Abstract
Allergic enteritis (AE) is a gastrointestinal form of food allergy. This study aimed to elucidate cellular and molecular mechanisms of AE using a murine model. To induce AE, BALB/c wild type (WT) mice received intraperitoneal sensitization with ovalbumin (an egg white allergen) plus ALUM and feeding an egg white (EW) diet. Microarray analysis showed enhanced gene expression of CC chemokine receptor (CCR) 8 and its ligand, chemokine CC motif ligand (CCL) 1 in the inflamed jejunum. Histological and FACS analysis showed that CCR8 knock out (KO) mice exhibited slightly less inflammatory features, reduced eosinophil accumulation but accelerated neutrophil accumulation in the jejunums, when compared to WT mice. The concentrations of an eosinophil chemoattractant CCL11 (eotaxin-1), but not of IL-5, were reduced in intestinal homogenates of CCR8KO mice, suggesting an indirect involvement of CCR8 in eosinophil accumulation in AE sites by inducing CCL11 expression. The potential of CCR8 antagonists to treat allergic asthma has been discussed. However, our results suggest that CCR8 blockade may promote neutrophil accumulation in the inflamed intestinal tissues, and not be a suitable therapeutic target for AE, despite the potential to reduce eosinophil accumulation. This study advances our knowledge to establish effective anti-inflammatory strategies in AE treatment.
Highlights
Allergic enteritis (AE) is a gastrointestinal form of food allergy
Microarray analysis showed that the gene expression of CCL1 and CCL8 was highly up-regulated in the jejunum of OVA-sensitized and egg white (EW)-diet fed (OVA/EW) wild type (WT) mice (41.66 and 47.91 folds respectively) when compared to that in the OVA-sensitized and casein-diet fed mice, i.e., the control group (OVA/CN WT mice; Fig. 2A and Table S1)
We have found a contribution of chemokine receptor 8 (CCR8) in eosinophil migration to the inflamed AE tissues
Summary
Allergic enteritis (AE) is a gastrointestinal form of food allergy. This study aimed to elucidate cellular and molecular mechanisms of AE using a murine model. Several studies showed an essential role of the CCR8/CCL1 axis in the recruitment of Th2 cells and the development of inflammation in murine models of allergic asthma or atopic dermatitis[18,19,20,21,22,23,24]. Based on these studies, the potential of CCR8 antagonists to treat allergic asthma has been discussed[25,26]. The importance of CCR8 in allergic asthma has been debated, since additional studies have shown a dispensable role of CCR8 in the recruitment of Th2 cells into inflamed respiratory tissues of experimental mice[27,28,29]
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