Protection against experimental allergic airway inflammation by the Schistosoma mansoni glycoprotein Omega-1


T A Gasan2; K Obieglo2; A Ozir-Fazalalikhan2; F Otto2; Y van Wijck2; A Schots3; M Yazdanbakhsh2; C H Hokke2; C Taube1; H H Smits2
1 Clinic of Pulmonary Medicine, University Hospital Essen, Germany;  2 Leiden University Medical Centre, Netherlands;  3 Wageningen University and Resarch Centre, Netherlands


Parasitic helminths, such as schistosomes, are proficient regulators of the host’s immune response, enabling individual worms to persist within hostile host tissues for decades. Chronic infection with Schistosoma mansoni is known protect against allergic airway inflammation (AAI) in mice, and to be associated with reduced Th2 responses to inhaled allergens in humans, despite a robust schistosome-specific Th2 responses. With this naturally occurring immunomodulatory capacity, schistosomes are an attractive source of novel AAI therapeutic molecules. We have previously shown that mice treated with an i.p. injection of intact Schistosoma mansoni eggs were protected against a subsequent induction of AAI by ovalbumin (OVA)/alum (Obieglo, 2018). One of the most abundantly secreted egg molecules is the glycoprotein omega-1 (ω1). This molecule has been shown to exhibit immunomodulatory effects: targeting mannose receptor (MR)-expressing dendritic cells via Lex-glycans and suppressing protein translation via its RNAse activity upon uptake in the cell (Everts, 2012). Here, we aimed to investigate the immunoregulatory properties of the egg-derived glycoprotein ω1 in an AAI mouse model.

Mice treated with two i.p. injections of plant-derived recombinant ω1 (50 µg/mouse – one week apart) were protected against a subsequent induction of AAI by ovalbumin (OVA)/alum, injected 4 and 10 days after the last ω1 administration. Administration of ω1 significantly inhibited pulmonary eosinophilia in response to allergic challenge and dampened local Th2 cytokines (IL-5, IL-13) in the lavage and the mediastinal lymph nodes. In addition, ω1 pre-treatment was linked to a reduced influx of pro-inflammatory, monocyte-derived dendritic cells into lung tissue of allergic mice, combined with lower levels of the monocyte-attractant chemokine CCL2 in the lavage fluid following allergen challenge. The induction of allergic inflammation in the OVA/Alum model critically depends on the trafficking of OVA from the peritoneal cavity (the injection site) into the mediastinal lymph nodes by inflammatory monocytes. To deduce the mechanism of ω1-induced protection in the OVA/Alum model, we examined what effects pre-treatment with ω1 has on the trafficking and processing of subsequent fluorescent-labelled OVA by inflammatory monocytes.

Pre-treatment with ω1 resulted in a significantly higher number of OVA-positive cells remaining in the peritoneal cavity 24 hours following OVA/alum injection and reduces trafficking of OVA-positive cells into the mediastinal lymph node and bone marrow compartment. Therefore, these data suggest that pre-treatment with ω1 may prevent the induction of an allergic response to OVA by reducing allergen trafficking towards the draining mediastinal lymph nodes. In future experiments we aim to look at what MR-expressing cell types ω1 is targeting and how this influences the function of these cells to inhibit migration of OVA carca

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