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Brief Definitive Report: Absence of regulatory IL‐10 enhances innate protection against filarial parasites by a neutrophil‐independent mechanism
Author(s) -
SIMONS J. E.,
GRAY C. A.,
LAWRENCE R. A.
Publication year - 2010
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.1365-3024.2010.01210.x
Subject(s) - neutrophilia , brugia malayi , immunology , biology , granulocyte , antibody , lymphatic filariasis , filariasis , helminths
Summary Brugia malayi causes the major tropical disease, lymphatic filariasis. Chronicity of disease is associated with generation of regulatory cells secreting IL‐10 and/or TGF‐β. Previous work has shown that the rate of microfilariae (Mf) clearance from the blood is mouse strain‐dependent. Here, we show that IL‐10 plays an important role in preventing the clearance of Mf. Indeed, anti‐IL‐10 antibody treatment increases the rate of Mf clearance from the bloodstream in both rapid‐Mf‐clearing CBA/Ca and slow‐clearing C57Bl/6 mice. In addition, IL‐10 −/− mice implanted intraperitoneally with Mf‐producing adult nematodes have significantly lower Mf, but not adults, in comparison with wild‐type mice at 3 weeks post‐implantation (p.i.). Clearance of Mf from the peritoneal cavity of IL‐10 −/− mice is associated with a dramatic infiltration of neutrophils. Furthermore, rapid‐Mf‐clearing CBA/Ca mice have a dramatic blood neutrophilia at 24 h p.i., whereas slow‐clearing C57Bl/6 mice show no such neutrophilia. Thus, neutrophils may play a role as effector cells in microfilarial infection. We therefore treated mice with anti‐granulocyte antibody to abolish neutrophil recruitment during Mf infection i.v. Although anti‐granulocyte treatment severely depleted neutrophils, it did not significantly reduce the rate of B. malayi Mf clearance either during primary infection or during a challenge following antigen sensitization.