Chronic eosinophilic pneumonia (CEP) is an eosinophilic lung disease that is typically diagnosed by a triad of clinical symptoms including pulmonary symptoms, eosinophilia and characteristic radiographic abnormalities. It requires a high index of suspicion given its overlap with other eosinophilic conditions and lack of a specific diagnostic test. The diagnosis is made after careful consideration of other secondary causes of eosinophilia, such as infectious, drugs, or toxic etiologies. CEP generally responds rapidly to treatment, which primarily consists of corticosteroid therapy, but relapses are common. Novel therapies are being explored as more information is being discovered about the pathophysiology of eosinophilic disease processes. Close follow-up is important given the difficulty in weaning patients from glucocorticoids with many patients developing sequelae of chronic glucocorticoid therapy. Therefore, exploring alternative treatments is of upmost importance.

Objective Inflammation in adipose tissues in obesity promotes insulin resistance and metabolic disease. The Duffy antigen receptor for chemokines (DARC) is a promiscuous non-signaling receptor expressed on erythrocytes and other cell types that modulates tissue inflammation by binding chemokines such as monocyte chemoattractant protein-1 (MCP-1) and by acting as a chemokine reservoir. DARC allelic variants are common in humans, but the role of DARC in modulating obesity-related metabolic disease is unknown. Methods We examined body weight gain, tissue adiposity, metabolic parameters and inflammatory marker expression in wild-type and DARC knockout mice fed a chow diet (CD) and high fat diet (HFD). Results Compared to wild-type mice, HFD-fed DARC knockout mice developed glucose intolerance and insulin resistance independent of increases in body weight or adiposity. Interestingly, insulin sensitivity was also diminished in lean male DARC knockout mice fed a chow diet. Insulin production was not reduced by DARC gene deletion, and plasma leptin levels were similar in HFD fed wild-type and DARC knockout mice. MCP-1 levels in plasma rose significantly in the HFD fed wild-type mice, but not in the DARC knockout mice. Conversely, adipose tissue MCP-1 levels were higher, and more macrophage crown-like structures were detected, in the HFD fed DARC knockout mice as compared with the wild-type mice, consistent with augmented adipose tissue inflammation that is not accurately reflected by plasma levels of DARC-bound MCP-1 in these mice.

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