Mechanisms Of Host Manipulation Research Articles

Metabolomics Provides New Insights into Host Manipulation Strategies by Asobara japonica (Hymenoptera: Braconidae), a Fruit Fly Parasitoid

Asobara japonica (Hymenoptera: Braconidae) is an endoparasitoid wasp that can successfully parasitize a wide range of host species across the Drosophila genus, including the invasive crop pest Drosophila suzukii. Parasitoids are capable of regulating the host metabolism to produce the nutritional metabolites for the survival of their offspring. Here, we intend to investigate the metabolic changes in D. melanogaster hosts after parasitization by A. japonica, using the non-targeted LC-MS (liquid chromatography-mass spectrometry) metabolomics analysis. In total, 3043 metabolites were identified, most of which were not affected by A. japonica parasitization. About 205 metabolites were significantly affected in parasitized hosts in comparison to non-parasitized hosts. The changed metabolites were divided into 10 distinct biochemical groups. Among them, most of the lipid metabolic substances were significantly decreased in parasitized hosts. On the contrary, most of metabolites associated with the metabolism of amino acids and sugars showed a higher abundance of parasitized hosts, and were enriched for a wide range of pathways. In addition, eight neuromodulatory-related substances were upregulated in hosts post A. japonica parasitization. Our results reveal that the metabolites are greatly changed in parasitized hosts, which might help uncover the underlying mechanisms of host manipulation that will advance our understanding of host-parasitoid coevolution.

Mechanisms of host manipulation by Neisseria gonorrhoeae.

Neisseria gonorrhoeae (also known as gonococcus) has been causing gonorrhoea in humans since ancient Egyptian times. Today, global gonorrhoea infections are rising at an alarming rate, in concert with an increasing number of antimicrobial-resistant strains. The gonococcus has concurrently evolved several intricate mechanisms that promote pathogenesis by evading both host immunity and defeating common therapeutic interventions. Central to these adaptations is the ability of the gonococcus to manipulate various host microenvironments upon infection. For example, the gonococcus can survive within neutrophils through direct regulation of both the oxidative burst response and maturation of the phagosome; a concerning trait given the important role neutrophils have in defending against invading pathogens. Hence, a detailed understanding of how N. gonorrhoeae exploits the human host to establish and maintain infection is crucial for combating this pathogen. This review summarizes the mechanisms behind host manipulation, with a central focus on the exploitation of host epithelial cell signaling to promote colonization and invasion of the epithelial lining, the modulation of the host immune response to evade both innate and adaptive defenses, and the manipulation of host cell death pathways to both assist colonization and combat antimicrobial activities of innate immune cells. Collectively, these pathways act in concert to enable N. gonorrhoeae to colonize and invade a wide array of host tissues, both establishing and disseminating gonococcal infection.

Wolbachiauses host microRNAs to manipulate host gene expression and facilitate colonization of the dengue vectorAedes aegypti

The obligate endosymbiont Wolbachia pipientis is found in a wide range of invertebrates where they are best known for manipulating host reproduction. Recent studies have shown that Wolbachia also can modulate the lifespan of host insects and interfere with the development of human pathogens in mosquito vectors. Despite considerable study, very little is known about the molecular interactions between Wolbachia and its hosts that might mediate these effects. Using microarrays, we show that the microRNA (miRNA) profile of the mosquito, Aedes aegypti, is significantly altered by the wMelPop-CLA strain of W. pipientis. We found that a host miRNA (aae-miR-2940) is induced after Wolbachia infection in both mosquitoes and cell lines. One target of aae-miR-2940 is the Ae. aegypti metalloprotease gene. Interestingly, expression of the target gene was induced after Wolbachia infection, ectopic expression of the miRNA independent of Wolbachia, or transfection of an artificial mimic of the miRNA into mosquito cells. We also confirmed the interaction of aae-miR-2940 with the target sequences using GFP as a reporter gene. Silencing of the metalloprotease gene in both Wolbachia-infected cells and adult mosquitoes led to a significant reduction in Wolbachia density, as did inhibition of the miRNA in cells. These results indicate that manipulation of the mosquito metalloprotease gene via aae-miR-2940 is crucial for efficient maintenance of the endosymbiont. This report shows how Wolbachia alters the host miRNA profile and provides insight into the mechanisms of host manipulation used by this widespread endosymbiont.