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Abstract Background Tobacco smoking alters the DNA methylation profiles of immune cells which may underpin some of the pathogenesis of smoking-associated diseases. To link smoking-driven epigenetic effects in specific immune cell types with disease risk, we isolated six leukocyte subtypes, CD14+ monocytes, CD15+ granulocytes, CD19+ B cells, CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells, from whole blood of 67 healthy adult smokers and 74 nonsmokers for epigenome-wide association study (EWAS) using Illumina 450k and EPIC methylation arrays. Results Numbers of smoking-associated differentially methylated sites (smCpGs) at genome-wide significance (p

Background: Tobacco smoking alters the DNA methylation profiles of immune cells which may underpin some of the pathogenesis of smoking-associated diseases. To link smoking-driven epigenetic effects in specific immune cell types with disease risk, we isolated six leukocyte subtypes, CD14+ monocytes, CD15+ granulocytes, CD19+ B cells, CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells, from whole blood of 67 healthy adult smokers and 74 nonsmokers for epigenome-wide association study (EWAS) using Illumina 450k and EPIC methylation arrays. Results: Numbers of smoking-associated differentially methylated sites (smCpGs) at genome-wide significance (p < 1.2 × 10−7) varied widely across cell types, from 5 smCpGs in CD8+ T cells to 111 smCpGs in CD19+ B cells. We found unique smoking effects in each cell type, some of which were not apparent in whole blood. Methylation-based deconvolution to estimate B cell subtypes revealed that smokers had 7.2% (p = 0.033) less naïve B cells. Adjusting for naïve and memory B cell proportions in EWAS and RNA-seq allowed the identification of genes enriched for B cell activation-related cytokine signaling pathways, Th1/Th2 responses, and hematopoietic cancers. Integrating with large-scale public datasets, 62 smCpGs were among CpGs associated with health-relevant EWASs. Furthermore, 74 smCpGs had reproducible methylation quantitative trait loci single nucleotide polymorphisms (SNPs) that were in complete linkage disequilibrium with genome-wide association study SNPs, associating with lung function, disease risks, and other traits. Conclusions: We observed blood cell-type-specific smCpGs, a naïve-to-memory shift among B cells, and by integrating genome-wide datasets, we identified their potential links to disease risks and health traits. [ABSTRACT FROM AUTHOR]

Erythrocytes, thrombocytes, lymphocytes and neutrophils were the principal blood cell types found in the blood of Clarias batrachus, Ophicephalus striatus, Oreochromis mossambicus and Oreochromis niloticus. Eosinophils and basophils were observed in Ophicephalus striatus but were absent in Clarias batrachus. Eosinophils but no basophils were seen in Oreochromis mossambicus and Oreochromis niloticus. Along with mature erythrocytes, immature, dividing, senile, and disintegrated erythrocytes were also observed from the circulating blood of the four fish species.From Clarias batrachus, eight species of helminths were recovered, namely, Cichlidogyrus sclerosus, Actinocleidus sp., Phyllodistomum sp., Opegaster minima, Gauhatiana batrachii, Bovienia serialis, Procamallanus darius, and Philometra sp. The parasites recovered from Ophicephalus striatus were Diplostomulum sp., Camallanus ophicephali, Arqulus indicus, and Lernaea cyprinacea. Cichlidogyrus sclerosus and Transversotrema laruei were collected from Oreochromis mossambicus and Oreochromis niloticus; from the latter, Gyrodactylus medius was also recovered. The average parasite burden was generally low.Parasitized and unparasitized fishes were active and appeared healthy. Blood values of parasitized fishes showed few significant differences from those of unparasitized fish groups. No parasitized fish group showed significant reduction in mean hematocrit and RBC count or significant increase in mean WBC count and mean % neutrophils in comparison with unparasitized group of the same fish species.

Abstract: Juvenile Senegalese soles (Solea senegalensis) were exposed to estuarine sediments through 28-day laboratory and in situ (field) bioassays. The sediments, collected from three distinct sites (a reference plus two contaminated) of the Sado Estuary (W Portugal) were characterized for total organic matter, redox potential, fine fraction and for the levels of metals, polycyclic aromatic hydrocarbons (PAHs) and organochlorines, namely polychlorinated biphenyls (PCBs) and dichloro diphenyl tricholoethane plus its main metabolites (DDTs). Genotoxicity was determined in whole peripheral blood by the single-cell gel electrophoresis (SCGE or “comet”) assay and by scoring erythrocytic nuclear abnormalities (ENA). Analysis was complemented with the determination of lipid peroxidation in blood plasma by the thiobarbituric acid reactive substances (TBARS) protocol and cell type sorting. The results showed that exposure to contaminated sediments induced DNA fragmentation and clastogenesis. Still, laboratory exposure to the most contaminated sediment revealed a possible antagonistic effect between metallic and organic contaminants that might have been enhanced by increased bioavailability. The laboratory assay caused a more pronounced increase in ENA whereas a very significant increase in DNA fragmentation was observed in field-tested fish exposed to the reference sediment, which is likely linked to increased lipid peroxidation that probably occurred due to impaired access to food. Influence of natural pathogens was ruled out by unaltered leukocyte counts. The statistical integration of data correlated lipid peroxidation with biological variables such as fish length and weight, whereas the genotoxicity biomarkers were more correlated to sediment contamination. It was demonstrated that laboratory and field bioassays for the risk assessment of sediment contamination may yield different genotoxicity profiles although both provided results that are in overall accordance with sediment contamination levels. While field assays may provide more ecologically relevant data, the multiple environmental variables may produce sufficient background noise to mask the true effects of contamination. [Copyright &y& Elsevier]