rP33 activates bacterial killing by chicken peripheral blood heterophils

The protection of poultry from infection by Salmonella is of major concern with regard to human health because Salmonella is a common bacterial cause of foodborne diseases, and protection without the use of antibiotics is preferable in order to avoid possible complications involving antibiotic resistance. Salmonella immune lymphokine (SILK), produced by stimulated splenic T cells from Salmonella Enteritidis-immunized chickens, has been shown to confer protection against Salmonella infection on day-old chicks without the use of antibiotics. This protection results from the potentiation of an immune response following treatment with SILK. This study was undertaken to analyze a component of SILK, identified as P33, that is the product of the chicken mim-1 gene. A recombinant derivative expressing a domain of P33 (rP33) has been shown to be chemotactic for heterophils and is therefore instrumental in eliciting the immune response characteristic of SILK-induced protection against Salmonella infection in chicks. We report here that rP33 possesses the ability to activate antimicrobial responses from heterophils. The killing of Salmonella Enteritidis by heterophils was increased by in vitro treatment of the cells with rP33. Treatment with rP33 also stimulated the degranulation of heterophils but did not induce an oxidative burst or upregulate phagocytosis. These results indicate that P33 is an active component of SILK, conferring protection against Salmonella Enteritidis by augmenting the antimicrobial activities of heterophils.