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. 2011 Nov 9:10:203.
doi: 10.1186/1476-511X-10-203.

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

Gamal Badr  1 , Mohamed Mohany, Ali Metwalli
Affiliations

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

Gamal Badr et al. Lipids Health Dis. .

Abstract

Background: Long 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.

Results: Flow 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.

Conclusion: Our 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.

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Figures

Figure 1
Figure 1
Surface expression of CXCR4 and CCR7 on B and T cells. Surface CXCR4 and CCR7 expression levels were analyzed with flow cytometry on B and T cells of the control mice (open histograms, thin line), diabetic mice (open histograms, black bold line) and diabetic mice supplemented with WP (gray-filled histograms, thin line) using anti-CXCR4-PE, anti-CCR7-PE and IgG (open histogram) isotype control antibodies. Histograms were gated based on viable B220+ B cells (A) and CD3+ T cells (B).
Figure 2
Figure 2
Impact of WP supplementation on actin polymerization in B cells. B cells were isolated from control (open circles), diabetic (closed black circles), and WP-treated diabetic groups (closed gray triangles). F-actin polymerization was measured in response to CXCL12 (A) and CCL21 (B). The results are expressed as the percentage changes in MFI (n = 10) ± SD as described in the Materials and Methods section.
Figure 3
Figure 3
Impact of WP supplementation on actin polymerization in T cells. T cells were isolated from the control (open circles), diabetic (closed black circles), and WP-treated diabetic groups (closed gray triangles). F-actin polymerization was measured in response to CXCL12 (A) and CCL21 (B). The results are expressed as the percentage changes in MFI (n = 8) ± SD as described in the Materials and Methods section.
Figure 4
Figure 4
Whey protein restores B cell chemotaxis in diabetic mice. Splenic B cells were isolated from 10 mice in each group and were analyzed for migration to CXCL12 and CCL21. Input populations and migrated cell populations were stained with B220-APC and IgD-PE/CD44-FITC. Representative dot plots of input cells and transmigrated cells to medium (without chemokine) versus medium containing CXCL12 for control mice are shown, including the input and transmigrated B cell population data. Data from one representative experiment are shown in panel A. The percentage of B cells from 10 different mice in the control (open bars), diabetic (closed, black bars) and WP-treated diabetic (closed, gray bars) groups that specifically migrated to chemokines are shown. The results are expressed as the mean specific migration ± SEM. *P < 0.05, diabetic vs. control; #P < 0.05, diabetic vs. WP-treated groups.
Figure 5
Figure 5
Whey protein restores T cell chemotaxis in diabetic mice. T cells were isolated from 10 mice in each group and analyzed for migration to CXCL12 and CCL21. Input populations and migrated cell populations were stained with CD3-FITC. The percentage of T cells from 10 different mice in the control (open bars), diabetic (closed, black bars) and WP-treated diabetic (closed, gray bars) groups that specifically migrated to chemokines are shown. The results are expressed as the mean specific migration ± SEM. *P < 0.05, diabetic vs. control; #P < 0.05, diabetic vs. WP-treated groups.
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