Tsutomu Komori1, Keiko Saito1, Noriyuki Sawa2, Yasuhiro Shibasaki3, Chie Kohchi4, Gen-Ichiro Soma4, Hiroyuki Inagawa5. 1. Kohkin Chemical Co. Ltd., Higashi-osaka, Osaka, Japan. 2. Tokushima Agriculture, Forestry and Fisheries Technology Support Center, Myozai-gun, Tokushima, Japan. 3. Nihon University, College of Bioresource Sciences, Fujisawa, Kanagawa, Japan. 4. Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan Macrophi Inc., Takamatsu-shi, Kagawa, Japan Control of Innate Immunity, Technology Research Association, Takamatsu-shi, Kagawa, Japan. 5. Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan Macrophi Inc., Takamatsu-shi, Kagawa, Japan Control of Innate Immunity, Technology Research Association, Takamatsu-shi, Kagawa, Japan PXS07205@nifty.ne.jp.
Abstract
BACKGROUND: Oral administration of lipopolysaccharide (LPS), a major outer-membrane component of Gram-negative bacteria, has been found to prevent infection in mammals and fish. Oral administration of LPS is believed to increase phagocytic activity and promote cytokine production, thus associating it with priming. The present study aimed to elucidate the effect of oral administration of LPS in birds, which phylogenetically lie between fish and mammals, using chickens as a model. MATERIALS AND METHODS: LPS derived from Pantoea agglomerans (LPSp) was added to the feed or water for oral administration to broiler chickens. For the survival assay and gene expression analysis (Genopal), LPSp was administered at a dose of 10 μg/kg of body weight (BW)/day. LPSp was administered at a dose of 0.2 μg/kg or 200 μg/kg to stimulate peripheral blood mononuclear phagocytosis (latex beads) and nitric oxide (NO) production. RESULTS: LPSp (10 μg/kg BW/day) administration significantly inhibited mortality in broiler chickens on commercial farms. Furthermore, oral administration resulted in a transient increase in phagocytic activity and improved the ability to produce NO. On examining splenic cytokine induction following intraperitoneal administration of LPS derived from Escherichia coli (LPSe), we found significantly increased interleukin (IL)-1β mRNA expression. CONCLUSION: Innate immunity activation in chickens, as seen in infection prevention, was induced by oral administration of LPSp. This infection prevention involved increased phagocytic activity and enhanced gene expression and appears to be a phylogenetically-preserved innate immunity mechanism. Copyright
BACKGROUND: Oral administration of lipopolysaccharide (LPS), a major outer-membrane component of Gram-negative bacteria, has been found to prevent infection in mammals and fish. Oral administration of LPS is believed to increase phagocytic activity and promote cytokine production, thus associating it with priming. The present study aimed to elucidate the effect of oral administration of LPS in birds, which phylogenetically lie between fish and mammals, using chickens as a model. MATERIALS AND METHODS: LPS derived from Pantoea agglomerans (LPSp) was added to the feed or water for oral administration to broiler chickens. For the survival assay and gene expression analysis (Genopal), LPSp was administered at a dose of 10 μg/kg of body weight (BW)/day. LPSp was administered at a dose of 0.2 μg/kg or 200 μg/kg to stimulate peripheral blood mononuclear phagocytosis (latex beads) and nitric oxide (NO) production. RESULTS:LPSp (10 μg/kg BW/day) administration significantly inhibited mortality in broiler chickens on commercial farms. Furthermore, oral administration resulted in a transient increase in phagocytic activity and improved the ability to produce NO. On examining splenic cytokine induction following intraperitoneal administration of LPS derived from Escherichia coli (LPSe), we found significantly increased interleukin (IL)-1β mRNA expression. CONCLUSION: Innate immunity activation in chickens, as seen in infection prevention, was induced by oral administration of LPSp. This infection prevention involved increased phagocytic activity and enhanced gene expression and appears to be a phylogenetically-preserved innate immunity mechanism. Copyright