The role of proboscis of the malaria vector mosquito Anopheles stephensi in host-seeking behavior

<p>Abstract</p> <p>Background</p> <p>The proboscis is an essential head appendage in insects that processes gustatory code during food intake, particularly useful considering that blood-sucking arthropods routinely reach vessels under the host skin using this proboscis as a probe.</p> <p>Results</p> <p>Here, using an automated device able to quantify CO₂-activated thermo (35°C)-sensing behavior of the malaria vector <it>Anopheles stephensi</it>, we uncovered that the protruding proboscis of mosquitoes contributes unexpectedly to host identification from a distance. Ablation experiments indicated that not only antennae and maxillary palps, but also proboscis were required for the identification of pseudo-thermo targets. Furthermore, the function of the proboscis during this behavior can be segregated from CO₂detection required to evoke mosquito activation, suggesting that the proboscis of mosquitoes divide the proboscis into a "thermo-antenna" in addition to a "thermo-probe".</p> <p>Conclusions</p> <p>Our findings support an emerging view with a possible role of proboscis as important equipment during host-seeking, and give us an insight into how these appendages likely evolved from a common origin in order to function as antenna organs.</p

Loop-mediated isothermal amplification applied to filarial parasites detection in the mosquito vectors: Dirofilaria immitis as a study model

<p>Abstract</p> <p>Background</p> <p>Despite recent advances in our understanding of the basic biology behind transmission of zoonotic infectious diseases harbored by arthropod vectors these diseases remain threatening public health concerns. For effective control of vector and treatment, precise sampling indicating the prevalence of such diseases is essential. With an aim to develop a quick and simple method to survey zoonotic pathogen-transmitting vectors, LAMP (loop-mediated isothermal amplification) was applied to the detection of filarial parasites using a filarial parasite-transmitting experimental model that included one of the mosquito vectors, <it>Aedes aegypti</it>, and the canine heartworm, <it>Dirofilaria immitis</it>.</p> <p>Results</p> <p>LAMP reactions amplifying the cytochrome oxidase subunit I gene demonstrated high sensitivity when a single purified <it>D. immitis </it>microfilaria was detected. Importantly, the robustness of the LAMP reaction was revealed upon identification of an infected mosquito carrying just a single parasite, a level easily overlooked using conventional microscopic analysis. Furthermore, successful detection of <it>D. immitis </it>in wild-caught mosquitoes demonstrated its applicability to field surveys.</p> <p>Conclusion</p> <p>Due to its simplicity, sensitivity, and reliability, LAMP is suggested as an appropriate diagnostic method for routine diagnosis of mosquito vectors carrying filarial parasites. This method can be applied to the survey of not only canine filariasis but also lymphatic filariasis, another major public health problem. Therefore, this method offers great promise as a useful diagnostic method for filarial parasite detection in endemic filariasis regions.</p

Intrinsic Tumor Suppression and Epithelial Maintenance by Endocytic Activation of Eiger/TNF Signaling in Drosophila

SummaryOncogenic alterations in epithelial tissues often trigger apoptosis, suggesting an evolutionary mechanism by which organisms eliminate aberrant cells from epithelia. In Drosophila imaginal epithelia, clones of cells mutant for tumor suppressors, such as scrib or dlg, lose their polarity and are eliminated by cell death. Here, we show that Eiger, the Drosophila tumor necrosis factor (TNF), behaves like a tumor suppressor that eliminates oncogenic cells from epithelia through a local endocytic JNK-activation mechanism. In the absence of Eiger, these polarity-deficient clones are no longer eliminated; instead, they grow aggressively into tumors. We show that in scrib clones endocytosis is elevated, which translocates Eiger to endocytic vesicles and leads to activation of apoptotic JNK signaling. Furthermore, blocking endocytosis prevents both JNK activation and cell elimination. Our data indicate that TNF signaling and the endocytic machinery could be components of an evolutionarily conserved fail-safe mechanism by which animals protect against neoplastic development

Multivariable analysis of host amino acids in plasma and liver during infection of malaria parasite <it>Plasmodium yoelii</it>

Abstract Background Malaria is the most significant human parasitic disease, and yet understanding of the energy metabolism of the principle pathogen, Plasmodium falciparum, remains to be fully elucidated. Amino acids were shown to be essential nutritional requirements since early times and much of the current knowledge of Plasmodium energy metabolism is based on early biochemical work, performed using basic analytical techniques, carried out almost exclusively on human plasma with considerable inter-individual variability. Methods In order to further characterize the fate of amino acid metabolism in malaria parasite, multivariate analysis using statistical modelling of amino acid concentrations (aminogram) of plasma and liver were determined in host infected with rodent malaria parasite, Plasmodium yoelii. Results and conclusion Comprehensive and statistical aminogram analysis revealed that P. yoelii infection caused drastic change of plasma and liver aminogram, and altered intra- and inter-correlation of amino acid concentration in plasma and liver. These findings of the interactions between amino acids and Plasmodium infection may provide insight to reveal the interaction between nutrients and parasites.</p

Plant Hormone Salicylic Acid Produced by a Malaria Parasite Controls Host Immunity and Cerebral Malaria Outcome

<div><p>The apicomplexan parasite <i>Toxoplasma gondii</i> produces the plant hormone abscisic acid, but it is unclear if phytohormones are produced by the malaria parasite <i>Plasmodium</i> spp., the most important parasite of this phylum. Here, we report detection of salicylic acid, an immune-related phytohormone of land plants, in <i>P</i>. <i>berghei</i> ANKA and <i>T</i>. <i>gondii</i> cell lysates. However, addition of salicylic acid to <i>P</i>. <i>falciparum</i> and <i>T</i>. <i>gondii</i> culture had no effect. We transfected <i>P</i>. <i>falciparum</i> 3D7 with the <i>nahG</i> gene, which encodes a salicylic acid-degrading enzyme isolated from plant-infecting <i>Pseudomonas</i> sp., and established a salicylic acid-deficient mutant. The mutant had a significantly decreased concentration of parasite-synthesized prostaglandin E₂, which potentially modulates host immunity as an adaptive evolution of <i>Plasmodium</i> spp. To investigate the function of salicylic acid and prostaglandin E₂ on host immunity, we established <i>P</i>. <i>berghei</i> ANKA mutants expressing <i>nahG</i>. C57BL/6 mice infected with <i>nahG</i> transfectants developed enhanced cerebral malaria, as assessed by Evans blue leakage and brain histological observation. The <i>nahG</i>-transfectant also significantly increased the mortality rate of mice. Prostaglandin E₂ reduced the brain symptoms by induction of T helper-2 cytokines. As expected, T helper-1 cytokines including interferon-γ and interleukin-2 were significantly elevated by infection with the <i>nahG</i> transfectant. Thus, salicylic acid of <i>Plasmodium</i> spp. may be a new pathogenic factor of this threatening parasite and may modulate immune function via parasite-produced prostaglandin E₂.</p></div

Identification of salicylic acid from <i>Plasmodium berghei</i> ANKA.

<p><i>P</i>. <i>berghei</i> ANKA was purified from infected mice blood, and salicylic acid (SA) was extracted, and analyzed by LC-triple TOF mass spectrometry. (A) Structural formula of SA. (B) LC chromatogram of SA standard (control) and <i>P</i>. <i>berghei</i> ANKA sample. (C) Fragmentation analysis of peaks in (B) (colored in aqua). Collision energy was 20 eV.</p

Parasite SA influences the cerebral malaria outcome.

<p>(A-C) Histological observation of infected mouse cerebellums. (A) Cerebellum infected by <i>nahG</i>-expressing parasites. Note the sequestrated leukocytes in microvessels. The inset image shows a higher magnification of the boxed portion. Phagocytized hemozoin is observed (arrowhead). (B) Brain of a mouse infected with <i>gfp</i>-expressing parasites. Slight microbleeding was observed, but no sequestrated vessels were found. (C) Brain of an uninfected control. Sections were stained by hematoxylin and eosin. (D) Evans blue leakage analysis of the severity of cerebral malaria. Photographs of brains from mice infected with <i>nahG</i>- (left upper) and <i>gfp-</i> (left middle) expressing parasites and uninfected controls (left bottom), and quantification of dye leakage (right). Mice (n = 5) were sacrificed at 6 days post-infection. Solid line, p<0.01; dashed line, p<0.05. C57BL/6 mice at 6 days post-infection were used for all experiments. Bar: 50 μm.</p