Further studies on the nutritional requirements of Colpoda duodenaria
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Journal of Cellular and Comparative Physiology↗
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Nature and time course of acclimation to aluminum in juvenile brook trout ( Salvelinus fontinalis ): II. Gill histology
Gill samples from juvenile brook trout ( Salvelinus fontinalis ) acclimated to low-level aluminum at pH 5.2 showed severe damage by day 4, with necrosis and fusion of secondary lamellae and hyperplasia and hypertrophy of mucous cells. Over the following 20 d, there was a continual process of repair with proliferation and hypertrophy of mucous cells. Qualitative analysis of gill samples plus physiology and mortality data collected in a companion study indicated progressive development (by day 10 onward) of increasing acclimation to Al. Quantitative analysis of gill samples on day 13 showed that mucous cell volume density had tripled and mucous cell area had doubled in Al-exposed fish compared with control fish. A lamellar fusion index showed evidence of fusion in Al-exposed fish by day 4 with recovery to nearly control levels by day 13. Physiological disturbances appear to be directly related to the histological changes observed in the gill epithelium. At the cellular level, changes in either mucous cell production and secretion or changes in mucus chemistry contribute, in part, to acclimation to Al.
Canadian Journal of Fisheries and Aquatic Sciences↗
Comparisons of stereological and other approaches for quantifying macrophage aggregates in piscine spleens
Macrophage aggregates (MA s) are focal accumulations of pigmented macrophages in the spleen and other tissues of fish. A central role of MA s is the clearance and destruction of degenerating cells and recycling of some cellular components. Macrophage aggregates also respond to chemical contaminants and infectious agents and may play a role in the adaptive immune response. Tissue damage or physiological stress can result in increased MA accumulation. As a result, MA s may be sensitive biomarkers of environmental stress in fish. Abundance of MA s in tissues has been reported in a variety of ways—most commonly as density, mean size, and relative area—but the utility of these estimates has not been compared. In this study, four different types of splenic MA abundance estimates (abundance score, density, relative area, and total volume) were compared in two fish populations (Striped Bass Morone saxatilis and White Perch M. americana ) with a wide range in ages. Stereological estimates of total volume indicated an increase in MA abundance with spleen volume, which generally corresponded to fish age, and with splenic infections (mycobacteria or trematode parasites). Abundance scores were generally limited in the ability to detect changes in MA abundance by these factors, whereas density estimates were greatly influenced by changes in spleen volume. In some instances, densities declined while the total volume of MA s and spleen volume increased. Experimentally induced acute stress resulted in a decrease in spleen volume and an increase in MA density, although the total volume of MA s remained unchanged. Relative area estimates accounted for the size and number of MA s but not for changes in organ volume. Total volume is an absolute measure of MA abundance irrespective of changes in organ volume or patterns of accumulation and may provide an improved means of quantifying MA s in the spleens of fish.
Maryland↗
Upper thermal limits of growth in brook trout and their relationship to stress physiology
Despite the threat of climate change, the physiological mechanisms responsible for reduced performance at high temperatures remain unclear for most species. Elevated but sublethal temperatures may act via endocrine and cellular stress responses to limit performance in important life-history traits such as growth. Here, brook trout ( Salvelinus fontinalis ) subjected to chronically elevated or daily oscillating temperatures were monitored for growth and physiological stress responses. Growth rate decreased at temperatures above 16°C and was negative at 24°C, with an estimated upper limit for positive growth of 23.4°C. Plasma cortisol increased with temperature and was 12- and 18-fold higher at 22 and 24°C, respectively, than at 16°C, whereas plasma glucose was unaffected by temperature. Abundance of heat shock protein 70 (HSP70) in the gill increased with temperature and was 11- and 56-fold higher at 22°C and 24°C, respectively, than at 16°C. There was no relationship between temperature and plasma Cl − , but there was a 53% and 80% decrease in gill Na + /K + -ATPase activity and abundance at 24°C in comparison with 16°C. Daily temperature oscillations of 4°C or 8°C (19–23°C or 17–25°C) were compared with 21°C controls. Growth rate decreased with temperature and was 43% and 35% lower by length and mass, respectively, in the 8°C daily oscillation treatment than in the controls. There was no effect of temperature oscillation on plasma cortisol or glucose levels. In contrast, gill HSP70 abundance increased with increasing daily oscillation and was 40- and 700-fold greater at 4°C and 8°C daily oscillation, respectively, than in the constant temperature controls. In individuals exposed to 17–25°C diel oscillations for 4 days and then allowed to recover at 21°C, gill HSP70 abundance was still elevated after 4 days recovery, but not after 10 days. Our results demonstrate that elevated temperatures induce cellular and endocrine stress responses and provide a possible mechanism by which growth is limited at elevated temperatures. Temperature limitations on growth may play a role in driving brook trout distributions in the wild.
Journal of Experimental Biology↗
IL-2 and IL-12 alter NK cell responsiveness to IFN-γ-inducible protein 10 by down-regulating CXCR3 expression
Cytokine treatment of NK cells results in alterations in multiple cellular responses that include cytotoxicity, cytokine production, proliferation, and chemotaxis. To understand the molecular mechanisms underlying these responses, microarray analysis was performed and the resulting gene expression patterns were compared between unstimulated, IL-2, IL-2 plus IL-12, and IL-2 plus IL-18-stimulated NK92 cells. RNase protection assays and RT-PCR confirmed microarray predictions for changes in mRNA expression for nine genes involved in cell cycle progression, signal transduction, transcriptional activation, and chemotaxis. Multiprobe RNase protection assay also detected changes in the expression of CCR2 mRNA, a gene that was not imprinted on the microarray. We subsequently expanded our search for other chemokine receptor genes absent from the microarray and found an IL-2- and IL-12-dependent decrease in CXCR3 receptor mRNA expression in NK92 cells. A detailed analysis of CXCR3 expression in primary NK cells revealed that an IL-2 and an IL-12 together significantly decreased the CXCR3 receptor mRNA and receptor surface expression by 6 and 24 h of treatment, respectively. This decrease in receptor expression was associated with a significant reduction in chemotaxis in the presence of IFN-γ-inducible protein-10. The decline in CXCR3 mRNA was due to transcriptional and posttranscriptional mechanisms as the addition of actinomycin D to IL-2- and IL-12-treated NK92 slightly altered the half-life of the CXCR3 mRNA. Collectively, these data suggest that IL-2 and IL-12 directly affect NK cell migratory ability by rapid and direct down-regulation of chemokine receptor mRNA expression. Natural killer (NK) cells are large granular lymphocytes that play an important role in the defense against virally infected or malignant cells (1). Their activity can be characterized as nonadaptive and independent of MHC restriction (1, 2). A variety of NK cell functions including cytotoxicity, proliferation, chemotaxis, and cytokine production are modulated by regulatory cytokines including IFN-αβ, IL-2, IL-12, IL-18, IL-10, and TNF (reviewed in Refs. 3 and 4). Because cytokines induce such a broad range of effects in NK cells, the potential for alterations in gene expression in stimulated cells is very great. To determine which genes are regulated in response to cytokine stimulation, our laboratory has used cDNA microarray technology to examine gene expression in NK cells. Microarray technology is very useful because it allows for large-scale examination of gene expression. Additionally, this technology has proved useful in identifying physiologically relevant gene expression patterns in eukaryotic systems such as yeast (5) and fibroblasts (6) as well as predicting patterns of gene expression in tumor cells (7, 8). To examine gene expression in response to cytokine stimulation, a human NK cell line, NK92, was stimulated with IL-2 alone or in combination with IL-12 or IL-18. These cytokines were chosen because of their ability to induce NK cell responses; however, little is known about the repertoire of genes that are activated by these cytokines. Microarray analysis of gene expression in NK92 cells identified a variety of genes whose mRNA expression patterns change in response to cytokine stimulation. The genes encoding the mRNAs are not specific to any one pathway; however, changes in cytokine, chemokine, and chemokine receptor gene mRNAs were prevalent. Our mRNA studies on chemokine receptor gene expression were extended to cell surface analysis of receptor densities in cytokine-treated primary NK cells. Using FACS analysis, we observed a significant decrease in CXCR3 receptor expression in NK cells treated for 24 h with IL-2 and IL-12 alone or in combination. Recently, alterations in chemokine receptor expression were reported in IL-2-stimulated NK cells (9); however, the cells were cultured in IL-2 for 8–10 days. In contrast, our data demonstrate that cytokines can modify chemokine receptor function within hours, thus supporting a model whereby cytokines, in particular IL-2 and IL-12, regulate chemokine receptor expression in a direct, rapid, and novel manner.
Journal of Immunology↗