title: Enhancement of natural and acquired immunity by Lactobacillus rhamnosus (HN001), Lactobacillus acidophilus (HN017) and Bifidobacterium lactis (HN019).
abstract: Consumption of lactic acid bacteria (LAB) has been suggested to confer a range of health benefits including stimulation of the immune system and increased resistance to malignancy and infectious illness. In the present study, the effects of feeding Lactobacillus rhamnosus (HN001, DR20), Lactobacillus acidophilus (HN017) and Bifidobacterium lactis (HN019, DR10) on in vivo and in vitro indices of natural and acquired immunity in healthy mice were examined. Mice were fed daily with L. rhamnosus, L. acidophilus or B. lactis (10(9) colony forming units) and their immune function was assessed on day 10 or day 28. Supplementation with L. rhamnosus, L. acidophilus or B. lactis resulted in a significant increase in the phagocytic activity of peripheral blood leucocytes and peritoneal macrophages compared with the control mice. The proliferative responses of spleen cells to concanavalin A (a T-cell mitogen) and lipopolysaccharide (a B-cell mitogen) were also significantly enhanced in mice given different LAB. Spleen cells from mice given L. rhamnosus, L. acidophilus or B. lactis also produced significantly higher amounts of interferon-gamma in response to stimulation with concanavalin A than cells from the control mice. LAB feeding had no significant effect on interleukin-4 production by spleen cells or on the percentages of CD4+, CD8+ and CD40+ cells in the blood. The serum antibody responses to orally and systemically administered antigens were also significantly enhanced by supplementation with L. rhamnosus, L. acidophilus or B. lactis. Together, these results suggest that supplementation of the diet with L. rhamnosus (HN001), L. acidophilus (HN017) or B. lactis (HN019) is able to enhance several indices of natural and acquired immunity in healthy mice.
authors.affiliation: Milk and Health Research Centre, Institute of Food, Nutrition and Human Health, Massey University, Palmerston North, New Zealand. h.s.gill@massey.ac.nz
authors.forename: H S
authors.initials: HS
authors.lastname: Gill
authors.forename: K J
authors.initials: KJ
authors.lastname: Rutherfurd
authors.forename: J
authors.initials: J
authors.lastname: Prasad
authors.forename: P K
authors.initials: PK
authors.lastname: Gopal
mesh_terms: D000818:Animals; D001644:Bifidobacterium / Q000276:immunology*; D007111:Immunity, Cellular; D007113:Immunity, Innate / Q000276:immunology*; D007116:Immunization, Passive; D016898:Interferon-alpha / Q000276:immunology; D007778:Lactobacillus / Q000276:immunology*; D008262:Macrophage Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010586:Phagocytes / Q000276:immunology; D010587:Phagocytosis; D013154:Spleen / Q000276:immunology
chemical_list: D016898:Interferon-alpha