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Biomedical subjects

B S Polla

Publications and source records attributed to B S Polla.

At least 91 records · Page 5Linked to original sources
PubMed1993

Phagocytosis of Staphylococcus aureus induces a selective stress response in human monocytes-macrophages (M phi): modulation by M phi differentiation and by iron.

Phagocytosis of microorganisms represents a stress not only for the phagocytosed agent but also for the host cell. We have investigated the stress response induced in human monocytes-macrophages (M phi) phagocytosing inactivated Staphylococcus aureus. Exposure of human M phi to S. aureus induced in these cells (i) a threefold increase in superoxide dismutase activity, (ii) a selective and differentiation-dependent induction of host heat shock protein synthesis (HSP70 but not HSP65), and (iii) de novo synthesis of heme oxygenase, but only when exogenous iron was added to the cultures. The coordinate upregulation of two scavenging enzymes and of HSP70 suggests that all three are part of cellular protective mechanisms against phagocytosis-related oxidative injury to host cells.

Cell Differentiation↗
PubMed1993

Spontaneous heat shock protein synthesis by alveolar macrophages in interstitial lung disease associated with phagocytosis of eosinophils.

Synthesis of heat shock proteins (HSPs) is induced in all cells and tissues after exposure to elevated temperatures, or a variety of other types of injury, including oxidative injury. We have previously reported that stress proteins are induced in monocytes-macrophages during phagocytosis of red blood cells. Receptor-mediated phagocytosis is associated with activation of the respiratory burst, generation of the lipid mediators of inflammation, and increased production of cytokines. Similar activation events have been described in the alveolar macrophage (AM) during pulmonary fibrosis. We therefore analysed the pattern of proteins synthesized by human AMs recovered by bronchoalveolar lavage (BAL) in interstitial lung disease, both under basal conditions and after in vitro exposure to heat or hydrogen peroxide (H2O2). In two out of the 17 cases studied, we observed a high alveolar eosinophilia (10 and 24%, respectively) and phagocytosis, by the AMs, of eosinophilic material. Whereas exposure to heat or H2O2 induced in all AMs the synthesis of the classical HSPs, in these two cases, we found spontaneous synthesis of HSPs and of a 32 kD oxidation-specific stress protein, haeme oxygenase (HO). Exposure of AM to purified eosinophil-derived proteins, such as major basic protein (MBP), eosinophil peroxidase (EPO), eosinophil-derived neurotoxin (EDN), alone or in combination, did not induce stress protein synthesis, further suggesting that phagocytosis is involved in this induction. Stress protein synthesis by AMs may represent a new cellular marker of pulmonary injury and eosinophilic inflammation, and an autoprotective mechanism against oxidative stress.

Adult↗
PubMed1992

[Salami and extrinsic allergic alveolitis: a new occupational disease in Switzerland].

The authors report a case of extrinsic allergic alveolitis in a patient working in an industrial butchery where she is involved in the preparation of dry sausages. The molds proliferating at the surface of these sausages, molds from the Penicillium family, are responsible for the disease. The respective value of laboratory tests such as the presence of precipitating antibodies and the analysis of the cellularity of the bronchoalveolar lavage are discussed. Whenever a patient presents with clinical symptoms suggestive of extrinsic allergic alveolitis a detailed search for any type of exposure linked to the professional milieu is required, so as to propose adequate modifications in work conditions or work place.

Alveolitis, Extrinsic Allergic↗
PubMed1992

Monocytes from patients with atopic dermatitis are primed for superoxide production.

To determine the potential role of monocytes (peripheral blood monocytes, PBMs) in the pathogenesis of atopic dermatitis (AD), we investigated whether PBMs from patients with severe AD are primed to generate toxic oxygen metabolites. To induce in vitro superoxide anion (O2-) production, we used either particulate (e.g., opsonized bacteria or zymosan) or soluble (e.g., phorbol esters) stimuli, which allowed us to test two distinct pathways for reduced nicotinamide-adenine dinucleotide phosphate activation. In addition, PBMs from the same patients were also examined for their levels of expression of the low-affinity receptor for IgE, Fc epsilon receptor 2 (CD23). We found that PBMs, but not peripheral blood neutrophils, from patients with AD were primed for O2- production as compared to PBMs from either normal control subjects or patients with allergic rhinitis. These cells also expressed increased levels of CD23, and there was a significant correlation between these two parameters. Since the monocytes infiltrating into the AD lesions bear CD23, our data suggest that in vivo priming of PBMs and increased O2- production may participate in the pathogenesis of this skin disease.

Adolescent↗
PubMed1992

Fatal anaphylactoid response to protamine after percutaneous transluminal coronary angioplasty.

A generalized skin erythema and severe hypotension developed following administration of protamine for the reversal of heparin anticoagulation after an unsuccessful attempt at percutaneous transluminal angioplasty in a patient who had never been exposed to protamines before. Evidence of classical pathway complement activation was present indicating that this reaction could have been triggered by a non-immunological mechanism. The patient could not adequately be resuscitated because of the presence of severe coronary artery disease.

Aged↗
PubMed1991

Flavonoids, but not protein kinase C inhibitors, prevent stress protein synthesis during erythrophagocytosis.

Erythrophagocytosis induces in monocytes-macrophages the synthesis of stress proteins including the classical heat shock proteins (HSPs) and heme oxygenase (HO). To evaluate the role of oxygen radicals in this induction, we used the antioxidant flavonoids quercetin and kaempferol. These compounds inhibited HSP and HO synthesis, the latter being more sensitive. Quercetin and kaempferol also are inhibitors of protein kinase C (PKC). In order to determine whether inhibition of stress protein synthesis by flavonoids was mediated by their antioxidant properties or by PKC inhibition, we also tested more specific PKC antagonists, staurosporine and H-7. Staurosporine (SS) and H-7 decreased the synthesis of HSP70 and HSP83 but had no effect on HO. These data suggest that (1) erythrophagocytosis-related oxygen radicals are involved in the induction of the stress response in phagocytic cells, (2) the induction of HSPs and HO is differentially regulated, and (3) the effects of flavonoids on HO are linked to their scavenging activity rather than to PKC modulation.

Cells, Cultured↗
PubMed1991

Heat shock protein induction in rat pancreatic islets by recombinant human interleukin 1 beta.

Interleukin 1 beta, potentiated by tumour necrosis factor alpha, is cytotoxic to pancreatic Beta cells in vitro. We have hypothesized that interleukin 1 beta induces oxygen free radicals in Beta cells. Since cytotoxicity induced by free radicals and by heat may activate the same cellular repair mechanism (the heat shock response), the aim of this study was to investigate the pattern of protein synthesis in isolated islets after exposure to interleukin 1 beta (150 pg/ml, 24 h), tumour necrosis factor alpha (50 ng/ml, 24 h) heat shock (43 degrees C, 30 min) and H2O2 (0.1 mmol/l, 20 min). By polyacrylamide gel electrophoresis, autoradiography, Western-blot analysis and partial peptide mapping of 35S-methionine labelled islets, interleukin 1 beta was found to induce a 73 kilodalton protein belonging to the heat shock protein family heat shock protein 70, a heat shock protein 90, and haem oxygenase. A minor induction of heat shock protein 73 and haem oxygenase was seen after H2O2. Interleukin 1 beta did not induce heat shock proteins in rat thyroid cells, rat mesangial cells or in human monocytes. Tumour necrosis factor alpha did not induce selective protein synthesis. Pre-exposure of islets to heat, tumour necrosis factor alpha, or H2O2 did not prevent the impairment of glucose-stimulated insulin release seen after 24 h of interleukin 1 beta exposure. The data are compatible with free radical induction by interleukin 1 beta. However, the heat shock response is not specific for oxidative injury, and previous studies have shown discrepant effects as to a protective effect of free radical scavengers against interleukin 1 beta-mediated beta-cytotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗