Changes in hemlock looper [Lepidoptera: Geometridae] pupal distribution through a 3-year outbreak cycle

La distribution des chrysalides de l’arpenteuse de la pruche, Lambdina fiscellaria, a été étudiée au cours d’un cycle épidémique d’une durée de trois ans près du Lac Princeton sur l’île d’Anticosti au Québec. Au total, 10 sapins ont été coupés et toutes les chrysalides ont été comptées sur le tronc et les branches (partie non-foliée vs foliée) de la cime inférieure, médiane et supérieure, ainsi que sur le tronc sous la cime. En condition préépidémique, les chrysalides ont principalement été trouvées sur les branches des cimes médianes et supérieures. Durant l’épidémie, la densité des chrysalides n’a pas augmenté dans ces sites de pupaison et les larves se sont surtout transformées en chrysalides sur le tronc, à partir du sol jusque dans la cime médiane, ainsi que sur les branches de la cime inférieure. Peu de chrysalides ont été trouvées sur la partie foliée des branches en période post-épidémique, la plupart étant trouvées sur la partie basale non-foliée qui apparaît comme un endroit préférentiel pour la pupaison de l'arpenteuse de la pruche. De façon à optimiser la détection des augmentations de populations dans les réseaux de surveillance, des pièges à chrysalides devraient être placés à hauteur de poitrine sur le tronc de sapins baumiers.The hemlock looper, Lambdina fiscellaria, pupal distribution was studied through a 3-year outbreak cycle near Lac Princeton on Anticosti Island in Quebec. Over the 3 years, 10 balsam fir trees were cut and all pupae were counted on the stem and branches (non-foliated vs foliated parts) of the lower, middle and upper crowns and on the stem below crown. In pre-outbreak conditions, pupae were mostly found on branches of the middle and upper crowns. During the outbreak, pupal density did not increase on these parts of the trees, since pupae were mostly found on the stem, from the ground to the middle crown, and on branches of the lower crown. Few pupae were found on the foliated portion of branches in post-outbreak conditions but most were found on the basal non-foliated part of branches, which appears to be a preferred location for hemlock looper pupation. In order to optimize detection of population increases in monitoring networks, we suggest using pupal traps at breast height on balsam fir trees

Salvia miltiorrhiza water-soluble extract, but not its constituent salvianolic acid B, abrogates LPS-induced NF-kappaB signalling in intestinal epithelial cells

Herbal medicine has become an increasing popular therapeutic alternative among patients suffering from various inflammatory disorders. The Salvia miltiorrhizae water-soluble extract (SME) have been shown to possess antioxidant and anti-inflammatory properties in vitro. However, the mechanism of action and impact of SME on LPS-induced gene expression is still unknown. We report that SME significantly abrogated LPS-induced IκB phosphorylation/degradation, NF-κB transcriptional activity and ICAM-1 gene expression in rat IEC-18 cells. Chromatin immunoprecipitation assay demonstrated that LPS-induced RelA recruitment to the ICAM-1 gene promoter was inhibited by SME. Moreover, in vitro kinase assay showed that SME directly inhibits LPS induced IκB kinase (IKK) activity in IEC-18 cells. To investigate the physiological relevance of SME inhibitory activity on NF-κB signalling, we used small intestinal explants and primary intestinal epithelial cells derived from a transgenic mouse expressing the enhanced green fluorescent protein (EGFP) under the transcriptional control of NF-κB cis-elements (cis-NF-κBEGFP). SME significantly blocked LPS-induced EGFP expression and IκBα phosphorylation in intestinal explants and primary IECs, respectively. However, salvianolic acid B, an activate component of SME did not inhibit NF-κB transcriptional activity and IκB phosphorylation/degradation in IEC-18 cells. These results indicate that SME blocks LPS-induced NF-κB signalling pathway by targeting the IKK complex in intestinal epithelial cells. Modulation of bacterial product-mediated NF-κB signalling by natural plant extracts may represent an attractive strategy towards the prevention and treatment of intestinal inflammation

Microbes and colorectal cancer: is there a relationship?

The human colon plays host to as many as 15,000–36,000 bacterial species, amounting to more than 100 trillion bacteria 1,2. The microbiota and their associated prokaryotic genome is an integral part of the host and uniquely contributes to various biologic processes such as maturation and development of the mucosal immune system, metabolic capacity, and intestinal epithelial cell proliferation and differentiation 3. An international effort is currently underway to catalogue the repertoire of microorganisms present in the intestines of healthy humans and of those with pathologic conditions. The human microbiome project—for which the U.S. National Institutes of Health has contributed more than $110 million—is aiming to determine the structure of the microbial community associated with the human body and the functions thereby served in health and disease 3,4

Environmental Determinants of Malaria Transmission Around the Koka Reservoir in Ethiopia

New dam construction is known to exacerbate malaria transmission in Africa as the vectors of malaria—Anopheles mosquitoes—use bodies of water as breeding sites. Precise environmental mechanisms of how reservoirs exacerbate malaria transmission are yet to be identified. Understanding of these mechanisms should lead to a better assessment of the impacts of dam construction and to new prevention strategies. Combining extensive multiyear field surveys around the Koka Reservoir in Ethiopia and rigorous model development and simulation studies, environmental mechanisms of malaria transmission around the reservoir were examined. Most comprehensive and detailed malaria transmission model, Hydrology, Entomology, and Malaria Transmission Simulator, was applied to a village adjacent to the reservoir. Significant contributions to the dynamics of malaria transmission are shaped by wind profile, marginal pools, temperature, and shoreline locations. Wind speed and wind direction influence Anopheles populations and malaria transmission during the major and secondary mosquito seasons. During the secondary mosquito season, a noticeable influence was also attributed to marginal pools. Temperature was found to play an important role, not so much in Anopheles population dynamics, but in malaria transmission dynamics. Change in shoreline locations drives malaria transmission dynamics, with closer shoreline locations to the village making malaria transmission more likely. Identified environmental mechanisms help in predicting malaria transmission seasons and in developing village relocation strategies upon dam construction to minimize the risk of malaria

The struggle within: Microbial influences on colorectal cancer:

Recently, an unprecedented effort has been directed at understanding the interplay between chronic inflammation and development of cancer, with the case of inflammatory bowel disease (IBD)-associated colorectal cancer at the forefront of this research endeavor. The last decade has been particularly fertile, with the discovery of numerous innovative paradigms linking various inflammatory, proliferative, and innate and adaptive immune signaling pathways to the development of colorectal cancer. Because of the preponderant role of the intestinal microbiota in the initiation and progression of IBD, recent efforts have been directed at understanding the relationship between bacteria and colorectal cancer. The microbiota and its collective genome, the microbiome, form a diverse and complex ecological community that profoundly impacts intestinal homeostasis and disease states. This review will discuss the differential influence of the microbiota on the development of IBD-associated colorectal cancer and highlight the role of innate immune sensor-dependent as well as -independent mechanisms in this pathology

MedZIM: Mediation analysis for Zero-Inflated Mediators with applications to microbiome data

The human microbiome can contribute to the pathogenesis of many complex diseases such as cancer and Alzheimer's disease by mediating disease-leading causal pathways. However, standard mediation analysis is not adequate in the context of microbiome data due to the excessive number of zero values in the data. Zero-valued sequencing reads, commonly observed in microbiome studies, arise for technical and/or biological reasons. Mediation analysis approaches for analyzing zero-inflated mediators are still lacking largely because of challenges raised by the zero-inflated data structure: (a) disentangling the mediation effect induced by the point mass at zero; and (b) identifying the observed zero-valued data points that are actually not zero (i.e., false zeros). We develop a novel mediation analysis method under the potential-outcomes framework to fill this gap. We show that the mediation effect of the microbiome can be decomposed into two components that are inherent to the two-part nature of zero-inflated distributions. The first component corresponds to the mediation effect attributable to a unit-change over the positive relative abundance and the second component corresponds to the mediation effect attributable to discrete binary change of the mediator from zero to a non-zero state. With probabilistic models to account for observing zeros, we also address the challenge with false zeros. A comprehensive simulation study and the applications in two real microbiome studies demonstrate that our approach outperforms existing mediation analysis approaches.Comment: Corresponding: Zhigang L

Sodium and its manifold impact on our immune system

The Western diet is rich in salt, and a high salt diet (HSD) is suspected to be a risk factor for cardiovascular diseases. It is now widely accepted that an experimental HSD can stimulate components of the immune system, potentially exacerbating certain autoimmune diseases, or alternatively, improving defenses against certain infections, such as cutaneous leishmaniasis. However, recent findings show that an experimental HSD may also aggravate other infections (e.g., pyelonephritis or systemic listeriosis). Here, we discuss the modulatory effects of a HSD on the microbiota, metabolic signaling, hormonal responses, local sodium concentrations, and their effects on various immune cell types in different tissues. We describe how these factors are integrated, resulting either in immune stimulation or suppression in various tissues and disease settings

Toll-Like Receptor 9-Dependent Macrophage Activation by Entamoeba histolytica DNA

Activation of the innate immune system by bacterial DNA and DNA of other invertebrates represents a pathogen recognition mechanism. In this study we investigated macrophage responses to DNA from the intestinal protozoan parasite Entamoeba histolytica. E. histolytica genomic DNA was purified from log-phase trophozoites and tested with the mouse macrophage cell line RAW 264.7. RAW cells treated with E. histolytica DNA demonstrated an increase in levels of tumor necrosis factor alpha (TNF-α) mRNA and protein production. TNF-α production was blocked by pretreatment with chloroquine or monensin. In fact, an NF-κB luciferase reporter assay in HEK cells transfected with human TLR9 demonstrated that E. histolytica DNA signaled through Toll-like receptor 9 (TLR9) in a manner similar to that seen with CpG-ODN. Immunofluorescence assays confirmed NF-κB activation in RAW cells, as seen by nuclear translocation of the p65 subunit. Western blot analysis demonstrated mitogen-activated protein kinase activation by E. histolytica DNA. E. histolytica DNA effects were abolished in MYD88−/− mouse-derived macrophages. In the context of disease, immunization with E. histolytica DNA protected gerbils from an E. histolytica challenge infection. Taken together, these results demonstrate that E. histolytica DNA is recognized by TLR9 to activate macrophages and may provide an innate defense mechanism characterized by the induction of the inflammatory mediator TNF-α