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B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection.

Nothelfer K, Arena ET, Pinaud L, Neunlist M, Mozeleski B, Belotserkovsky I, Parsot C, Dinadayala P, Burger-Kentischer A, Raqib R, Sansonetti PJ, Phalipon A - J. Exp. Med. (2014)

Bottom Line: The induction of a type three secretion apparatus (T3SA)-dependent B cell death is observed in the human CL-01 B cell line in vitro, as well as in mouse B lymphocytes in vivo.The presence of bacterial co-signals is required to sensitize B cells to apoptosis and to up-regulate tlr2, thus enhancing IpaD binding.Apoptotic B lymphocytes in contact with Shigella-IpaD are detected in rectal biopsies of infected individuals.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institut Pasteur, INSERM U786, Unité de Pathogénie Microbienne Moléculaire, 75015 Paris, FranceInstitut Pasteur, INSERM U786, Unité de Pathogénie Microbienne Moléculaire, 75015 Paris, France.

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S. flexneri induces B cell death dependent on the T3SA in vivo. (A) Total cell count in murine LNs after footpad infection with S. flexneri. Cells were counted 24 and 48 h after WT and T3SA− infection. (B) Percentages of CD19+ B cells in murine popliteal LNs 24 and 48 h after footpad infection. (C) Percentages of PI+ CD19+ B cells in murine popliteal LNs 48 h after footpad infection. (D) Percentages of CD4+ T cells in murine popliteal LNs 48 h after footpad infection. (E) Number of CFUs for WT and T3SA− bacteria in murine LNs 48 h after footpad infection. Two independent experiments with each 5 mice per group (10 LNs) were performed and data are presented as mean ± SEM. Asterisks indicate statistical significant differences between WT and T3SA−, determined by Mann-Whitney Student’s t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
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fig3: S. flexneri induces B cell death dependent on the T3SA in vivo. (A) Total cell count in murine LNs after footpad infection with S. flexneri. Cells were counted 24 and 48 h after WT and T3SA− infection. (B) Percentages of CD19+ B cells in murine popliteal LNs 24 and 48 h after footpad infection. (C) Percentages of PI+ CD19+ B cells in murine popliteal LNs 48 h after footpad infection. (D) Percentages of CD4+ T cells in murine popliteal LNs 48 h after footpad infection. (E) Number of CFUs for WT and T3SA− bacteria in murine LNs 48 h after footpad infection. Two independent experiments with each 5 mice per group (10 LNs) were performed and data are presented as mean ± SEM. Asterisks indicate statistical significant differences between WT and T3SA−, determined by Mann-Whitney Student’s t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Mentions: A murine model of footpad infection with WT and T3SA− bacteria was performed as previously described (Salgado-Pabón et al., 2013) to assess the potential induction of B cell death by S. flexneri in vivo. Consistent with the priming of an immune response, the total cell number increased in the draining LNs of infected mice as compared with uninfected ones, with no difference between WT and T3SA− bacteria (Fig. 3 A). In contrast, despite an increase of the percentage of CD19+ B lymphocytes upon infection, the B cell compartment was significantly reduced in LNs upon infection with WT bacteria as compared with the T3SA− strain (Fig. 3 B). Accordingly, WT bacteria induced higher B cell death than the T3SA− strain (Fig. 3 C). Differences in the percentages of CD4+ T lymphocytes inversely correlated with the percentages of CD19+ cells, indicating that the reduction of the cellular compartment was specific to B lymphocytes (Fig. 3 D). Similar bacterial counts were detected in the LNs after infection with either Shigella strain (Fig. 3 E). S.flexneri thus causes murine B cell death in vivo in a T3SA-dependent manner.


B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection.

Nothelfer K, Arena ET, Pinaud L, Neunlist M, Mozeleski B, Belotserkovsky I, Parsot C, Dinadayala P, Burger-Kentischer A, Raqib R, Sansonetti PJ, Phalipon A - J. Exp. Med. (2014)

S. flexneri induces B cell death dependent on the T3SA in vivo. (A) Total cell count in murine LNs after footpad infection with S. flexneri. Cells were counted 24 and 48 h after WT and T3SA− infection. (B) Percentages of CD19+ B cells in murine popliteal LNs 24 and 48 h after footpad infection. (C) Percentages of PI+ CD19+ B cells in murine popliteal LNs 48 h after footpad infection. (D) Percentages of CD4+ T cells in murine popliteal LNs 48 h after footpad infection. (E) Number of CFUs for WT and T3SA− bacteria in murine LNs 48 h after footpad infection. Two independent experiments with each 5 mice per group (10 LNs) were performed and data are presented as mean ± SEM. Asterisks indicate statistical significant differences between WT and T3SA−, determined by Mann-Whitney Student’s t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4042640&req=5

fig3: S. flexneri induces B cell death dependent on the T3SA in vivo. (A) Total cell count in murine LNs after footpad infection with S. flexneri. Cells were counted 24 and 48 h after WT and T3SA− infection. (B) Percentages of CD19+ B cells in murine popliteal LNs 24 and 48 h after footpad infection. (C) Percentages of PI+ CD19+ B cells in murine popliteal LNs 48 h after footpad infection. (D) Percentages of CD4+ T cells in murine popliteal LNs 48 h after footpad infection. (E) Number of CFUs for WT and T3SA− bacteria in murine LNs 48 h after footpad infection. Two independent experiments with each 5 mice per group (10 LNs) were performed and data are presented as mean ± SEM. Asterisks indicate statistical significant differences between WT and T3SA−, determined by Mann-Whitney Student’s t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Mentions: A murine model of footpad infection with WT and T3SA− bacteria was performed as previously described (Salgado-Pabón et al., 2013) to assess the potential induction of B cell death by S. flexneri in vivo. Consistent with the priming of an immune response, the total cell number increased in the draining LNs of infected mice as compared with uninfected ones, with no difference between WT and T3SA− bacteria (Fig. 3 A). In contrast, despite an increase of the percentage of CD19+ B lymphocytes upon infection, the B cell compartment was significantly reduced in LNs upon infection with WT bacteria as compared with the T3SA− strain (Fig. 3 B). Accordingly, WT bacteria induced higher B cell death than the T3SA− strain (Fig. 3 C). Differences in the percentages of CD4+ T lymphocytes inversely correlated with the percentages of CD19+ cells, indicating that the reduction of the cellular compartment was specific to B lymphocytes (Fig. 3 D). Similar bacterial counts were detected in the LNs after infection with either Shigella strain (Fig. 3 E). S.flexneri thus causes murine B cell death in vivo in a T3SA-dependent manner.

Bottom Line: The induction of a type three secretion apparatus (T3SA)-dependent B cell death is observed in the human CL-01 B cell line in vitro, as well as in mouse B lymphocytes in vivo.The presence of bacterial co-signals is required to sensitize B cells to apoptosis and to up-regulate tlr2, thus enhancing IpaD binding.Apoptotic B lymphocytes in contact with Shigella-IpaD are detected in rectal biopsies of infected individuals.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institut Pasteur, INSERM U786, Unité de Pathogénie Microbienne Moléculaire, 75015 Paris, FranceInstitut Pasteur, INSERM U786, Unité de Pathogénie Microbienne Moléculaire, 75015 Paris, France.

Show MeSH
Related in: MedlinePlus