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M Sabol

Publications and source records attributed to M Sabol.

7 recordsLinked to original sources

Glucocorticoids decrease c-fos expression in human nasal polyps in vivo.

BACKGROUND: Activated c-fos binds to jun proteins to form the activation protein 1 (AP-1) transcription factor that regulates cytokine and other proinflammatory genes. c-Fos may play a key role in nasal polyp formation. Glucocorticoids may exert their anti-inflammatory effects through an interaction of glucocorticoid receptors with AP-1 that leads to mutual inactivation of both factors, and a "default" termination of AP-1 mediated gene activation. This may explain the beneficial effects of glucocorticoids in the treatment of nasal polyps. METHODS: To test this hypothesis in humans in vivo the immunohistochemical expression of c-fos-immunoreactive material (c-fos-irm) was assessed in nasal polyps from eight steroid naive subjects, polyps from eight subjects treated with topical beclomethasone dipropionate (BDP), and normal inferior turbinate nasal mucosa (n = 6). RESULTS: mRNA for c-fos was detected in all nasal polyps and normal mucosa. In contrast, c-fos-irm was present in all steroid naive subjects but in only two of the eight subjects treated with BDP (p = 0.007, two-tailed Fisher's exact test). c-Fos-irm was expressed solely in epithelial cells and glandular structures; it was expressed in normal epithelium and glands, but the staining intensity was low. CONCLUSION: Glucocorticoids appear to modulate expression of c-fos-irm and possibly AP-1 in human airway epithelial cells in vivo.

Adult↗

Mucoglycoprotein hypersecretion in allergic rhinitis and cystic fibrosis.

There is little information about specific changes in submucosal gland exocytosis in diseases such as allergic rhinitis (AR), nonallergic rhinitis (NAR), and cystic fibrosis (CF). Nasal lavage fluids were collected from normal, AR, NAR, and CF subjects. Concentrations of lysozyme, Alcian blue-staining mucoglycoconjugate material (AB + m), and human high-molecular-weight mucoglycoconjugates recognized by the 7F10 murine monoclonal antibody [7F10-immunoreactive mucoglycoconjugates (7F10-irm)] were measured. AB + m and 7F10-irm were characterized by Sepharose-2B column chromatography and glycosidase digestion. 7F10-irm was increased in CF (2.4-fold; P = 0.001) and AR (12.7-fold; P = 0.00007) subjects. AB + m was increased in CF (1.8-fold; P = 0.049) and AR (1.2-fold; P = 0.07) subjects. There were no changes in NAR subjects. On Sepharose-2B columns, AB + m peaks were at 1.3-3.0 x 10(6) and 0.36-0.65 x 10(6) Da. 7F10-irm showed four distinct peaks at 1.5, 1.2, 0.85, and 0.53 x 10(6) Da that were nearly identical in both normal and CF samples. Sialic acid was present in both 7F10-irm and AB + m. 7F10-irm and AB + m are mutually exclusive sialylated mucoglycoproteins that are significantly induced in AR and CF but not in NAR.

Animals↗

Hyaluronan is exocytosed from serous, but not mucous cells, of human nasal and tracheobronchial submucosal glands.

BACKGROUND: Hyaluronan is a large, nonsulfated glycosaminoglycan that is a major component of many extracellular matrices. Secretion of hyaluronan has been associated with inflammation in the lungs and other tissues. The purpose of the present study was to determine the distribution of hyaluronan in human respiratory tissues and to determine if hyaluronan was present in human nasal secretions. METHOD: Hyaluronan was localized in histological sections of human nasal and tracheobronchial mucosa using a biotinlabeled affinity-purified hyaluronan binding probe derived from cartilage proteoglycan (b-PG) (Green et al. Exp Cell Res 1988; 178:224-32). Subjects had saline nasal provocation to collect baseline nasal secretions, then ate chili peppers to provoke parasympathetic cholinergic nasal glandular secretion (gustatory provocation). Total protein and hyaluronan concentrations were measured in the lavage fluids. RESULTS: Staining for hyaluronan was intense in basement membranes of epithelium, glands and vessels, and perivascular adventitia. Many epithelial cells contained hyaluronan, but the staining intensity was less than that on the basolateral aspects of these cells. Submucosal gland serous cells contained variable amounts of hyaluronan. Hyaluronan was not present in goblet cells, submucosal gland mucous cells, or sub-basement membrane collagen deposits. The gustatory, parasympathetic stimulus induced a 4-fold increase in hyaluronan secretion (P < 0.01) and a 3.5-fold increase in total protein release (P < 0.0010). Hyaluronan accounted for 75% to 80% of the polymeric uronic acids in human nasal secretions. CONCLUSION: Hyaluronan was present human respiratory epithelial cells and submucosal gland serous cells and was exocytosed in response to parasympathetic stimulation. This distribution suggests roles in packaging cationic proteins in serous cells, cellular adhesion to basement membranes, and activation of macrophages in airway lumens.

Bronchi↗

Oncogene-induced basement membrane invasiveness in human mammary epithelial cells.

Expression of the intermediate filament protein vimentin, and loss of the cellular adhesion protein uvomorulin (E-cadherin) have been associated with increased invasiveness of established human breast cancer cell lines in vitro and in vivo. In the current study, we have further examined these relationships in oncogenically transformed human mammary epithelial cells. A normal human mammary epithelial strain, termed 184, was previously immortalized with benzo[a]pyrene, and two distinct sublines were derived (A1N4 and 184B5). These sublines were infected with retroviral vectors containing a single or two oncogenes of the nuclear, cytoplasmic, and plasma membrane-associated type (v-rasH, v-rasKi, v-mos, SV40T and c-myc). All infectants have been previously shown to exhibit some aspects of phenotypic transformation. In the current study, cellular invasiveness was determined in vitro using Matrigel, a reconstituted basement membrane extract. Lineage-specific differences were observed with respect to low constitutive invasiveness and invasive changes after infection with ras, despite similar ras-induced transformation of each line. Major effects on cellular invasiveness were observed after infection of the cells with two different oncogenes (v-rasH + SV40T and v-rasH + v-mos). In contrast, the effects of single oncogenes were only modest or negligible. All oncogenic infectants demonstrated increased attachment to laminin, but altered secretion of the 72 kDa and 92 kDa gelatinases was not associated with any aspect of malignant progression. Each of the two highly invasive double oncogene transformants were vimentin-positive and uvomorulin-negative, a phenotype indicative of the epithelial-mesenchymal transition (EMT) previously associated with invasiveness of established human breast cancer cell lines. Weakly invasive untransformed mammary epithelial cells in this study were positive for both vimentin and uvomorulin, suggesting that uvomorulin may over-ride the otherwise vimentin-associated invasiveness.

Animals↗

[Modification of a panoptic method of staining isolated cells].

A simple and rapid method of isolated cell staining was achieved by modification of the Pappenheim's method. It is based on the following steps: (1) dilution of commonly used stock solutions May-Grünwald (1:1), Giemsa-Romanowsky (1.25% v/v), (2) reverse sequence of the used staining solutions in comparison with the original method, (3) shorter time of procedure (5 min/slide), (4) utilization of distilled water of pH 5.1-5.6 for dilution of solutions and rinsing of slides, (5) it is not necessary to add serum to cell suspensions. The presented histological method is suitable for cytomorphological examination of cells. It can be applied in routine hematological laboratories not equipped with cytospins. (Fig. 5, Ref. 6.).

Animals↗

Effect of short-term ethanol intake on antibody-dependent cell-mediated cytotoxicity (ADCC) in rats.

The present study was designed to evaluate the effect of short ethanol intake on ADCC activity in blood and spleen mononuclear cells. Wistar rats were fed a standard diet and drank 0.1 M ethanol solution for three days. Glucose and water controls were used in this experiment. Increased ADCC activity was found in ethanol consuming rats in the blood and spleen as compared to both controls. Our findings support the assumption that ADCC may play an important role in liver disease of alcoholics.

Alcohol Drinking↗