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Biomedical subjects

P Stierna

Publications and source records attributed to P Stierna.

64 records · Page 4Linked to original sources

Experimental sinusitis in rabbits induced by aerobic and anaerobic bacteria: models for research in sinusitis.

Experimental acute sinusitis can be induced in New Zealand white rabbits by Streptococcus pneumoniae serotype 3, or the anaerobe Bacteroides fragilis, after blocking of the sinus ostium. Histological examination of the sinus mucosa in both models reveals edema, dilated venules, leukocytic infiltration, goblet cell formation, as well as localized epithelial lesions. In comparison the bacteroides sinusitis enhances a more pronounced and long-lasting tissue reaction, including periosteal thickening and new bone formation. The sinus mucosal blood flow as measured with microspheres Sn113 is increased as compared to control side in pneumococcal sinusitis. An increased lactate concentration of sinus secretions as well as in the pathological sinus mucosa indicates an anaerobic metabolism. Furthermore, a decreased ATP-content of the sinus mucosa suggests an energy depletion which could impair epithelial function. The anaerobic milieu of the sinus secretion is probably created by the leukocytes as analyzed by the separation of the D- and L-form of lactate.

Animals↗

Autoradiographic findings in experimental sinusitis in rabbits.

In order to study the effect of a purulent infection in the sinus cavity on the uptake of radionuclide in the surrounding bone, two series of experiments were performed; one using 45Ca-chloride (T1/2 = 153 d), that was given intravenously in a dose of 50 MBq to the previously infected animal, and in the other 99Tcm-DP was used in a dose of 530-1600 MBq. The animals were killed 4-6 hours later and analyzed using an autoradiographic technique and histological examination. Chronic unilateral infection of the maxillary sinus was induced experimentally according to the technique described by Kumlien and Schiratzki (1985). An acute unilateral maxillary sinusitis was induced experimentally according to Johansson et al. (1988). An increased uptake of 99Tcm-DP in the bone surrounding the sinus cavity with an infected mucosa could be seen. This uptake could be seen four days after induction of an acute, purulent, pneumococcal sinusitis, and five months after the induction of an purulent, chronic sinusitis. No increase in uptake could be seen in the mucosa of the sinus with purulent infection. The beta-emitting nuclide gave better resolution in autoradiography than did the gamma-emitting nuclide, and would give better possibilities in identifying structures; however, the specificity to bone of 45Ca was not high enough to be suitable.

Animals↗

Serum antibody response to Bacteroides fragilis in experimental sinusitis.

Maxillary sinusitis was induced in New Zealand white rabbits by local inoculation of 10(6) colony-forming units of Bacteroides fragilis NCTC 9343, and the serum IgG, IgA and IgM antibody responses to cell wall antigens were studied. Prior to inoculation, and one, two, three and four weeks after induction, serum samples were obtained and analysed for antibodies to the lipopolysaccharide and the capsular polysaccharide. Capsular polysaccharide from B. fragilis ATCC 23745 was used as control. The rise in IgG activity against NCTC 9343 capsular polysaccharide and lipopolysaccharide was most marked and sustained throughout the four weeks. The increases in IgA concentration were moderate and sometimes transient, and a more pronounced IgA increase was seen with IFA than with EIA. The IgM peak levels were weak and usually declined within two to three weeks. The development of antibody to the lipopolysaccharide was similar to that of the NCTC 9343 capsular polysaccharide antibodies, though somewhat delayed in time. No significant increase in antibody to the control capsular polysaccharide was seen.

Animals↗

Lectin expression during wound healing of the rabbit sinus mucosa: a study of regenerating epithelium and early polyp formation.

Lectin expression during wound healing of the rabbit sinus mucosa was examined. Positive UEA-I staining was evident on squamous or cuboidal as well as columnar regenerating epithelial cells (RE cells). PNA staining of columnar RE cells first became evident after neuraminidase treatment, while squamous or cuboidal RE cells stained positively with PNA alone. Fucosylation within RE cells thus occurred from a relatively early period, and sialylation followed at later stages. Ingrowing epithelial cells of early polyp formation stained negatively with UEA-I, indicating that unfucosylated RE cells may represent aberrant cellular behavior. We concluded that these patterns of lectin staining indicate a functional maturation as well as an integration of regenerating mucosa.

Animals↗

Association of bronchopneumonia with sinusitis due to Bordetella bronchiseptica in an experimental rabbit model.

An animal model for rhinogenic sinusitis was developed in rabbits naturally colonized with Bordetella bronchiseptica. It was found that ostial occlusion predisposes the sinus to invasion with this opportunistic bacterium and subsequent sinusitis as a result of reduced local host defense. In addition to the inflammatory lesions in the sinus, bronchitis and pneumonia were found in 84% of the experimental rabbits, suggesting that ostial dysfunction can also contribute to infectious disease of the lower respiratory tract. In such a model it is possible to study the significance of asymptomatic carriage of potential pathogens after ostial occlusion.

Animals↗

Effects of topical budesonide treatment on glucocorticoid receptor mRNA down-regulation and cytokine patterns in nasal polyps.

UNLABELLED: The effects of a topically applied corticosteroid, budesonide, on the expression of glucocorticoid receptor (GR) mRNA and regulation of pro-inflammatory cytokine patterns in patients with nasal polyps were evaluated. All patients were eligible for surgical polypectomy, and a majority of them had been treated with nasal steroids. Patients were given 400 microg b.i.d. (group A, n = 11), 200 microg b.i.d. (group B, n = 10), or no treatment (group C, n = 15) during two months before polypectomy. Morning serum cortisol was analyzed on the day of surgery. Surgically removed polyps were taken for analysis of GR mRNA expression by solution hybridization. Remaining tissue was cryostat-sectioned, whereafter quantification of the cytokines interleukin 1beta, interleukin 2, interleukin 4, interleukin 5, interleukin 6, interleukin 10, tumor necrosis factor alpha, and interferon gamma was made by immunohistochemistry and digitized image analysis. No significant differences among the three groups were found for any of the parameters investigated. CONCLUSION: nasal polyps do not respond with down-regulation of GR mRNA or cytokines following topical corticosteroid treatment. The proposed corticosteroid resistance may be inherent, or induced by a change of local tissue bioavailability.

Administration, Topical↗

Expression of P-glycoprotein 170 in nasal mucosa may be increased with topical steroids.

The synthesis of P-glycoprotein 170 (P-gp), a "multidrug resistance" protein capable of extruding various drugs including 11-OH steroids from human cells, can be upregulated by certain glucocorticosteroids. This study demonstrates the presence of P-gp in the columnar surface epithelium and in glandular acini of healthy nasal mucosa with immunohistochemical technique. Furthermore, nasal polyps from 5 of 17 patients treated with clinical doses of a topical nasal steroid, budesonide, appear to show a stronger staining intensity for P-gp than polyps from 13 untreated patients. This suggests the possibility of local P-gp gene induction by topical glucocorticoid treatment. Upregulation of P-gp synthesis appears as a new possible cause of relative resistance to topical steroid medication in patients with nasal inflammatory disease.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Gram negative sinusitis: a bacteriologic and histologic study in rabbits.

Recent investigations of chronic sinusitis that is "recalcitrant" to traditional medical and surgical therapy indicate that gram negative bacteria are frequently involved, most commonly Pseudomonas aeruginosa. Analysis of infection-induced histopathologic changes in the underlying sinus mucosa may provide important insight into the recalcitrant nature of these infections. Therefore, the aim of this investigation is to experimentally induce sinus infection in the rabbit with Pseudomonas aeruginosa, a bacterium commonly associated with "recalcitrant sinusitis," and evaluate the histopathologic findings. A unilateral maxillary sinusitis was induced in 33 New Zealand white rabbits. Histologic analysis at 4, 14, 21, and 28 days revealed a moderate inflammation that persisted throughout the study period. Initial changes included edema, loss of submucosal glands, and ulceration. Fibroplasia and bone remodeling were evident throughout the study. Epithelial plaque formation occurred early in the infection, whereas goblet cell formation was a later change. Experimental sinusitis induced by Pseudomonas aeruginosa causes an intense transmucosal injury. The histopathologic injury and response to Pseudomonas aeruginosa appears to be more intense than that noted on previous investigations of experimental sinusitis using other bacteria. The significant histopathologic changes noted could explain the recalcitrant nature of gram negative sinusitis observed clinically in patients.

Animals↗

The relationship of nasal polyps, infection, and inflammation.

The role of infection as cause or effect in nasal polyps is debated. In experimentally induced sinusitis in rabbits, polyps are frequent. The initial polyp formation sequence involves multiple epithelial disruptions with proliferating granulation tissue. Regenerating epithelial branches spread into the underlying connective tissue, where intraepithelial microcavities give rise to a polyp body from the adjacent mucosa. Clinical as well as experimental studies indicate that nasal polyp formation and growth are activated and perpetuated by an integrated process of mucosal epithelium, matrix, and inflammatory cells, which in turn may be initiated by both infectious and noninfectious inflammation. The complexity of the pathophysiologic events in nasal polyposis is reinforced by the finding that epithelial desquamation, combined with infection or inflammation, will initiate polyp formation. Systemic glucocorticosteroids inhibit polyp formation as well as growth of pathogenic bacteria in the sinuses of rabbits with experimental infection. Therapeutic use of corticosteroids in polyp disease, combined with antibiotics or surgery, should be modified in relation to long-term progression, intensity variations, and predisposing conditions.

Animals↗

Histopathological observations in chronic maxillary sinusitis.

Biopsy samples from the maxillary sinus mucosa of patients with purulent, non-purulent and recurrent sinusitis were studied histologically and compared with those from a maxillary sinus of patients with no previous history of sinus disease on the side of sampling. Basement membrane thickening, atypical gland formation, goblet cell hyperplasia, mononuclear inflammatory cell infiltration and subepithelial oedema were observed in all groups irrespective of the appearance of the effusion. Although the inflammatory variables in selected areas of the mucosa seemed to show an increase in severity with the increasingly severe forms of sinusitis, neither the endoscopic mucosal appearance nor the nature of the sinus effusion corresponded to any specific histological pattern.

Basement Membrane↗