Effects of undenatured whey protein supplementation on CXCL12- and CCL21-mediated B and T cell chemotaxis in diabetic mice

Lipids in Health and Disease

Research

Ali Metwalli¹  Mohamed Mohany²  Gamal Badr³ 

[1] Food Science Department, College of Agriculture and Food Science, King Saud University, Saudi Arabia;Zoology Department, College of Science, King Saud University, Saudi Arabia;Zoology Department, College of Science, King Saud University, Saudi Arabia;Zoology Department, Faculty of Science, Assiut University, Egypt;

关键词: B cells;    chemotaxis;    diabetes mellitus;    F-actin polymerization;    T cells;    whey protein;   

DOI  :  10.1186/1476-511X-10-203

 received in 2011-10-11, accepted in 2011-11-09,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundLong and persistent uncontrolled diabetes tends to degenerate the immune system and leads to an increased incidence of infection. Whey proteins (WPs) enhance immunity during early life and have a protective role in some immune disorders. In this study, the effects of camel WP on the chemotaxis of B and T cells to CXCL12 and CCL21 in diabetic mice were investigated.ResultsFlow cytometric analysis of the surface expressions of CXCR4 (CXCL12 receptor) and CCR7 (CCL21 receptor) on B and T cells revealed that the surface expressions of CXCR4 and CCR7 were not significantly altered in diabetic and WP-supplemented diabetic mice compared with control mice. Nevertheless, B and T lymphocytes from diabetic mice were found to be in a stunned state, with a marked and significant (P < 0.05) decrease in CXCL12- and CCL21-mediated actin polymerization and subsequently, a marked decrease in their chemotaxis. WP supplementation in the diabetes model was found to significantly increase CXCL12- and CCL21-mediated actin polymerization and chemotaxis in both B and T cells.ConclusionOur data revealed the benefits of WP supplementation in enhancing cytoskeletal rearrangement and chemotaxis in B and T cells, and subsequently improving the immune response in diabetic mice.

【 授权许可】

CC BY   
© Badr et al; licensee BioMed Central Ltd. 2011