Bone marrow stromal cells attenuate sepsis via prostaglandin E 2 -dependent reprogramming of host macrophages to increase their interleukin-10 production methods
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Effect of BMSCs on plasma cytokine concentrations
Alterations in vascular permeability are central to the pathogenesis of sepsis-induced organ injury, and the benefits of BMSC treatment in reducing vascular permeability have already been reported -. We studied this in the peritoneum, lung, liver and kidney by measuring Evans blue dye leakage 24 h after CLP. CLP surgery significantly increased peritoneal, liver and renal vascular permeability ( P < 0.01, P < 0.01 and P < 0.001, respectively); all three were significantly ( P < 0.05, P < 0.05 and P < 0.05, respectively) decreased in mice treated with BMSCs ( online).
Molecular basis of the BMSC-macrophage interaction
To understand the molecular basis of the interaction between BMSCs and macrophages, we performed a series of experiments in vitro and in vivo. Wild-type BMSCs showed NF-κB activation 30 min after LPS stimulation ( ). In a number of cell types, NF-κB has been shown to induce prostaglandin production and release through a pathway involving cyclooxygenase-2 (COX2; refs. - ). BMSCs have been shown to produce prostaglandin E 2 and possibly affect other immune cells via EP1-EP4 receptors,. We found a significant increase in the expression and activity of COX2 (which produces the substrate for prostaglandin synthase enzymes) in BMSCs 3 h and 5 h after LPS stimulation ( ), but when the BMSCs were treated with an antibody to TNF-α or collected from Tlr4 -/- mice, the COX2 expression did not change ( ). This suggested that prostaglandin E 2 might indeed be re...
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Mouse care was in full compliance with the US NIH criteria for the care and use of laboratory animals in research and all studies were approved by the Animal Care and Use Committee of the NIDDK and NIDCR, NIH. Aged (42-44 weeks old) male C57BL/6 mice (NIH) had free access to water and chow before and after surgery. In addition, 8-12-week-old males with a variety of genetic manipulations were used as listed in the online. All reagents used are summarized in online.
Polymicrobial cecal ligation and puncture sepsis
We performed CLP as previously described, with some modifications, in C57BL/6 mice,. We ligated the cecum by silk 4-0 and punctured it twice with a 21-gauge needle, gently squeezed it to express a small amount of fecal material and then returned it to the central abdominal cavity. In sham-operated mice, we located the cecum but neither ligated nor punctured it. We closed the abdominal incision in two layers with 6-0 nylon sutures. After surgery, we gave 1 ml per 30 g body weight of pre-warmed normal saline. All mice received antibiotic and fluid therapy subcutaneously (a combination of imipenem and cilastatin; 14 mg per kg in 1.5 ml of normal saline at 6 h and 7 mg per kg in 1.5 ml of normal saline at 18 h after surgery). The details of the tissue harvest are described in the.
Treatment of cecal ligation and puncture mice with bone marrow stromal cells
We injected one million BMSCs in 0.3 ml sterile PBS via the tail vein. We gave untreated control mice 0.3 ml sterile PBS with no cells. There was no difference in organ injury, cytokine abundance, Evans blue dye level or pathology in the sham-operated mice with or without BMSC injection. Details of cell isolation and culture are provided in the.
Survival studies
We assessed survival after surgery every 6 h within the first 48 h and then every 8 h for 4 d. We began antibiotic injection and fluid resuscitation 6 h after CLP by subcutaneous injection and repeated it every 12 h for 4 d. We killed all mice at the end of the fourth day.
Ex vivo studies on isolated lung monocytes and macrophages
We killed septic mice 6 h after CLP induction with or without intravenous injection of 1 million BMSCs. We removed the lungs, minced them into small pieces and incubated the pieces in RPMI 1640 medium with 1% penicillin-streptomycin and 1% glutamine for 30 min at 37 °C 5% CO 2 in the presence of collagenase type 1 (300 U ml -1 ) and DNase I (50 U ml -1 ) (Worthington Biochemicals). After the incubation, we filtered the cell suspension through a 70-µm cell strainer and then washed it with complete RPMI medium. We incubated the resulting cells for 15 min at 4 °C with CD11b magnetic beads and subsequently applied them to MS columns (Miltenyi) for the positive selection of CD11b cells. The cell purity of the CD11b + cells, as assessed by FACS analysis, was greater than 97%. After washing, we plated the isolated cells in 96-well plates at a concentration of 50,00...
Macrophage-bone marrow stromal cells coculture experiments
First, we plated macrophages in 96-well plates at a concentration of 40,000 cells per 200 µl. After 1 h, we removed the supernatants and added either 40,000 BMSCs in fresh medium or fresh medium alone to the wells. As a control, we plated BMSCs without macrophages. After an overnight incubation, we added LPS to the cocultures to reach a final concentration of 1 µg ml -1. We collected supernatants 1, 3, 5 and 7 h after the stimulation and performed ELISA (R&D Systems) on the samples to detect the released IL-10. For the transwell or conditioned medium experiments, we either added BMSCs on the insert membrane of the transwell system (HTS Transwell 0.4-µm pore size poly-carbonate membrane, from Corning Incorporated) or added conditioned medium diluted 1:1 with fresh medium to the macrophages. For generation of BMSC-conditioned medium, we cultured BMSCs in complete m...
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Evidence quotes (8)
Alterations in vascular permeability are central to the pathogenesis of sepsis-induced organ injury, and the benefits of BMSC treatment in reducing vascular permeability have already been reported -. We studied this in the peritoneum, lung, liver and kidney by measuring Evans blue dye leakage 24 h after CLP. CLP surgery significantly increased peritoneal, liver and renal vascular permeability ( P < 0.01, P < 0.01 and P < 0.001, respectively); all three were significantly ( P < 0.05, P < 0.05 and P < 0.05, respectively) decreased in mice treated with BMSCs ( online).
To understand the molecular basis of the interaction between BMSCs and macrophages, we performed a series of experiments in vitro and in vivo. Wild-type BMSCs showed NF-κB activation 30 min after LPS stimulation ( ). In a number of cell types, NF-κB has been shown to induce prostaglandin production and release through a pathway involving cyclooxygenase-2 (COX2; refs. - ). BMSCs have been shown to produce prostaglandin E 2 and possibly affect other immune cells via EP1-EP4 receptors,. We found a significant increase in the expression and activity of COX2 (which produces the substrate for prostaglandin synthase enzymes) in BMSCs 3 h and 5 h after LPS stimulation ( ), but when the BMSCs were treated with an antibody to TNF-α or collected from Tlr4 -/- mice, the COX2 expression did not change ( ). This suggested that prostaglandin E 2 might indeed be responsible for reprogramming the macrophages. For this reason, we measured the amount of prostaglandin E 2 in the coculture medium and found a significant increase in its concentration after LPS stimulation ( ). This increase was eliminated if the BMSCs lacked TLR4 or if they were incubated with anti...
Mouse care was in full compliance with the US NIH criteria for the care and use of laboratory animals in research and all studies were approved by the Animal Care and Use Committee of the NIDDK and NIDCR, NIH. Aged (42-44 weeks old) male C57BL/6 mice (NIH) had free access to water and chow before and after surgery. In addition, 8-12-week-old males with a variety of genetic manipulations were used as listed in the online. All reagents used are summarized in online.
We performed CLP as previously described, with some modifications, in C57BL/6 mice,. We ligated the cecum by silk 4-0 and punctured it twice with a 21-gauge needle, gently squeezed it to express a small amount of fecal material and then returned it to the central abdominal cavity. In sham-operated mice, we located the cecum but neither ligated nor punctured it. We closed the abdominal incision in two layers with 6-0 nylon sutures. After surgery, we gave 1 ml per 30 g body weight of pre-warmed normal saline. All mice received antibiotic and fluid therapy subcutaneously (a combination of imipenem and cilastatin; 14 mg per kg in 1.5 ml of normal saline at 6 h and 7 mg per kg in 1.5 ml of normal saline at 18 h after surgery). The details of the tissue harvest are described in the.
We injected one million BMSCs in 0.3 ml sterile PBS via the tail vein. We gave untreated control mice 0.3 ml sterile PBS with no cells. There was no difference in organ injury, cytokine abundance, Evans blue dye level or pathology in the sham-operated mice with or without BMSC injection. Details of cell isolation and culture are provided in the.
We assessed survival after surgery every 6 h within the first 48 h and then every 8 h for 4 d. We began antibiotic injection and fluid resuscitation 6 h after CLP by subcutaneous injection and repeated it every 12 h for 4 d. We killed all mice at the end of the fourth day.
We killed septic mice 6 h after CLP induction with or without intravenous injection of 1 million BMSCs. We removed the lungs, minced them into small pieces and incubated the pieces in RPMI 1640 medium with 1% penicillin-streptomycin and 1% glutamine for 30 min at 37 °C 5% CO 2 in the presence of collagenase type 1 (300 U ml -1 ) and DNase I (50 U ml -1 ) (Worthington Biochemicals). After the incubation, we filtered the cell suspension through a 70-µm cell strainer and then washed it with complete RPMI medium. We incubated the resulting cells for 15 min at 4 °C with CD11b magnetic beads and subsequently applied them to MS columns (Miltenyi) for the positive selection of CD11b cells. The cell purity of the CD11b + cells, as assessed by FACS analysis, was greater than 97%. After washing, we plated the isolated cells in 96-well plates at a concentration of 50,000 cells per well per 200 µl RPMI medium (with 10% FBS, 1% glutamine and 1% penicillin-streptomycin) containing 10 µg ml -1 LPS (from Escherichia coli O111:B4, Sigma). We incubated cells for 1, 3, 5 and 7 h after stimulation and collected supernatants sequentially from wells dedicated...
First, we plated macrophages in 96-well plates at a concentration of 40,000 cells per 200 µl. After 1 h, we removed the supernatants and added either 40,000 BMSCs in fresh medium or fresh medium alone to the wells. As a control, we plated BMSCs without macrophages. After an overnight incubation, we added LPS to the cocultures to reach a final concentration of 1 µg ml -1. We collected supernatants 1, 3, 5 and 7 h after the stimulation and performed ELISA (R&D Systems) on the samples to detect the released IL-10. For the transwell or conditioned medium experiments, we either added BMSCs on the insert membrane of the transwell system (HTS Transwell 0.4-µm pore size poly-carbonate membrane, from Corning Incorporated) or added conditioned medium diluted 1:1 with fresh medium to the macrophages. For generation of BMSC-conditioned medium, we cultured BMSCs in complete medium. After 3 d, we collected supernatants, spun them down to remove possible cell contamination (500 g for 10 min) and stored the resulting supernatants at -20 °C until further use. Further details on ELISA and western blotting are in the.
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