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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 innate immune response in PPs in three groups.A) Expressions of TLR4, NF-κB and IFN-γ in the PPs of the terminal ileum in three groups (Immunohistochemical staining, ×200 magnification). B) Semi-quantitation for positive staining intensity of TLR4, NF-κB and IFN-γ in the PPs. Data were showed as the mean ± SD of 5 animals per group. *, compared with the NC group, P<0.05. #, compared with the IIR group, P<0.05.
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pone.0133692.g004: The innate immune response in PPs in three groups.A) Expressions of TLR4, NF-κB and IFN-γ in the PPs of the terminal ileum in three groups (Immunohistochemical staining, ×200 magnification). B) Semi-quantitation for positive staining intensity of TLR4, NF-κB and IFN-γ in the PPs. Data were showed as the mean ± SD of 5 animals per group. *, compared with the NC group, P<0.05. #, compared with the IIR group, P<0.05.

Mentions: The expressions of TLR4, NF-κB and IFN-γ in macaque intestine were significantly increased in the IIR group, compared to their weak expressions in the NC group, p<0.05 (Fig 4A and 4B). SST treatment significantly down-regulated the expressions of TLR4, NF-κB and IFN-γ in the PPs, compared to the IIR group, p<0.05 (Fig 4A and 4B). Therefore, with the supplementation of SST after IIR, these data support that, the activated innate immunity in the germline centers of PPs was significantly inhibited.


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 innate immune response in PPs in three groups.A) Expressions of TLR4, NF-κB and IFN-γ in the PPs of the terminal ileum in three groups (Immunohistochemical staining, ×200 magnification). B) Semi-quantitation for positive staining intensity of TLR4, NF-κB and IFN-γ in the PPs. Data were showed as the mean ± SD of 5 animals per group. *, compared with the NC group, P<0.05. #, compared with the IIR group, P<0.05.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0133692.g004: The innate immune response in PPs in three groups.A) Expressions of TLR4, NF-κB and IFN-γ in the PPs of the terminal ileum in three groups (Immunohistochemical staining, ×200 magnification). B) Semi-quantitation for positive staining intensity of TLR4, NF-κB and IFN-γ in the PPs. Data were showed as the mean ± SD of 5 animals per group. *, compared with the NC group, P<0.05. #, compared with the IIR group, P<0.05.
Mentions: The expressions of TLR4, NF-κB and IFN-γ in macaque intestine were significantly increased in the IIR group, compared to their weak expressions in the NC group, p<0.05 (Fig 4A and 4B). SST treatment significantly down-regulated the expressions of TLR4, NF-κB and IFN-γ in the PPs, compared to the IIR group, p<0.05 (Fig 4A and 4B). Therefore, with the supplementation of SST after IIR, these data support that, the activated innate immunity in the germline centers of PPs was significantly inhibited.

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