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Synthesis of heat shock proteins (HSPs) following cellular stress is a response shared by many organisms. Amongst the HSP family, the ∼70 kDa HSPs are the most evolutionarily conserved with intracellular chaperone and extracellular immunoregulatory functions. This study focused on the effects of larval excretory-secretory products (ESPs) from the parasite Schistosoma mansoni on HSP70 protein expression levels in haemocytes (defence cells) from its snail intermediate host Biomphalaria glabrata. S. mansoni larval stage ESPs are known to interfere with haemocyte physiology and behaviour. Haemocytes from two different B. glabrata strains, one which is susceptible to S. mansoni infection and one which is resistant, both showed reduced HSP70 protein levels following 1 h challenge with S. mansoni ESPs when compared to unchallenged controls; however, the reduction observed in the resistant strain was less marked. The decline in intracellular HSP70 protein persisted for at least 5 h in resistant snail haemocytes only. Furthermore, in schistosome-susceptible snails infected by S. mansoni for 35 days, haemocytes possessed approximately 70% less HSP70. The proteasome inhibitor, MG132, partially restored HSP70 protein levels in ESP-challenged haemocytes, demonstrating that the decrease in HSP70 was in part due to intracellular degradation. The extracellular signal-regulated kinase (ERK) signalling pathway appears to regulate HSP70 protein expression in these cells, as the mitogen-activated protein-ERK kinase 1/2 (MEK1/2) inhibitor, U0126, significantly reduced HSP70 protein levels. Disruption of intracellular HSP70 protein expression in B. glabrata haemocytes by S. mansoni ESPs may be a strategy employed by the parasite to manipulate the immune response of the intermediate snail host.
Synthesis of heat shock proteins (HSPs) following cellular stress is a response shared by many organisms. Amongst the HSP family, the ∼70 kDa HSPs are the most evolutionarily conserved with intracellular chaperone and extracellular immunoregulatory functions. This study focused on the effects of larval excretory-secretory products (ESPs) from the parasite Schistosoma mansoni on HSP70 protein expression levels in haemocytes (defence cells) from its snail intermediate host Biomphalaria glabrata. S. mansoni larval stage ESPs are known to interfere with haemocyte physiology and behaviour. Haemocytes from two different B. glabrata strains, one which is susceptible to S. mansoni infection and one which is resistant, both showed reduced HSP70 protein levels following 1 h challenge with S. mansoni ESPs when compared to unchallenged controls; however, the reduction observed in the resistant strain was less marked. The decline in intracellular HSP70 protein persisted for at least 5 h in resistant snail haemocytes only. Furthermore, in schistosome-susceptible snails infected by S. mansoni for 35 days, haemocytes possessed approximately 70% less HSP70. The proteasome inhibitor, MG132, partially restored HSP70 protein levels in ESP-challenged haemocytes, demonstrating that the decrease in HSP70 was in part due to intracellular degradation. The extracellular signal-regulated kinase (ERK) signalling pathway appears to regulate HSP70 protein expression in these cells, as the mitogen-activated protein-ERK kinase 1/2 (MEK1/2) inhibitor, U0126, significantly reduced HSP70 protein levels. Disruption of intracellular HSP70 protein expression in B. glabrata haemocytes by S. mansoni ESPs may be a strategy employed by the parasite to manipulate the immune response of the intermediate snail host.
Parasites can harm hosts and influence populations, communities, and ecosystems. However, parasites are reciprocally affected by population‐ and community‐level dynamics. Understanding feedbacks between infection dynamics and larger‐scale epidemiological and ecological processes could improve predictions and reveal novel control methods. We evaluated how exploitative resource competition among hosts, a fundamental aspect of population biology, influences within‐host infection dynamics of the widespread human parasite Schistosoma mansoni in its intermediate host, Biomphalaria glabrata. We added size‐dependent consumption of shared resources to a parameterized bioenergetics model to predict a priori the growth, parasite production, and survival of an infected focal host coexisting with an uninfected conspecific competitor in an experiment that varied competitor size. The model quantitatively anticipated that competitors disrupt growth and parasite production and that these effects increase with competitor size. Fitting the model to these data improved its match to host survivorship. Thus, resource competition alters infection dynamics, there are strong size asymmetries in these effects, and size‐asymmetric resource competition effects on infection dynamics can be accurately predicted by bioenergetics theory. More broadly, this framework can assess parasite transmission and control in other contexts, such as in resource competitive host communities, or in response to eutrophication, food supplementation, or culling.
), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights.Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) v The history of research on the relationships between Biomphalaria spp. and larval trematodes, particularly Schistosoma mansoni, is long, active, and ongoing today. Snails of the genus Biomphalaria are of significant medical importance with many species living in freshwater habitats associated with human settlements; many of these snail species are obligate intermediate hosts of the human blood fluke S. mansoni, the causative agent of hepatosplenic schistosomiasis. This parasitic disease continues to disrupt the lives of about 200 million people in over 70 countries and prevents these individuals from otherwise reasonable expectations of healthy and productive lives. Furthermore, it is estimated that within the developing world, especially in sub-Saharan Africa, more than 700 million people are at risk of becoming infected, despite the efforts to control transmission in human and snail populations by mass chemotherapy and the use of molluscicides. Several factors, such as the absence of a schistosome vaccine, the recent appearance of resistance to antischistosome drugs, and human activities that expand snail habitats, have increased the need for a better understanding of schistosome-snail interactions. In recent years, the application of new technologies has contributed to the accumulation of considerable new information on this topic that may be of great use to biomedical scientists.In addition to the impact of Biomphalaria spp. on public health, these snails are also interesting models for the study of other topics such as population biology, including genetics and demography, proteomics, invertebrate immunobiology, mating systems, and biogeography, among others. Biomphalaria spp. snails have been extensively used as experimental biological models contributing significantly to new developments in many areas studied by biomedical scientists. Extensive coverage of these topics is included in this book, also considering trematode species other than schistosomes.The aim of the present book is to provide an overview of the recent advances in the Biomphalaria spp.-larval trematode interactions, especially in Biomphalariaschistosome systems. Emphasis is placed on gaps in our knowledge that must be filled to gain a better understanding of the relationships in these host-parasite systems. This may be critical for a deeper knowledge of the transmission of schistosomiasis and other snail-borne parasitic diseases. Pref...
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