Document Detail


Locust cellular defense against infections: Sites of pathogen clearance and hemocyte proliferation.
MedLine Citation:
PMID:  25281274     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The locust cellular defense is mediated by hemocytes and hematopoietic tissue. In Locusta migratoria, the hemocytes and hematopoietic tissue mutually assist each other in clearing invading pathogens from circulation. A β-1, 3-glucan infection induces nodule formation and apoptotic, TUNEL positive, cells in the hematopoietic tissue and massive loss of hemocytes in the circulation, calling for instant proliferation of hemocytes and hematopoietic tissue cells to assure continued host cellular defense. As the locust hematopoietic tissue persists at the adult stage, it was originally designated as being the major source for the replenishment process. Revisiting post infection hemocyte proliferation, using immunofluorescence based tests for DNA synthesis and mitosis, evidenced the lack of β-1, 3-glucan induced cell proliferation in the hematopoietic tissue. Instead these tests identified the circulating hemocytes as the major source for hemocyte replenishment in the circulation. The hematopoietic tissue, however, undergoes a continuous, slow and infection independent regeneration, thereby accumulating potential phagocytes despite infection, and might serve a prophylactic role in containing pathogens in this swarming insect.
Authors:
Tewodros Firdissa Duressa; Ria Vanlaer; Roger Huybrechts
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-30
Journal Detail:
Title:  Developmental and comparative immunology     Volume:  -     ISSN:  1879-0089     ISO Abbreviation:  Dev. Comp. Immunol.     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-10-4     Completed Date:  -     Revised Date:  2014-10-5    
Medline Journal Info:
Nlm Unique ID:  7708205     Medline TA:  Dev Comp Immunol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 Elsevier Ltd. All rights reserved.
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