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L Michel

Publications and source records attributed to L Michel.

At least 19 recordsLinked to original sources
PubMed1995

The nitric oxide donors, azide and hydroxylamine, inhibit the programmed cell death of cytokine-deprived human eosinophils.

Azide and hydroxylamine release nitric oxide (NO) enzymatically in biological conditions. We observed that both compounds were able to inhibit in vitro the programmed cell death of human eosinophils from peripheral blood. This protective effect could be mimicked by permeable cGMP analogs and by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Moreover, the soluble guanylate cyclase inhibitor LY-83583 inhibited in a dose-response manner the effects of the NO donors. Consequently, via the increase of eosinophil survival, NO could contribute to the amplification of inflammatory and allergic processes. This effect appears to be mediated, at least in part, by the soluble guanylate pathway.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Mapping of the pyrophosphate binding sites of beef heart mitochondrial F1-ATPase by photolabelling with azidonitrophenyl [alpha-32P]pyrophosphate.

4-Azido-2-nitrophenyl [alpha-32P]pyrophosphate (azido-[alpha-32P]PPi) mimics ADP and PPi by some of its binding properties when assayed in the absence of photoirradiation with mitochondrial F1-ATPase. Upon photoirradiation, both alpha- and beta-subunits of F1-ATPase were covalently labelled. Following chemical and enzymatic cleavages of each of the two photolabelled subunits, peptides containing the covalently bound radioactivity were separated by HPLC and identified by amino acid sequencing. Bound azido-[alpha-32P]PPi was found to be concentrated in two distant sequences of the alpha-subunit, namely Asp194-Thr221 and Lys386-Met437, and in a single sequence of the beta-subunit Glu294-Met358 with most of the photoprobe bound to beta-Tyr-311 and beta-Tyr-345. These results are discussed in terms of a model in which the pyrophosphate binding sites of F1 are located in regions of the alpha- and beta-subunits exposed at the interface between the two subunits and correspond to non-catalytic and catalytic adenine nucleotide binding sites, respectively.

Affinity Labels↗
PubMed1995

Exogenous nitric oxide elicits chemotaxis of neutrophils in vitro.

Nitric oxide (NO) has been shown to be both an intercellular and intracellular messenger. We propose here that exogenous NO induces chemotactic locomotion of human neutrophils. Indeed, when human neutrophils were placed in a gradient of a nitric oxide donor (S-nitroso-N-acetylpenicillamine; SNAP), a directed locomotion was induced, as evidenced by experiments of chemotaxis under agarose. Degraded SNAP (i.e., SNAP solution which had previously released NO) did not induce directed locomotion. Moreover, oxyhemoglobin, a scavenger of free NO, suppressed the chemotactic effect of SNAP, whereas LY-83583, a soluble guanylate cyclase inhibitor, inhibited the SNAP-mediated chemotaxis in a dose-response manner. Other unrelated NO donors, SIN-1 and S-nitroso-cysteine--a natural S-nitroso-compound, also induced a directed locomotion of neutrophils. Taken together, these in vitro experiments indicate that exogenous NO could mediate the chemotaxis of neutrophils and thus suggest that NO could contribute to neutrophil recruitment in vivo.

Aminoquinolines↗
PubMed1995

Human eosinophils in culture undergo a striking and rapid shrinkage during apoptosis. Role of K+ channels.

In the absence of appropriate stimulus, eosinophils in vitro rapidly exhibit the features of apoptotic cells (nuclear pycnosis, cell shrinkage, DNA fragmentation). By using electronic cell sizing, we precisely measured the volume distribution of human eosinophils during apoptosis. We observed that apoptosis of eosinophils was accompanied by a marked cell volume decrease (approximately 60%). Moreover, analysis of the volume distribution in different experimental conditions (kinetics of apoptosis, inhibition of apoptosis by cytokines) revealed that the cell shrinkage, once triggered, was a fast process in which the intermediate states between normal and shrunken volume had a short half-life. As a model of apoptosis, the eosinophil model allowed us to test the hypothesis that apoptotic cell shrinkage was linked to osmotic changes due to leakage of internal ions. Indeed, in the presence of K+ channel blockers, the shrinkage was inhibited in a dose-dependent manner. In conclusion, our results suggest that eosinophil shrinkage during apoptosis is a striking and rapid phenomenon and osmotic changes due to K+ efflux could be responsible, at least in part, of the volume decrease.

Apoptosis↗
PubMed1995

Abdominal pain: do not forget Thorotrast!

The use of Thorotrast (25% thorium dioxide), a radiologic contrast agent used up until the mid-1950s, was associated with a wide range of malignancies, mainly of hepatic origin. We report a case of Thorotrast-induced hepatocarcinoma in an 82-year-old woman.

Aged↗
PubMed1995

Lipolysis-stimulated receptor: a newcomer on the lipoprotein research scene.

It has been widely accepted that the remnants of the intestinally-derived lipoprotein chylomicrons, i.e., chylomicron remnants (CMR), are cleared from the circulation by a receptor genetically distinct from the well-known LDL-receptor. This second receptor was initially considered as a receptor specific for apo E, in contrast to the LDL-receptor, which binds both apo B and apoE. This article critically examines the current dogma of the putative CMR receptor, as well as both supporting and conflicting evidence for the recently-proposed identity of this receptor with the LDL-receptor related protein (LRP). Next, we introduce the lipolysis-stimulated receptor, LSR, which bears all the biochemical characteristics of the CMR receptor. In addition, the apparent number of LSR expressed in the liver is inversely correlated with nonfasting levels of plasma triglycerides. A change in LSR expression and parallel inverse change in plasma triglycerides is observed in rats treated with hyperlipidemic (retinoic acid) or hypolipidemic (fish oil in MaxEPA) agents, indicating that LSR represents a definite target for pharmacological management of hyperlipidemia. In support of this notion is the observation that MaxEPA, which causes an increase in LSR expression, also reduces both plasma triglyceride and cholesterol levels in the thus far intractable homozygous Watanabe heritable hyperlipidemic rabbit.

Animals↗
PubMed1994

Internalization of surface HLA-DR molecules by human epidermal Langerhans cells: analysis by flow cytometry and confocal microscopy.

Langerhans cells (LC) play a pivotal role in antigen processing and presentation to T cells during delayed-type hypersensitivity reaction in the skin. Antigen presentation involves the interaction between the class II molecules of MHC (HLA-DR) expressed by LC and T receptor of CD4+ T lymphocytes. It is now recognized that class II molecules are internalized into LC and can be associated with processed immunogenic peptides. This process involves receptor-mediated endocytosis. The aim of this study was to investigate the time-course of endocytosis of HLA-DR by freshly isolated human LC. Epidermal cells, obtained from normal skin samples, were labeled by indirect immunofluorescence using anti-HLA-DR monoclonal antibodies (MAb). The cell suspension was incubated at 37 degrees C for different periods (15, 30, 45, 60 and 90 min) and then analyzed by flow cytometry and confocal microscopy. Flow cytometry analysis showed decreased HLA-DR molecule expression by LC after incubation at 37 degrees C. Confocal microscopic analysis showed different strain patterns depending on the incubation time: (1) T = 0, continuous peripheral staining; (2) T = 15 min, patchy peripheral staining; (3) T = 30 min, patches or intracellular vesicular staining; (4) T = 45 min, intracellular vesicular staining; (5) T = 60 min, diffuse intracellular staining; (6) T = 90 min, aggregated staining. In our study model, flow cytometry provides quantitative information for the HLA-DR endocytosis, whereas confocal microscopy provides qualitative results concerning the intracellular distribution of internalized HLA-DR molecules.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1992

Photolabeling of the phosphate binding site of chloroplast coupling factor 1 with [32P]azidonitrophenyl phosphate.

Chloroplast F1-ATPase (CF1) was photolabeled by a radiolabeled photoactivatable derivative of Pi, 4-azido-2-nitrophenyl [32P]phosphate (ANPP). The radioactivity was localized in the beta subunit of CF1. Upon cleavage of the beta subunit by cyanogen bromide, the predominantly labeled peptide was recovered, which was subsequently subjected to tryptic digestion. A tryptic peptide (spanning Ile312-Arg354), was found to contain nearly all the covalently bound radioactivity. By Edman degradation, the labeled amino acid residues were identified as Tyr328, Val329 and Pro330. The labeled beta-Tyr328 of CF1 is the equivalent of beta-Tyr311 of F1 from beef heart mitochondria, which was previously found to be photolabeled by ANPP [J. Garin et al. (1989) Biochemistry 28, 1442-1448].

Affinity Labels↗
PubMed1992

The ATP synthase (F0-F1) complex in oxidative phosphorylation.

The transmembrane electrochemical proton gradient generated by the redox systems of the respiratory chain in mitochondria and aerobic bacteria is utilized by proton translocating ATP synthases to catalyze the synthesis of ATP from ADP and P(i). The bacterial and mitochondrial H(+)-ATP synthases both consist of a membranous sector, F0, which forms a H(+)-channel, and an extramembranous sector, F1, which is responsible for catalysis. When detached from the membrane, the purified F1 sector functions mainly as an ATPase. In chloroplasts, the synthesis of ATP is also driven by a proton motive force, and the enzyme complex responsible for this synthesis is similar to the mitochondrial and bacterial ATP synthases. The synthesis of ATP by H(+)-ATP synthases proceeds without the formation of a phosphorylated enzyme intermediate, and involves co-operative interactions between the catalytic subunits.

Amino Acid Sequence↗
PubMed1992

Leukotriene B4 and platelet-activating factor in human skin.

Acute inflammatory reactions are characterized by leukocyte infiltration associated with increases in vascular permeability and in local blood flow. Leukocyte infiltration can be induced by chemotactic factors such as leukotriene B4 (LTB4) and paf-acether (formerly known as platelet-activating factor) that can be generated within inflammatory lesions. Vascular permeability and increase in blood flow are also affected by LTB4 and paf-acether, as well as by several other substances, including histamine and prostaglandins. Derived from arachidonic acid via the 5 lipo-oxygenase pathway, LTB4 is one of the most potent leukocyte chemotactic substances known. Intradermal injections of LTB4 induce dermal neutrophil infiltration in animal models and in humans. Topical application of LTB4 to human skin induces intraepidermal micro-abscesses containing numerous intact neutrophils. LTB4 has been found to be increased in psoriatic lesions, but its synthesis by epidermal cells remains undecided. Like other leukotrienes, LTB4 can stimulate DNA synthesis in cultured human epidermal keratinocytes. However, receptors for LTC4 but not for LTB4 have been found on human keratinocytes in culture. Paf-acether is an ether-linked phospholipid identified as 1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine and is considered to be one of the most potent mediators of acute allergic and inflammatory reactions. For instance, intradermal injection of paf-acether induces inflammatory events such as neutrophil infiltration and increase in vascular permeability. Recent data suggest that cutaneous cells, such as fibroblasts and keratinocytes, are capable of producing paf and that paf is released during the development of allergic cutaneous reactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Dermatitis↗
PubMed1992

[Extracorporeal gallbladder lithotripsy: technology, practical methods, results and current value].

Extracorporeal shock wave lithotripsy of gallstones is a safe and well-tolerated procedure. Patients are now treated without general anesthesia and, increasingly, on an outpatient basis. Skin petechiae and transient hematuria are the most common side effects. Episodes of biliary colic are common in the follow-up period, but more serious adverse side effects such as cholecystitis and pancreatitis are distinctly uncommon. It is estimated that only 15% to 20% of all patients with symptomatic cholelithiasis are suitable lithotripsy candidates. As our knowledge of the procedure grows, it seems clear that the best results are obtained in patients with solitary radiolucent stones less than or equal to 20 mm, with stone-free rates at 12 months above 80%, for this selected group of patients. Adjuvant oral bile-acid dissolution therapy should be used in conjunction with gallstone lithotripsy. Gallstone recurrence remains to be established by clinical studies. Therapy for gallstones in 1991 has to be reevaluated by an interdisciplinary approach, taking into account not only open cholecystectomy, but also other modalities such as medical dissolution, laparoscopic surgery, percutaneous cholecystolithotomy and extra-corporeal shock wave lithotripsy. The appeal of the laparoscopic approach will substantially reduce the pool of patients for lithotripsy. Nevertheless, lithotripsy will continue to be a viable treatment option for patients with a single radiolucent stone. It is an outpatient procedure and doesn't require any incision or general anesthesia.

Bile Acids and Salts↗
PubMed1992

[Studying the mast cell. Recent data].

In the light of recently published data, the mast cell can now be viewed as a key cell, not only in allergic reactions such as immediate hypersensitivity responses, but also in a broad spectrum of other biologic responses including host-parasite interactions, nonspecific inflammatory reactions, fibrosis, angiogenesis, tissue reconstruction, and wound healing. Nevertheless the molecular basis for the intervention of mast cells in many of these biologic responses is still unclear. Very recent studies have demonstrated that mast cells are capable of producing a wide range of cytokines, a property which may influence various physiologic, immunologic and disease processes. Furthermore, although substantial differences have been reported between mast cells located in different tissues, the reasons and mechanisms underlying this heterogeneity long remained obscure. The recent development of two original experimental approaches, i.e., in vitro culture of mast cells, mainly derived from mouse bone marrow precursors, and replenishment of mast cell-deficient mice, has provided new insight into the mechanisms by which tissue microenvironment influence of regulation mast cell phenotype. Extrapolation to humans of data obtained in rodents is, however, hazardous. In the review presented here, the most recent data from the literature provide the basis for outlining avenues of research which can be expected, in the near or remote future, to solve what mast cell experts term "the riddle of the mast cells".

Animals↗
PubMed1991

Paf-acether in human skin.

Paf is a phospholipid mediator present in human skin which induces inflammatory events, such as neutrophil infiltration and increased vascular permeability. Recent data suggest that cutaneous cells, such as fibroblasts and keratinocytes, produce paf and that paf is released during allergic cutaneous reactions. It is tempting to speculate that paf may contribute to the development of various skin disorders with acute and chronic skin inflammation. Paf antagonists may help in bringing answers to this hypothesis and may offer new prospects for the treatment of cutaneous inflammatory diseases.

Humans↗
PubMed1991

Cyclosporin A inhibits the antigen-presenting functions of freshly isolated human Langerhans cells in vitro.

Cyclosporin A (CsA) is a strong inhibitor of skin allograft rejection. It has been also reported to act, not only on helper T cells, but also on the antigen-presenting functions of mouse epidermal cells (EC) enriched in Langerhans cells (LC). We tested the effects of CsA on the human allogeneic mixed epidermal cell-lymphocyte reaction (MECLR) using whole EC and freshly isolated LC as stimulator cells. Results were as follows. 1) CsA inhibited the lymphocyte proliferative response in a dose-dependent fashion, by about 80% for a CsA concentration of 10(-7) M. To evaluate the effects of the drug on the two cell populations involved in MECLR, stimulator EC and responder PBMC were separately pulsed for 2 h with CsA, washed, and combined to form MECLR. Inhibition by CsA of the alloantigen-dependent lymphocyte proliferation appeared to be multifactorial, because CsA-pulsed EC and CsA-pulsed effector PBMC led to identical reductions of 40% each in proliferation. 2) The nature of EC sensitivity to CsA during MECLR was then analyzed after freshly separating highly purified CD1-positive LC (greater than 95%) and LC-depleted EC (mainly keratinocytes), using an immunomagnetic particle technique. When responder PBMC were cultured with CsA-pulsed LC, a highly significant reduction of lymphocyte proliferation was observed, indicating that CsA has direct effects on LC. 3) Some of the possible mechanisms by which CsA might act on LC were studied. Substantial IL-1 activity and PGE2 amounts were induced during MECLR by LC and keratinocytes, but CsA did not act via these factors. Neither did it significantly modify HLA-DR, DQ, or DP antigen expressions on EC. In conclusion, CsA directly inhibits antigen presentation by human LC. This inhibition may partly explain the beneficial effects of CsA on skin allografts and certain cutaneous immune reactions.

Adolescent↗
PubMed1991

Soluble CD23 increases IL-3 induction of histamine synthesis by human bone marrow cells.

Interleukin 3 (IL-3) and soluble CD23 (sCD23/IgERII) have similar capacities to induce basophil development from human bone marrow (BM) precursors. IL-3 also has the capacity to induce de novo histamine synthesis from human BM cells. In the present study, we examined the effect of sCD23 on histamine synthesis by human BM cells and its relationship with IL-3. Our data showed that recombinant 25 KDa sCD23, although on its own failed to induce histamine release, significantly enhanced IL-3-stimulated histamine synthesis by BM cells. These data provide further support for the cytokine-like role of sCD23 on hematopoietic cells.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1990

Recurrent pleuro-pericarditis due to gastrodiaphragmatic fistula.

A 61-year-old woman presented with recurrent pleuro-pericarditis following Nissen fundoplication. A diagnosis of anterior gastrodiaphragmatic fistula was made. The suspected etiology of the fistula was local ischemia. This kind of fistula, although exceptional, should always be considered in the presence of unexplained recurrent pleuro-pericarditis after fundoplication.

Diaphragm↗