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The schistosomulicidal activity and the production of IL‐1 and TNF‐α by peritoneal macrophages from infected mice and their potentiation by muramyl tripeptide‐phosphatidyl ethanolamine (MTP‐PE) treatment
Author(s) -
SEGER M.,
GOLD D.,
LENGY J.,
PAULI H.,
KEISARI Y.
Publication year - 1993
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1993.tb00618.x
Subject(s) - immunostimulant , monokine , biology , tumor necrosis factor alpha , muramyl dipeptide , macrophage , immunology , endocrinology , medicine , interleukin , cytokine , pharmacology , immune system , biochemistry , in vitro
Summary Production of TNF‐α and IL‐1 by adherent peritoneal exudate macrophages (APEM) was monitored for 20 weeks in Schistosoma mansoni infected mice in comparison to their schistosomulicidal activity. LPS‐triggered IL‐1 and TNF‐α production by APEM peaked 10 weeks post infection (p.i.) and declined thereafter. The schistosomulicidal activity of APEM also peaked after 10 weeks but remained elevated thereafter. Infected mice were also treated with the immunostimulator liposomal muramyl tripeptide‐phosphatidyl ethanolamine (MTP‐PE) 6 or 10 weeks p.i., and their APEM were tested 4 weeks later. APEM from such treated animals showed elevated IL‐1 and TNF‐α production when treatment commenced 6 weeks p.i., while their schistosomulicidal activity increased when treatment commenced either 6 or 10 weeks p.i. The L‐arginine inhibitor, N G monomethyl arginine, markedly inhibited the schistosomulicidal activity but not the IL‐1 and TNF‐α production of APEM. Our results show that monokine production increases during the acute phase of infection and declines during its chronic phase, while macrophage schistosomulicidal activity remains constant throughout. Furthermore, TNF‐α or IL‐1 may play a minor role in APEM mediated killing of schistosomula.