Comparison of the effect of autoclaved and non-autoclaved live soil exposure on the mouse immune system

Abstract Background: Lack of exposure to the natural microbial diversity of the environment has been linked to dysregulation of the immune system and numerous noncommunicable diseases, such as allergies and autoimmune disorders. Our previous studies suggest that contact with soil material, rich in naturally occurring microbes, could have a beneficial immunoregulatory impact on the immune system in mice and humans. However, differences in the immunomodulatory properties of autoclaved, sterile soil material and non-autoclaved, live soil material have not been compared earlier. Results: In this study, we exposed C57BL/6 mice to autoclaved and live soil powders that had the same rich microbiota before autoclaving. We studied the effect of the soil powders on the mouse immune system by analyzing different immune cell populations, gene expression in the gut, mesenteric lymph nodes and lung, and serum cytokines. Both autoclaved and live soil exposure were associated with changes in the immune system. The exposure to autoclaved soil resulted in higher levels of Rorγt, Inos and Foxp3 expression in the colon. The exposure to live soil was associated with elevated IFN-γ concentration in the serum. In the mesenteric lymph node, exposure to live soil reduced Gata3 and Foxp3 expression, increased the percentage of CD8 + T cells and the expression of activation marker CD80 in XCR1⁺SIRPα⁻ migratory conventional dendritic cell 1 subset. Conclusions: Our results indicate that exposure to the live and autoclaved soil powders is not toxic for mice. Exposure to live soil powder slightly skews the immune system towards type 1 direction which might be beneficial for inhibiting type 2-related inflammation. Further studies are warranted to quantify the impact of this exposure in experimental type 2 inflammation

Rotifer communities under variable predation-turbulence combinations

The effects of water turbulence on rotifer communities were experimentally studied under different predation pressures. When the larvae of the phantom midge (Chaoborus flavicans) were present in turbulent water, the abundance of most rotifer taxa was enhanced. Especially the genera Chromogaster, Keratella, Polyarthra, and Trichocerca, increased in abundance. In calm water, chaoborids did not affect the rotifer community. In turbulent water predation by chaoborids was targeted more towards cladocerans (Bosmina sp.) and predation pressure on rotifers was relaxed. Additionally, reduced competition with cladocerans probably contributed to the increase of rotifer abundance. Turbulence alone had no significant effect on rotifer abundance because their individual size was small compared with the diameter of the turbulent eddies. The study suggested that the effects of turbulence on rotifers is not direct but takes place through changed predator-prey relations, i.e., the effect depends on the abundance of invertebrate predators. In aquatic ecosystems with a high density of chaoborids, increasing turbulence can considerably increase the abundance of rotifers.Peer reviewe

Heme oxygenase-1 repeat polymorphism in septic acute kidney injury

Abstract Acute kidney injury (AKI) is a syndrome that frequently affects the critically ill. Recently, an increased number of dinucleotide repeats in the HMOX1 gene were reported to associate with development of AKI in cardiac surgery. We aimed to test the replicability of this finding in a Finnish cohort of critically ill septic patients. This multicenter study was part of the national FINNAKI study. We genotyped 300 patients with severe AKI (KDIGO 2 or 3) and 353 controls without AKI (KDIGO 0) for the guanine–thymine (GTn) repeat in the promoter region of the HMOX1 gene. The allele calling was based on the number of repeats, the cut off being 27 repeats in the S–L (short to long) classification, and 27 and 34 repeats for the S–M–L₂ (short to medium to very long) classification. The plasma concentrations of heme oxygenase-1 (HO-1) enzyme were measured on admission. The allele distribution in our patients was similar to that published previously, with peaks at 23 and 30 repeats. The S-allele increases AKI risk. An adjusted OR was 1.30 for each S-allele in an additive genetic model (95% CI 1.01–1.66; p = 0.041). Alleles with a repeat number greater than 34 were significantly associated with lower HO-1 concentration (p<0.001). In septic patients, we report an association between a short repeat in HMOX1 and AKI risk