Journal
NUTRITION
Volume 19, Issue 3, Pages 270-274Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0899-9007(02)01060-2
Keywords
polymorphonuclear neutrophil; probiotics; Bifidobacterium longum; cytosine; adhesion molecule; recruitment
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OBJECTIVE: Dietary restriction impairs polymorphonuclear neutrophil (PMN) recruitment into the local inflammatory site, resulting in susceptibility to infection. Probiotics enhance host immunity via conditioning host intestinal microflora. Oral administration of Bifidobacterium longum culture condensate (BCC) in a diet-restricted marine peritonitis model may enhance PMN recruitment into the inflammatory site. METHODS: Male ICR mice (n = 40) were assigned in equal numbers to control or BCC groups and subjected to 75% restricted food intake for 7 d. During dietary restriction, controls received only standard mouse chow, whereas the BCC group received standard mouse chow containing 1% BCC. Mice were killed before (0 h) or after (2 or 4 h) intraperitoneal glycogen injection. Peritoneal lavage fluid and exudative cells were recovered by, peritoneal lavage. Peritoneal exudative cell number was counted. Taper necrosis factor-alpha, interleukin-6, macrophage inflammatory protein-2, and interleukin-10 concentrations in peritoneal lavage-fluid were determined by enzyme-linked immuosorbent assay. CD11b, CD18; CD31, and CD62L expressions on circulating PMNs were measured by flow cytometry. RESULTS: Oral BCC administration unregulated PMN recruitment into the peritoneal cavity and increased peritoneal fluid cytokine concentrations as well as CD18 and CD62L expressions on circulating PMNs during glycogen-induced peritonitis. CONCLUSIONS: Oral BCC administration in a diet-restricted marine peritonitis model augmented P recruitment into the inflammatory site by upregulating cytokine concentrations in the local inflammatory site and adhesion molecule expression on circulating PMNs. Oral BCC administration may be a favorable modality for improving dietary restriction-induced host immunosuppression. (C)Elsevier Science Inc. 2003.
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