Abstract
Association between gut dysbiosis and neurogenic diseases, such as hypertension, has been described. The aim of this study was to investigate whether changes in the gut microbiota alter gut-brain interactions inducing changes in blood pressure (BP). Recipient normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were orally gavaged with donor fecal contents from SHR and WKY. We divided the animals into four groups: WKY transplanted with WKY microbiota (W-W), SHR with SHR (S-S), WKY with SHR (W-S) and SHR with WKY (S-W). Basal systolic BP (SBP) and diastolic BP (DBP) were reduced with no change in heart rate as a result of fecal microbiota transplantation (FMT) from WKY rats to SHR. Similarly, FMT from SHR to WKY increased basal SBP and DBP. Increases in both NADPH oxidase-driven reactive oxygen species production and proinflammatory cytokines in brain paraventricular nucleus linked to higher BP drop with pentolinium and plasmatic noradrenaline (NA) levels were found in the S-S group as compared to the W-W group. These parameters were reduced by FMT from WKY to SHR. Increased levels of pro-inflammatory cytokines, tyrosine hydroxylase mRNA levels and NA content in the proximal colon, whereas reduced mRNA levels of gap junction proteins, were found in the S-S group as compared to the W-W group. These changes were inhibited by FMT from WKY to SHR. According to our correlation analyses, the abundance of Blautia and Odoribacter showed a negative correlation with high SBP. In conclusion, in SHR gut microbiota is an important factor involved in BP control, at least in part, as consequence of its effect on neuroinflammation and the sympathetic nervous system activity.
Highlights
Abundant evidence has demonstrated the association between gut dysbiosis and neurogenic diseases, such as hypertension (Mell et al, 2015; Yang et al, 2015)
Direct Systolic blood pressure (SBP) and diastolic blood pressure (DBP) values were increased by fecal microbiota transplantation (FMT) from spontaneously hypertensive rats (SHR) to WKY as compared to the with WKY microbiota (W-W) group, and reduced in SHR after FMT from WKY as compared to FMT from SHR to SHR, leading to a significant strain versus FMT interaction
We found that Reactive Oxygen Species (ROS) production (Figure 3A), NADPH oxidase activity (Figure 3B) and the mRNA levels of NADPH oxidase subunits, NOX-1, NOX4, p47phox, and p22phox (Figure 3C) and pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-17a, and interferon (IFN)-γ (Figures 4A–E) in brain paraventricular nucleus (PVN) were higher in the SHR with SHR (S-S) group than those found in the W-W group, and were reduced by FMT from WKY rats to SHR
Summary
Abundant evidence has demonstrated the association between gut dysbiosis and neurogenic diseases, such as hypertension (Mell et al, 2015; Yang et al, 2015). Increased sympathetic activity to the gut could result in dysbiosis, increased gut permeability and inflammatory status, leading to an imbalance in the gut content of short-chain fatty acids (SCFAs)producing bacteria and in the plasma levels of lipopolysaccharide (LPS). These metabolic and structural microbial products, working together, elevate sympathetic drive to the BM and other lymphoid organs, and may act as modulators for BM cell activity by increasing the proliferation and release of myeloid progenitors and other pro-inflammatory cells. This increase in myeloid progenitor cells contributes to an increase in peripheral and central inflammation that could be a critical event for the establishment of hypertension
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