S. Aureus modulates IL-1R8 expression during intramammary infection in goat

Mastitis is a mammary gland inflammation usually with a bacterial aetiology. Invading pathogens activate the immune response engaging leukocytes and epithelial cells of the udder. A tight regulation of the innate immune system is necessary to avoid exaggerated and detrimental responses. Different regulatory mechanisms are known to inhibit proinflammatory signaling, such as soluble receptors, decoy receptors, receptor antagonists and miRNAs. Among these IL-1R8 is a negative regulator of ILRs and TLRs signaling, preventing damages caused by inflammation. To better understand the role of IL-1R8 in goat mammary gland, a model of S. aureus intramammary infection (IMI) has been established. Goats were infused with PBS in the right udder and with S. aureus in the left udder, and mammary biopsies were collected 30 hours post infection. Given that no data are available on IL-1R8 in goat, we first studied its pattern of expression in a panel of goat healthy organs and tissues. Then we investigated the role of IL-1R8 during IMI, comparing its expression in healthy and infected tissues. IL-1R8 messenger was ubiquitously expressed with very high levels in pancreas, mammary gland, spleen and lymph nodes. IL-1R8 was mainly expressed by ductal epithelial cells but, during S. aureus infection, was down-modulated in ductal cells and up-regulated in antigen presenting cells (APCs). We can conclude that IL-1R8 is ubiquitously expressed in goat tissues, with higher levels in organs with a predominant epithelial component and in lymphoid tissues. IL-1R8 down-modulation after S. aureus infection by ductal cells could lead to an exaggerated inflammatory response, whereas its up-regulation by APCs could impair pathogen clearance by infiltrating immune cells.