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Bone marrow dendritic cells from mice with an altered microbiota provide interleukin 17A-dependent protection against Entamoeba histolytica colitis.

Burgess SL, Buonomo E, Carey M, Cowardin C, Naylor C, Noor Z, Wills-Karp M, Petri WA - MBio (2014)

Bottom Line: Most importantly, this work demonstrates that the microbiome can mediate protection against an enteric infection via extraintestinal effects on bone marrow-derived dendritic cells.Entamoeba histolytica is the causative agent of amebiasis, an infectious disease that contributes significantly to morbidity and mortality due to diarrhea in the developing world.The demonstration of immune-mediated protection due to communication from the microbiome to the bone marrow represents an emerging field of study that will yield unique approaches to the development of these treatments.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, USA.

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BMDCS from SFB-colonized mice migrated to the lamina propria of SFB-free mice upon adoptive transfer via the intraperitoneal route. Bone marrow cells (500,000) from SFB+ or SFB− mice were CFSE stained and adoptively transferred to 5-week-old CBA/J mice free of SFB. Flow cytometry for CFSE staining was performed on single cells isolated from spleens, Peyer’s patches (PP), mesenteric lymph nodes (MLN), and lamina propria (LP). *, P < 0.05.
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fig4: BMDCS from SFB-colonized mice migrated to the lamina propria of SFB-free mice upon adoptive transfer via the intraperitoneal route. Bone marrow cells (500,000) from SFB+ or SFB− mice were CFSE stained and adoptively transferred to 5-week-old CBA/J mice free of SFB. Flow cytometry for CFSE staining was performed on single cells isolated from spleens, Peyer’s patches (PP), mesenteric lymph nodes (MLN), and lamina propria (LP). *, P < 0.05.

Mentions: To test if the increase in DCs in the gut of SFB+ mice was due to a direct effect on the bone marrow, BMDCs from SFB-colonized and SFB-free mice were adoptively transferred to SFB− mice. For in vivo transfers, day 6 BMDC from SFB− and SFB+ mice were matured with LPS (1 µg/ml), and 16 h later, cells were stained with carboxyfluorescein succinimidyl ester (CFSE; 10 nM), and 5 × 105 cells were administered via intraperitoneal injection. CFSE+ BMDC were detected in the lamina propria but only from SFB+ mice (Fig. 4). The ability of SFB+ BMDCs to home to the gut may help explain the increased numbers of DCs seen in the lamina propria of SFB-colonized mice during E. histolytica infection (Fig. 2E). These results were consistent with other studies that have shown that adoptive transfer of LPS-matured BMDCs results in DC trafficking to the intestine (28, 29, 35).


Bone marrow dendritic cells from mice with an altered microbiota provide interleukin 17A-dependent protection against Entamoeba histolytica colitis.

Burgess SL, Buonomo E, Carey M, Cowardin C, Naylor C, Noor Z, Wills-Karp M, Petri WA - MBio (2014)

BMDCS from SFB-colonized mice migrated to the lamina propria of SFB-free mice upon adoptive transfer via the intraperitoneal route. Bone marrow cells (500,000) from SFB+ or SFB− mice were CFSE stained and adoptively transferred to 5-week-old CBA/J mice free of SFB. Flow cytometry for CFSE staining was performed on single cells isolated from spleens, Peyer’s patches (PP), mesenteric lymph nodes (MLN), and lamina propria (LP). *, P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4222101&req=5

fig4: BMDCS from SFB-colonized mice migrated to the lamina propria of SFB-free mice upon adoptive transfer via the intraperitoneal route. Bone marrow cells (500,000) from SFB+ or SFB− mice were CFSE stained and adoptively transferred to 5-week-old CBA/J mice free of SFB. Flow cytometry for CFSE staining was performed on single cells isolated from spleens, Peyer’s patches (PP), mesenteric lymph nodes (MLN), and lamina propria (LP). *, P < 0.05.
Mentions: To test if the increase in DCs in the gut of SFB+ mice was due to a direct effect on the bone marrow, BMDCs from SFB-colonized and SFB-free mice were adoptively transferred to SFB− mice. For in vivo transfers, day 6 BMDC from SFB− and SFB+ mice were matured with LPS (1 µg/ml), and 16 h later, cells were stained with carboxyfluorescein succinimidyl ester (CFSE; 10 nM), and 5 × 105 cells were administered via intraperitoneal injection. CFSE+ BMDC were detected in the lamina propria but only from SFB+ mice (Fig. 4). The ability of SFB+ BMDCs to home to the gut may help explain the increased numbers of DCs seen in the lamina propria of SFB-colonized mice during E. histolytica infection (Fig. 2E). These results were consistent with other studies that have shown that adoptive transfer of LPS-matured BMDCs results in DC trafficking to the intestine (28, 29, 35).

Bottom Line: Most importantly, this work demonstrates that the microbiome can mediate protection against an enteric infection via extraintestinal effects on bone marrow-derived dendritic cells.Entamoeba histolytica is the causative agent of amebiasis, an infectious disease that contributes significantly to morbidity and mortality due to diarrhea in the developing world.The demonstration of immune-mediated protection due to communication from the microbiome to the bone marrow represents an emerging field of study that will yield unique approaches to the development of these treatments.

View Article: PubMed Central - PubMed

Affiliation: Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia, USA.

Show MeSH
Related in: MedlinePlus