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Spontaneously Hypertensive Rats is Susceptible to Bacteria Translocation from Gut to Peripheral Tissues
Author(s) -
Zhang Bojun,
Nelson James W,
Bryan Robert M,
Durgan David J
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.709.1
Subject(s) - cecum , bacteria , inflammation , dysbiosis , neuroinflammation , spleen , lipopolysaccharide , chromosomal translocation , endocrinology , biology , medicine , gut flora , microbiology and biotechnology , immunology , biochemistry , genetics , gene
Cerebral small vessel disease (CSVD) is an inflammatory disease characterized by blood‐brain barrier (BBB) breakdown and neuroinflammation. We previous observed that spontaneously hypertensive stroke‐prone rats (SHRSPs) exhibit gut dysbiosis. Furthermore, transplanting SHRSPs with control gut microbiota significantly reduced makers associated with inflammation. Since the gut microbiome is a potential source of inflammation, we hypothesize that bacteria translocating from gut to brain induce neuroinflammation in CSVD. To test our hypothesis, we determined the efficiency of fluorescent‐labeled bacteria (GFP‐ E. coli JJ1901, chloramphenicol resistant) translocation in WKY and SHRSP rats. A single dose of E. coli JJ1901 [≈10 9 colony forming units (CFUs)] was administered to WKY and SHRSP rats (11–15 weeks old) through oral gavage. Peripheral tissues, brain, and cecum content were collected 2 hours later, homogenized, and plated on culture plates. The number of CFUs was counted 24 hours later. When compared to WKY rats, SHRSP showed significantly increased bacteria translocation to peripheral tissues (liver, spleen, and abdominal adipose tissue; n=7, p <0.05). In addition, more bacteria translocation incidents were found in SHRSPs compared to WKY rats (5/7 in SHRSP vs. 3/7 in WKY). However, similar level of acute bacteria translocation to brain was observed in both groups. To assess translocation rates of the chronically colonized bacteria, as opposed to the acute effects following gavage, colonization was established in newborn rat pups by administrating E. coli JJ1901 (≈10 9 CFUs) to pregnant mother rats through oral gavage. Bacteria colonization in the offspring of the gavaged rats was confirmed by plating diluted fecal samples on culture plates. Colonized SHRSPs (15 weeks old) showed significantly increased bacteria translocation to peripheral tissues when compared to WKY controls. Additionally, SHRSPs demonstrated a trend towards increased translocation of E. coli JJ1901 to the brain than WKY rats. We conclude that translocation of gut bacteria can be an underlying source responsible for inflammation in pathological states. Support or Funding Information National Heart, Lung, and Blood Institute R01HL134838 (D.J. Durgan), and by National Institute of Neurological Disorders and Stroke R01NS080531 (R.M. Bryan) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .