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Somatostatin Improved B Cells Mature in Macaques during Intestinal Ischemia-Reperfusion.

Liu L, Tan Q, Hu B, Wu H, Wang C, Liu R, Tang C - PLoS ONE (2015)

Bottom Line: In vitro, somatostatin significantly inhibited IL-6 and promoted IgM by increasing the expression of both PAX-5 and BLIMP-1 in the proinflammatory condition.Intestinal ischemia-reperfusion resulted in the proliferation of unmatured B cells which were involved in the augmentation of innate immunity.Somatostatin, with a bi-directional regulation function on innate as well as adaptive immunity of B cells, greatly improved B cells mature in macaques during ischemia-reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.

ABSTRACT

Aims: Intestinal ischemia-reperfusion has been taken as an important pathophysiological process for multiple organ dysfunctions in critical patients. Recent studies reported that dual expression programs of the B cells receptors and Toll-like receptors on B-lymphocytes permit these ubiquitous cells to integrate both adaptive and innate immune functions. Our previous studies found that somatostatin inhibited the intestinal inflammatory injury after ischemia-reperfusion in macaques. However, the changes of B cells and the effects of somatostatin on B cells after intestinal ischemia-reperfusion were unclear.

Methods: 15 macaques were divided into control, intestinal ischemia-reperfusion and somatostatin pretreatment groups. Immunohistochemistry was performed to identify the distributions of adaptive and innate immunity markers in the iliac mucosa. Hmy2.cir B lymphoblastoid cell line was cultured in vitro study. Enzyme-linked immunosorbent assay was used to measure IgM, IL-6 and SIgA, and the expressions of B cells transcription factors, PAX-5 and BLIMP-1, were detected by Western blotting.

Results: B2 lymphocytes in normal Peyer's patches were presented the phenotype of PAX-5+CD20+CD5-. Ischemia-reperfusion increased the numbers and sizes of Peyer's patches but with PAX-5+CD20-CD5- B cells, an unmatured set of B cells. Somatostatin partly kept the phenotype of mature B cells during ischemia-reperfusion. The innate immunity of B cells was inhibited whereas the adaptive immunity was increased in the intestinal mucosa in the somatostatin group, compared to the ischemia-reperfusion group. In vitro, somatostatin significantly inhibited IL-6 and promoted IgM by increasing the expression of both PAX-5 and BLIMP-1 in the proinflammatory condition.

Conclusion: Intestinal ischemia-reperfusion resulted in the proliferation of unmatured B cells which were involved in the augmentation of innate immunity. Somatostatin, with a bi-directional regulation function on innate as well as adaptive immunity of B cells, greatly improved B cells mature in macaques during ischemia-reperfusion. Preventive supplements of somatostatin may greatly limit intestinal injury and bacterial translocation during ischemia-reperfusion.

No MeSH data available.


Related in: MedlinePlus

The effects of SST on the viability of Hmy2.cir, expression of PAX-5, Blimp-1, IL-6 and production of IgM in vitro.Hmy2.cir, a human B lymphoblastoid cell line, were incubated with LPS (10 μg/ml), SST (10−9 mol/L) and IFN-γ (500 μ/ml) for 72 h. Experiments were divided into three pairs of group: control vs SST; LPS vs LPS+SST; LPS+IFN-γ vs LPS+IFN-γ+SST. A) Viability of Hmy2.cir measured by MTT assay in three pairs of groups. B) Expression of PAX-5 and Blimp-1 in three pairs of groups (Western blotting). C) IgM concentration in three pairs of groups (ELISA). D) Expressions of IL-6 in three pairs of groups (ELISA). Representatives of three independent experiments were shown and the experiments were triplicated.
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pone.0133692.g005: The effects of SST on the viability of Hmy2.cir, expression of PAX-5, Blimp-1, IL-6 and production of IgM in vitro.Hmy2.cir, a human B lymphoblastoid cell line, were incubated with LPS (10 μg/ml), SST (10−9 mol/L) and IFN-γ (500 μ/ml) for 72 h. Experiments were divided into three pairs of group: control vs SST; LPS vs LPS+SST; LPS+IFN-γ vs LPS+IFN-γ+SST. A) Viability of Hmy2.cir measured by MTT assay in three pairs of groups. B) Expression of PAX-5 and Blimp-1 in three pairs of groups (Western blotting). C) IgM concentration in three pairs of groups (ELISA). D) Expressions of IL-6 in three pairs of groups (ELISA). Representatives of three independent experiments were shown and the experiments were triplicated.

Mentions: There was no effect of SST (10−9 mol/L) on the viability of Hmy2.cir, a human B lymphoblastoid cell line in the late stage of B cell development. Either LPS alone or combined with IFN-γ significantly increased the viability of Hmy2.cir, p<0.05. However, SST only dramatically reduced the viability of Hmy2.cir stimulated by LPS+IFN-γ (Fig 5A).


Somatostatin Improved B Cells Mature in Macaques during Intestinal Ischemia-Reperfusion.

Liu L, Tan Q, Hu B, Wu H, Wang C, Liu R, Tang C - PLoS ONE (2015)

The effects of SST on the viability of Hmy2.cir, expression of PAX-5, Blimp-1, IL-6 and production of IgM in vitro.Hmy2.cir, a human B lymphoblastoid cell line, were incubated with LPS (10 μg/ml), SST (10−9 mol/L) and IFN-γ (500 μ/ml) for 72 h. Experiments were divided into three pairs of group: control vs SST; LPS vs LPS+SST; LPS+IFN-γ vs LPS+IFN-γ+SST. A) Viability of Hmy2.cir measured by MTT assay in three pairs of groups. B) Expression of PAX-5 and Blimp-1 in three pairs of groups (Western blotting). C) IgM concentration in three pairs of groups (ELISA). D) Expressions of IL-6 in three pairs of groups (ELISA). Representatives of three independent experiments were shown and the experiments were triplicated.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4519283&req=5

pone.0133692.g005: The effects of SST on the viability of Hmy2.cir, expression of PAX-5, Blimp-1, IL-6 and production of IgM in vitro.Hmy2.cir, a human B lymphoblastoid cell line, were incubated with LPS (10 μg/ml), SST (10−9 mol/L) and IFN-γ (500 μ/ml) for 72 h. Experiments were divided into three pairs of group: control vs SST; LPS vs LPS+SST; LPS+IFN-γ vs LPS+IFN-γ+SST. A) Viability of Hmy2.cir measured by MTT assay in three pairs of groups. B) Expression of PAX-5 and Blimp-1 in three pairs of groups (Western blotting). C) IgM concentration in three pairs of groups (ELISA). D) Expressions of IL-6 in three pairs of groups (ELISA). Representatives of three independent experiments were shown and the experiments were triplicated.
Mentions: There was no effect of SST (10−9 mol/L) on the viability of Hmy2.cir, a human B lymphoblastoid cell line in the late stage of B cell development. Either LPS alone or combined with IFN-γ significantly increased the viability of Hmy2.cir, p<0.05. However, SST only dramatically reduced the viability of Hmy2.cir stimulated by LPS+IFN-γ (Fig 5A).

Bottom Line: In vitro, somatostatin significantly inhibited IL-6 and promoted IgM by increasing the expression of both PAX-5 and BLIMP-1 in the proinflammatory condition.Intestinal ischemia-reperfusion resulted in the proliferation of unmatured B cells which were involved in the augmentation of innate immunity.Somatostatin, with a bi-directional regulation function on innate as well as adaptive immunity of B cells, greatly improved B cells mature in macaques during ischemia-reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.

ABSTRACT

Aims: Intestinal ischemia-reperfusion has been taken as an important pathophysiological process for multiple organ dysfunctions in critical patients. Recent studies reported that dual expression programs of the B cells receptors and Toll-like receptors on B-lymphocytes permit these ubiquitous cells to integrate both adaptive and innate immune functions. Our previous studies found that somatostatin inhibited the intestinal inflammatory injury after ischemia-reperfusion in macaques. However, the changes of B cells and the effects of somatostatin on B cells after intestinal ischemia-reperfusion were unclear.

Methods: 15 macaques were divided into control, intestinal ischemia-reperfusion and somatostatin pretreatment groups. Immunohistochemistry was performed to identify the distributions of adaptive and innate immunity markers in the iliac mucosa. Hmy2.cir B lymphoblastoid cell line was cultured in vitro study. Enzyme-linked immunosorbent assay was used to measure IgM, IL-6 and SIgA, and the expressions of B cells transcription factors, PAX-5 and BLIMP-1, were detected by Western blotting.

Results: B2 lymphocytes in normal Peyer's patches were presented the phenotype of PAX-5+CD20+CD5-. Ischemia-reperfusion increased the numbers and sizes of Peyer's patches but with PAX-5+CD20-CD5- B cells, an unmatured set of B cells. Somatostatin partly kept the phenotype of mature B cells during ischemia-reperfusion. The innate immunity of B cells was inhibited whereas the adaptive immunity was increased in the intestinal mucosa in the somatostatin group, compared to the ischemia-reperfusion group. In vitro, somatostatin significantly inhibited IL-6 and promoted IgM by increasing the expression of both PAX-5 and BLIMP-1 in the proinflammatory condition.

Conclusion: Intestinal ischemia-reperfusion resulted in the proliferation of unmatured B cells which were involved in the augmentation of innate immunity. Somatostatin, with a bi-directional regulation function on innate as well as adaptive immunity of B cells, greatly improved B cells mature in macaques during ischemia-reperfusion. Preventive supplements of somatostatin may greatly limit intestinal injury and bacterial translocation during ischemia-reperfusion.

No MeSH data available.


Related in: MedlinePlus