Immune function of bovine leukocytes after in vitro exposure to selected heavy metals

OBJECTIVE: To study effects of in vitro exposure of bovine leukocytes to mercury, cadmium, and lead on phagocytosis, natural killer cell activity, and lymphocyte proliferation. SAMPLE POPULATION: Leukocytes from 6 nonpregnant Holstein heifers. PROCEDURE: Leukocytes were exposed in vitro to the aforementioned metals, and leukocyte functions were assessed. RESULTS: Phagocytosis was suppressed by 10(-5) to 10(-7) M CdCl2 and by 10(-5) and 10(-6) M HgCl2, but not 10(-7) M HgCl2 nor 10(-4) to 10(-6) M PbCl2. Spontaneous and concanavalin A- or phytohemagglutinin-stimulated proliferation of metal-treated bovine blood mononuclear cells was not significantly different from that of nontreated control cells, except for enhanced spontaneous proliferation in response to 10(-5) M HgCl2. When proliferation was expressed as a stimulation index, a dose-dependent increase of spontaneous proliferation was observed in response to exposure to HgCl2 and PbCl2. Compared with response to 10(-6) or 10(-7) M CdCl2, reduction of mitogen-induced and spontaneous proliferation was observed on exposure to 10(-5) M CdCl2. Natural killer cell activity against YAC-1 target cells, evaluated by flow cytometry, was decreased only in cells exposed to 10 M HgCl2. CONCLUSION AND CLINICAL RELEVANCE: Bovine leukocytes are susceptible to the immunomodulatory effects of in vitro exposure to heavy metals at concentrations equal to or higher than those at which similar effects are seen for leukocytes from most other animal species for which data are available for comparison. Exception is phagocytosis, which is severely affected by low concentrations of CdCl2 and HgCl2 in cattle. Reduction of defense mechanisms on exposure to metals could lead to increased susceptibility to potential pathogens.     

Early weaning of winter flounder (Pseudopleuronectes americanus Walbaum) larvae on a commercial microencapsulated diet

Like most small marine fish larvae, the stomachs of winter flounder Pseudopleuronectes americanus are undeveloped at first feeding and have relatively reduced digestive capacity. This work was undertaken to test whether larvae at the onset of stomach differentiation (larval size about 5.5 mm) could be early weaned onto a commercial microencapsulated diet. We assessed the effect of early weaning by first comparing growth performance (standard length, total protein content and age at metamorphosis) of larvae fed enriched live prey from first feeding to a size of 5.5 mm and then reared on three different feeding regimes until metamorphosis: (1) live prey (LP) as a control group; (2) mixed feeding of live prey and microencapsulated diet (LP‐ME); (3) exclusively microencapsulated diet (ME) after fast weaning over 4 days (to a larval size of 6.2 mm). No differences were observed between larval development in the two first groups, which began metamorphosis at 40 days old. The larvae of the third group showed significantly slower growth that resulted in a delay of 4 days in the onset of metamorphosis. Differences in live prey availability between the treatments and the short transition period to allow the larvae to adapt to the new diet were identified as possible contributing factors to the slower growth and to the delay in metamorphosis of early weaned larvae. In a second experiment, the transitional weaning period was increased until the larvae were 6.6 mm in length. Weaning at that size resulted in no slowing of growth or delay in metamorphosis, suggesting that the feeding schedule was adequate.     

The conservation status of Sabellaria alveolata (L.) (Polychaeta: Sabellariidae) reefs in the Bay of Mont‐Saint‐Michel

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Mechanisms of evolution in Rickettsia conorii and R. prowazekii

Rickettsia conorii is an obligate intracellular bacterium that causes Mediterranean spotted fever in humans. We determined the 1,268,755-nucleotide complete genome sequence of R. conorii, containing 1374 open reading frames. This genome exhibits 804 of the 834 genes of the previously determined R. prowazekii genome plus 552 supplementary open reading frames and a 10-fold increase in the number of repetitive elements. Despite these differences, the two genomes exhibit a nearly perfect colinearity that allowed the clear identification of different stages of gene alterations with gene remnants and 37 genes split in 105 fragments, of which 59 are transcribed. A 38-kilobase sequence inversion was dated shortly after the divergence of the genus.     

Excitation Gap in the Normal State of Underdoped Bi2Sr2CaCu2O8+delta

Angle-resolved photoemission experiments reveal evidence of an energy gap in the normal state excitation spectrum of the cuprate superconductor Bi2Sr2CaCu2O8+delta. This gap exists only in underdoped samples and closes around the doping level at which the superconducting transition temperature Tc is a maximum. The momentum dependence and magnitude of the gap closely resemble those of the dx2-y2 gap observed in the superconducting state. This observation is consistent with results from several other experimental techniques, which also indicate the presence of a gap in the normal state. Some possible theoretical explanations for this effect are reviewed.     

Myelin-associated glycoprotein as a functional ligand for the Nogo-66 receptor

Axonal regeneration in the adult central nervous system (CNS) is limited by two proteins in myelin, Nogo and myelin-associated glycoprotein (MAG). The receptor for Nogo (NgR) has been identified as an axonal glycosyl-phosphatidyl-inositol (GPI)-anchored protein, whereas the MAG receptor has remained elusive. Here, we show that MAG binds directly, with high affinity, to NgR. Cleavage of GPI-linked proteins from axons protects growth cones from MAG-induced collapse, and dominant-negative NgR eliminates MAG inhibition of neurite outgrowth. MAG-resistant embryonic neurons are rendered MAG-sensitive by expression of NgR. MAG and Nogo-66 activate NgR independently and serve as redundant NgR ligands that may limit axonal regeneration after CNS injury.     

Botrytis pseudocinerea, a new cryptic species causing gray mold in French vineyards in sympatry with Botrytis cinerea

Botrytis cinerea is a major crop pathogen infesting >220 hosts worldwide. A cryptic species has been identified in some French populations but the new species, B. pseudocinerea, has not been fully delimited and established. The aim of this study was to distinguish between the two species, using phylogenetic, biological, morphological, and ecological criteria. Multiple gene genealogies confirmed that the two species belonged to different, well-supported phylogenetic clades. None of the morphological criteria tested (spore size, germination rate, or mycelial growth) was able to discriminate between these two species. Sexual crosses between individuals from the same species and different species were carried out. Only crosses between individuals from the same species were successful. Moreover, population genetics analysis revealed a high level of diversity within each species and a lack of gene flow between them. Finally, a population survey over time showed that B. cinerea was the predominant species but that B. pseudocinerea was more abundant in spring, on floral debris. This observation could not be explained by temperature adaptation in tests carried out in vitro or by aggressiveness on tomato or bean leaves. This study clearly establishes that B. cinerea and B. pseudocinerea constitute a complex of two cryptic species living in sympatry on several hosts, including grapevine and blackberry. We propose several biological or molecular tools for unambiguous differentiation between the two species. B. pseudocinerea probably makes a negligible contribution to gray mold epidemics on grapevine. This new species has been deposited in the MycoBank international database.     

Modulation of juvenile brook trout (Salvelinus fontinalis) cellular immune system after Aeromonas salmonicida challenge

In fish, the first line of defence against infectious microorganisms is based on non-specific cellular immune mechanisms (innate immunity). In this study, we measured the non-specific immune parameters (natural cytotoxic cells (NCC) activity, lymphoproliferation, percentage of phagocytosis and phagocytic activity) in brook trout (Salvelinus fontinalis) infected by a virulent strain of Aeromonas salmonicida. Eight days post-infection, the mortality of infected fish reached 70%. A transient immunostimulation of the NCC activity was noticed 24h post-infection, but there was no significant difference at 48 h. Then, infection of brook trout with A. salmonicida induced a biphasic immune response. At 24h post-infection, lymphoproliferation was drastically depressed but returned to control level at 96 h. A slight increase in the percentage of phagocytosis and the phagocytic activity was noticed throughout the experiment. Conversely the cell mortality was significantly higher in infected fish compared to control. The modulation of immunological parameters might reveal important clues on how innate immunity might protect fish from bacterial infections.     

Is acetyl/butyrylcholine specificity a marker for insecticide‐resistance mutations in insect acetylcholinesterase?

Substrate specificity has been widely studied in vertebrate cholinesterases and it has been shown that two phenylalanines in the acyl pocket of acetylcholinesterase govern the acceptance of the acetyl/butyryl moiety of the choline esters. As an insecticide‐resistance mutation has been evidenced in the acyl pocket of Drosophila melanogaster and Musca domestica acetylcholinesterase we investigated the possibility of linking changes in acetyl/butyrylthiocholine specificity with mutations in insect acetylcholinesterase. We thus analyzed the effect of 28 mutations in Drosophila enzyme on acetyl/butyrylthiocholine, N‐methyl/N‐propyl‐carbamates and ethyl/methyl‐paraoxon preference. It appeared that the highest changes on acetyl/butyrylthiocholine and N‐propyl/N‐methyl‐carbamates preference were due to mutations in the acyl pocket. Nevertheless, other insecticide‐resistance mutations, not located in the acyl pocket, also modified these substrate preferences. Moreover, the effect of mutations in the acyl pocket was hidden when some other insecticide‐resistance mutations were combined in the enzyme. Consequently, acetyl/butyrylthiocholine preference alteration cannot be used as a marker to localize a mutation in the insect AChE. © 2000 Society of Chemical Industry