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Particles from the Echinococcus granulosus laminated layer inhibit IL-4 and growth factor-driven Akt phosphorylation
Paula I Seoane1, Dominik Rückerl2, Cecilia Casaravilla1
1Cátedra de Inmunología, Departamento de Biociencias (Facultad de Química) e Instituto de Química Biológica (Facultad de Ciencias), Universidad de la República, Montevideo, Uruguay.
Abstract:
Proliferation of macrophages is a hallmark of inflammation in many type 2 settings including helminth infections. The cellular expansion is driven by the type 2 cytokine interleukin-4 (IL-4), as well as by M-CSF, which also controls homeostatic levels of tissue resident macrophages. Cystic echinococcosis, caused by the tissue-dwelling larval stage of the cestode Echinococcus granulosus, is characterised by normally subdued local inflammation. Infiltrating host cells make contact only with the acellular protective coat of the parasite, called laminated layer, particles of which can be ingested by phagocytic cells. Here we report that a particulate preparation from this layer (pLL) strongly inhibits the proliferation of macrophages in response to IL-4 or M-CSF. In addition, pLL also inhibits IL-4-driven up-regulation of Relm-α, without similarly affecting Chitinase-like 3 (Chil3/Ym1). IL-4-driven cell proliferation and up-regulation of Relm-α are both known to depend on the phosphatidylinositol (PI3K)/Akt pathway, which is dispensable for induction of Chil3/Ym1. Exposure to pLL in vitro inhibited Akt activation in response to proliferative stimuli, providing a potential mechanism for its activities. Our results suggest that the E. granulosus laminated layer exerts some of its anti-inflammatory properties through inhibition of PI3K/Akt activation and consequent limitation of macrophage proliferation.
Insights
The Echinococcus granulosus laminated layer (pLL) inhibits macrophage proliferation driven by interleukin-4 (IL-4) or M-CSF. This suggests pLL has anti-inflammatory properties by blocking the PI3K/Akt pathway.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Macrophage proliferation is key in type 2 inflammation, driven by IL-4 and M-CSF.
- Cystic echinococcosis exhibits subdued inflammation, with host cells contacting the parasite's laminated layer (LL).
Purpose of the Study:
- To investigate the effect of Echinococcus granulosus laminated layer particles (pLL) on macrophage proliferation.
- To elucidate the molecular mechanisms underlying pLL's impact on macrophage responses.
Main Methods:
- In vitro experiments using pLL with macrophages stimulated by IL-4 or M-CSF.
- Analysis of macrophage proliferation, Relm-α and Chil3/Ym1 expression.
- Assessment of PI3K/Akt pathway activation.
Main Results:
- pLL significantly inhibited IL-4 or M-CSF-induced macrophage proliferation.
- pLL suppressed IL-4-driven Relm-α upregulation but not Chil3/Ym1.
- pLL exposure inhibited Akt activation in response to proliferative stimuli.
Conclusions:
- The E. granulosus laminated layer possesses anti-inflammatory properties.
- pLL limits macrophage proliferation by inhibiting the PI3K/Akt pathway.
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