Abstract
Several insect innate immune mechanisms are activated in response to infection by entomopathogenic nematodes (EPNs). In this review, we focus on the coagulation of hemolymph, which acts to stop bleeding after injury and prevent access of pathogens to the body cavity. After providing a general overview of invertebrate coagulation systems, we discuss recent findings in Drosophila melanogaster which demonstrate that clots protect against EPN infections. Detailed analysis at the cellular level provided insight into the kinetics of the secretion of Drosophila coagulation factors, including non-classical modes of secretion. Roughly, clot formation can be divided into a primary phase in which crosslinking of clot components depends on the activity of Drosophila transglutaminase and a secondary, phenoloxidase (PO)-dependent phase, characterized by further hardening and melanization of the clot matrix. These two phases appear to play distinct roles in two commonly used EPN infection models, namely Heterorhabditis bacteriophora and Steinernema carpocapsae. Finally, we discuss the implications of the coevolution between parasites such as EPNs and their hosts for the dynamics of coagulation factor evolution.
Highlights
The life cycle of entomopathogenic nematodes (EPNs) requires that they breach epithelial barriers and create wounds in order to reach the hemolymph, where they complete their life cycle. Once inside their insect hosts, many EPN species release symbiotic pathogenic bacteria of the genera Photorhabdus or Xenorhabdus [1]. Both the nematodes and their bacteria contribute to the success of EPN infections
We showed that hemocyte-derived activities of mammalian macrophages and granulocytes through their ability to phagocytose and release hemocyte coagulation factors and (2) crystal cells (CC)
We showed that hemocytederived staysthe within the of vicinity of hemocytes that are in trapped in similar the clot,tosimilar to what was within vicinity hemocytes that are trapped the clot, what was found in found in horseshoe clots [24,41]
Summary
The life cycle of entomopathogenic nematodes (EPNs) requires that they breach epithelial barriers and create wounds in order to reach the hemolymph, where they complete their life cycle Once inside their insect hosts, many EPN species release symbiotic pathogenic bacteria of the genera Photorhabdus or Xenorhabdus [1]. To varying extents, both the nematodes and their bacteria contribute to the success of EPN infections. EPN infections are known to induce immune factors, such as antimicrobial peptides, the two major immune pathways involved (imd and Toll) are shown to be dispensable for EPN control upon infection of Drosophila melanogaster with Heterorhabditis bacteriophora/Photorhabdus luminescens [2]
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