bronchoconstriction. METHODS: In a double-blind, randomized, crossover study, 12 subjects with stable asthma were treated intravenously with MK-571 (160 mg), a selective and potent LTD4-receptor antagonist, or placebo, 20 minutes before each of two challenges involving exercise at a level previously demonstrated to cause a fall of at least 20 percent in the forced expiratory volume in one second (FEV1). The two exercise challenges were separated by one week. The results of the challenges were expressed as both the maximal fall in FEV1 after exercise and the time to recovery from bronchoconstriction. RESULTS: Treatment with MK-571 attenuated exercise-induced bronchoconstriction in all the subjects. The mean (+/- SEM) maximal percent decrease in FEV1 after exercise was 25.2 +/- 3.5 percent in the subjects taking placebo and 9.2 +/- 2.5 percent in the subjects taking MK-571 (P less than 0.001). The mean percent inhibition for the entire group was 69.5 percent. The mean time to recovery after exercise was 33.4 +/- 4.0 minutes in the placebo group and 8.4 +/- 2.5 minutes in the MK-571 group (P less than 0.001). CONCLUSIONS: This study demonstrates that pretreatment with a potent and selective LTD4 antagonist markedly attenuates exercise-induced bronchoconstriction, and it suggests that LTD4 is a major mediator of this type of bronchoconstriction.
Asthma, Exercise-Induced↗
The inhibitory influence of tracheal mucosa mounted in close proximity to canine trachealis.
Reduced smooth muscle contractile responses to agonists occur in the presence of epithelium, perhaps due to the release of an epithelium-derived relaxing factor (EpDRF). It is not clear whether the release of EpDRF requires the direct attachment of the epithelium to the smooth muscle. In the present study, using isolated canine tracheal smooth muscle strips, we examined whether the inhibitory effects of airway mucosa require the attachment of the mucosa to smooth muscle. The smooth muscle contractile responses to acetylcholine and histamine were reduced in the presence of airway mucosa, whether the mucosa was attached or in close proximity. The inhibitory effect mediated by the airway mucosa therefore is not dependent on mucosal attachment to smooth muscle. This phenomenon appears to be due to the release of a soluble, short-acting mediator from the airway mucosa.
Acetylcholine↗
Urinary leukotriene E4 levels during early and late asthmatic responses.
The sulphidopeptide leukotrienes C4 and D4 (LTC4, LTD4) are potent bronchoconstrictor mediators, released from human lung fragments after challenge with specific allergens in vitro. The purpose of this study was to measure urinary LTE4 (metabolite of LTC4 and LTD4) in subjects undergoing inhalation challenges with allergens or occupational sensitizing agents in the laboratory. Eighteen subjects with previously documented isolated early asthmatic responses (EARs), isolated late asthmatic responses (LARs), or dual (both early and late) asthmatic responses were studied. Urinary LTE4 levels increased in subjects who developed either isolated EARs (mean fall in FEV1, 27.98%) or early responses preceding LARs (mean fall in FEV1, 15.01%). The baseline levels of LTE4 were 150.26 (SEM, 49.5) pg/mg of creatinine in the isolated responders and 66.60 (SEM, 13.5) pg/mg of creatinine in the dual responders. These levels increased to 1816 (SEM, 606.1) pg/mg of creatinine (p = 0.041) and 174.80 (SEM, 40.1) pg/mg of creatinine (p = 0.025), respectively, after the EAR. The degree of maximal bronchoconstriction during the EAR correlated with the levels of LTE4 (r = 0.68; p = 0.001). No significant increase in urinary LTE4 levels occurred during the LAR. These results suggest that the LTE4 precursors, LTC4 and LTD4, are important bronchoconstrictor mediators causing EARs after allergen inhalation.
Administration, Inhalation↗
Production of immunoglobulin A protease by Streptococcus pneumoniae from animals.
Human isolates of Streptococcus pneumoniae tested by traditional immunochemical methods produce a protease that cleaves human immunoglobulin A1 (IgA1) into Fab and Fc fragments. The protease may be an important virulence factor, but studies of its pathogenetic significance have been hampered by lack of a suitable animal model. Since S. pneumoniae is a respiratory pathogen for several species of animals, we sought to determine whether isolates of this organism from animals with pneumococcal infection, including fatal diplococcal pneumonia, produced an IgA protease. Isolates from six animal species including the mouse, rat, dog, guinea pig, rhesus monkey, and chimpanzee were tested for protease activity against IgA preparations from the mouse, rat, dog, guinea pig, rabbit, rhesus and cynomolgus monkeys, gorilla, and human. Cleavage of IgA was demonstrated by the appearance of Fc fragments in Western blots (immunoblots) treated with specific antisera. All these isolates except that from the guinea pig produced a protease that cleaved IgA of human, rhesus monkey, and gorilla origin. Cleavage was inhibited by 5 mM EDTA. IgA cleavage from the other species could not be demonstrated. Although S. pneumoniae can colonize the respiratory tracts of several animal species, it is a significant pathogen principally of humans and some other primates. Our data suggest that some species of nonhuman primates including the rhesus monkey could be suitable for experimental studies on the significance of IgA protease in the pathogenesis of pneumococcal disease.
Animals↗
Tachyphylaxis to inhaled methacholine in normal but not asthmatic subjects.
Methacholine inhalation tests measure airway responsiveness in asthmatic and normal subjects. Tachyphylaxis occurs with repeated methacholine inhalations in normal subjects. The purpose of this study was to examine the time course and mechanisms of methacholine tachyphylaxis in normal subjects and to determine whether this occurs in mildly asthmatic subjects. Fifteen normal and nine asthmatic subjects were studied on 2 study days, at least 48 h apart. Each day, two inhalation tests were carried out. On one day, subjects performed two methacholine inhalation tests 3 h later by a methacholine test. Results were expressed as the provocation concentration causing a 20% fall in forced expiratory volume in 1 s (FEV1), (PC20). All normal subjects developed methacholine tachyphylaxis. The mean PC20 increased from 47.3 mg/ml (%SE 1.34) to 115.6 (%SE 1.51) (P less than 0.0001) in a 3-h interval. This increase lasted for greater than or equal to 6 h (P = 0.012). Asthmatic subjects did not develop methacholine tachyphylaxis. Their mean methacholine PC20s were 1.6 mg/ml (%SE 1.4) and 1.5 (%SE 1.4) (P = 0.75) 3 h later. In two other series of experiments, normal subjects were pretreated with the cyclooxygenase inhibitors indomethacin (100 mg/day) or flurbiprofen (150 mg/day) or a placebo for 3 days before two methacholine tests 3 h apart. Both indomethacin and flurbiprofen significantly inhibited the development of methacholine tachyphylaxis. These results confirm that methacholine tachyphylaxis occurs in normal subjects, lasts greater than or equal to 6 h, and may occur through the release of inhibitory prostaglandins. By contrast, methacholine tachyphylaxis does not occur in asthmatic subjects.
Administration, Inhalation↗
Serologic survey for Actinobacillus capsulatus in free-ranging snowshoe hares (Lepus americanus) from Alaska and Alberta.
A plate agglutination method was developed to test sera from free-ranging snowshoe hares (Lepus americanus) captured in Alaska (USA) or Alberta (Canada) for antibody against Actinobacillus capsulatus. Antiserum against A. capsulatus was prepared in a domestic rabbit. A concentrated suspension of formalin-killed A. capsulatus was prepared for use as an antigen. Serum antibody prevalence for hares was 98 of 239 (41%) in Alaska and 51 of 111 (46%) in Alberta. Prevalence in Alaska peaked in 1981 corresponding to a peak in hare population density. Seasonal prevalence peaked in May in Alaska. Prevalence at one capture site in Alaska was significantly higher than at four other sites. There was no difference in sex-specific prevalence for either Alaska or Alberta.
Actinobacillus↗
Immune mediated hemolytic anemia associated with antilymphocyte globulin therapy in dogs.
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Anemia, Hemolytic↗
The effect of oral prostaglandin E1 on airway responsiveness in asthmatic subjects.
Prostaglandin E1 (PGE1) is a bronchodilator in humans, but the effect of this prostaglandin on airway responsiveness in asthmatic subjects is not known. The purpose of this study was to examine the effect of oral PGE1 treatment on airway responsiveness to inhaled histamine and methacholine in asthmatic subjects. The subjects had inhalation tests performed on separate study days over a period of 2 weeks. PGE1 (200 micrograms 4 times daily) or placebo was taken in a double-blind fashion for 4 consecutive days. Each week, after three days of treatment, a histamine or methacholine inhalation test was performed on one day, followed by an inhalation test with the alternative agonist the following day. Baseline forced expired volume in 1 s (FEV1) values were similar before each inhalation test on each study day (P = 0.81). However, both histamine and methacholine airway responsiveness decreased following PGE1 treatment. The mean provocative concentration of histamine causing a 20% fall in FEV1 (PC20 histamine) on the placebo day was 1.47 mg/ml (%SD 3.05) and was 2.35 mg/ml (%SD 2.72) (p less than 0.005) during PGE1 treatment period. Similarly the PC20 methacholine was 1.84 mg/ml (%SD 2.30) on the placebo day and was 2.53 mg/ml (%SD 2.06) during PGE1 treatment period (p = 0.025). This study demonstrates that oral PGE1, administered in doses which did not change airway caliber, can reduce airway responsiveness in mild asthmatics.
Administration, Oral↗