Exposure to a Social Stressor Induces Translocation of Commensal Lactobacilli to the Spleen and Priming of the Innate Immune System.
Studies have shown that exposure to psychological stressors leads to inflammation throughout the body. This has been widely studied using social disruption (SDR), a social stressor that involves repeated social defeat in subordinate mice. Exposure to SDR increases serum cytokine levels, results in accumulation of spleen CD11b+myeloid cells, and primes macrophages for increased cytokine and microbicidal activity. Our previous studies showed that intestinal microbes are necessary for SDR-enhancement of innate immunity. In this study, we show that SDR increases spleen CD11b+Ly6CintermLy6G+neutrophil and CD11b+Ly6ChiLy6G-monocyte numbers compared with control mice. Further, we found that neutrophils and monocytes from stressor-exposed mice expressed higher levels of IL-1β mRNA. To determine whether bacterial translocation may contribute to these effects, bacterial 16S rRNA was quantified using quantitative real-time RT-PCR with bacterial group-specific primers. Exposure to the SDR stressor specifically increasedLactobacillusRNA in the spleen, which localized in spleen monocytes. The increased spleen levels ofLactobacillus16S rRNA in SDR mice positively correlated with increased levels of IL-1β and IL-23 mRNA. Our findings indicate that during stressor exposure,Lactobacillus spp.can translocate to the spleen and prime the innate immune system for enhanced reactivity.
Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210.|Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210.
William P
WP
Lafuse
Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210.|Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210.
Rachel
R
Gearinger
Department of Pediatrics, The Ohio State University, Columbus, OH 43210.|Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43210; and.
Sydney
S
Fisher
Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210.|Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210.
Connor
C
Nealer
Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43210; and.
Amy R
0000-0001-9882-3854
AR
Mackos
Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210; Michael.bailey2@nationwidechildrens.org.|Department of Pediatrics, The Ohio State University, Columbus, OH 43210.|Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43210; and.|Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH 43210.
Michael T
MT
Bailey
D000818:Animals; D018988:Bacterial Translocation; D002478:Cells, Cultured; D004781:Environmental Exposure / Q000009:adverse effects; D007113:Immunity, Innate; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D053759:Interleukin-23 / Q000235:genetics / Q000378:metabolism; D007778:Lactobacillus / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D013154:Spleen / Q000276:immunology* / Q000382:microbiology; D013315:Stress, Psychological / Q000276:immunology* / Q000382:microbiology; D013559:Symbiosis; D015854:Up-Regulation
D053583:Interleukin-1beta; D053759:Interleukin-23; D012336:RNA, Ribosomal, 16S