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Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy.
Hepatology. 2015 Oct; 62(4):1260-71.Hep

Abstract

Altered gut microbiome is associated with systemic inflammation and cirrhosis decompensation. However, the correlation of the oral microbiome with inflammation in cirrhosis is unclear. Our aim was to evaluate the oral microbiome in cirrhosis and compare with stool microbiome. Outpatients with cirrhosis (with/without hepatic encephalopathy [HE]) and controls underwent stool/saliva microbiome analysis (for composition and function) and also systemic inflammatory evaluation. Ninety-day liver-related hospitalizations were recorded. Salivary inflammation was studied using T helper 1 cytokines/secretory immunoglobulin A (IgA), histatins and lysozyme in a subsequent group. A total of 102 patients with cirrhosis (43 previous HE) and 32 age-matched controls were included. On principal component analysis (PCA), stool and saliva microbiome clustered far apart, showing differences between sites as a whole. In salivary microbiome, with previous HE, relative abundance of autochthonous families decreased whereas potentially pathogenic ones (Enterobacteriaceae, Enterococcaceae) increased in saliva. Endotoxin-related predicted functions were significantly higher in cirrhotic saliva. In stool microbiome, relative autochthonous taxa abundance reduced in previous HE, along with increased Enterobacteriaceae and Enterococcaceae. Cirrhotic stool microbiota demonstrated a significantly higher correlation with systemic inflammation, compared to saliva microbiota, on correlation networks. Thirty-eight patients were hospitalized within 90 days. Their salivary dysbiosis was significantly worse and predicted this outcome independent of cirrhosis severity. Salivary inflammation was studied in an additional 86 age-matched subjects (43 controls/43 patients with cirrhosis); significantly higher interleukin (IL)-6/IL-1β, secretory IgA, and lower lysozyme, and histatins 1 and 5 were found in patients with cirrhosis, compared to controls.

CONCLUSIONS

Dysbiosis, represented by reduction in autochthonous bacteria, is present in both saliva and stool in patients with cirrhosis, compared to controls. Patients with cirrhosis have impaired salivary defenses and worse inflammation. Salivary dysbiosis was greater in patients with cirrhosis who developed 90-day hospitalizations. These findings could represent a global mucosal-immune interface change in cirrhosis.

Authors+Show Affiliations

Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Microbiome Analysis Center, George Mason University, Manassas, VA.Department of Microbiology, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Department of Biostatistics, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, VA.Microbiome Analysis Center, George Mason University, Manassas, VA.Microbiome Analysis Center, George Mason University, Manassas, VA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

25820757

Citation

Bajaj, Jasmohan S., et al. "Salivary Microbiota Reflects Changes in Gut Microbiota in Cirrhosis With Hepatic Encephalopathy." Hepatology (Baltimore, Md.), vol. 62, no. 4, 2015, pp. 1260-71.
Bajaj JS, Betrapally NS, Hylemon PB, et al. Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy. Hepatology. 2015;62(4):1260-71.
Bajaj, J. S., Betrapally, N. S., Hylemon, P. B., Heuman, D. M., Daita, K., White, M. B., Unser, A., Thacker, L. R., Sanyal, A. J., Kang, D. J., Sikaroodi, M., & Gillevet, P. M. (2015). Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy. Hepatology (Baltimore, Md.), 62(4), 1260-71. https://doi.org/10.1002/hep.27819
Bajaj JS, et al. Salivary Microbiota Reflects Changes in Gut Microbiota in Cirrhosis With Hepatic Encephalopathy. Hepatology. 2015;62(4):1260-71. PubMed PMID: 25820757.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Salivary microbiota reflects changes in gut microbiota in cirrhosis with hepatic encephalopathy. AU - Bajaj,Jasmohan S, AU - Betrapally,Naga S, AU - Hylemon,Phillip B, AU - Heuman,Douglas M, AU - Daita,Kalyani, AU - White,Melanie B, AU - Unser,Ariel, AU - Thacker,Leroy R, AU - Sanyal,Arun J, AU - Kang,Dae Joong, AU - Sikaroodi,Masoumeh, AU - Gillevet,Patrick M, Y1 - 2015/05/06/ PY - 2014/12/12/received PY - 2015/03/19/revised PY - 2015/03/26/accepted PY - 2015/3/31/entrez PY - 2015/3/31/pubmed PY - 2016/1/20/medline SP - 1260 EP - 71 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 62 IS - 4 N2 - UNLABELLED: Altered gut microbiome is associated with systemic inflammation and cirrhosis decompensation. However, the correlation of the oral microbiome with inflammation in cirrhosis is unclear. Our aim was to evaluate the oral microbiome in cirrhosis and compare with stool microbiome. Outpatients with cirrhosis (with/without hepatic encephalopathy [HE]) and controls underwent stool/saliva microbiome analysis (for composition and function) and also systemic inflammatory evaluation. Ninety-day liver-related hospitalizations were recorded. Salivary inflammation was studied using T helper 1 cytokines/secretory immunoglobulin A (IgA), histatins and lysozyme in a subsequent group. A total of 102 patients with cirrhosis (43 previous HE) and 32 age-matched controls were included. On principal component analysis (PCA), stool and saliva microbiome clustered far apart, showing differences between sites as a whole. In salivary microbiome, with previous HE, relative abundance of autochthonous families decreased whereas potentially pathogenic ones (Enterobacteriaceae, Enterococcaceae) increased in saliva. Endotoxin-related predicted functions were significantly higher in cirrhotic saliva. In stool microbiome, relative autochthonous taxa abundance reduced in previous HE, along with increased Enterobacteriaceae and Enterococcaceae. Cirrhotic stool microbiota demonstrated a significantly higher correlation with systemic inflammation, compared to saliva microbiota, on correlation networks. Thirty-eight patients were hospitalized within 90 days. Their salivary dysbiosis was significantly worse and predicted this outcome independent of cirrhosis severity. Salivary inflammation was studied in an additional 86 age-matched subjects (43 controls/43 patients with cirrhosis); significantly higher interleukin (IL)-6/IL-1β, secretory IgA, and lower lysozyme, and histatins 1 and 5 were found in patients with cirrhosis, compared to controls. CONCLUSIONS: Dysbiosis, represented by reduction in autochthonous bacteria, is present in both saliva and stool in patients with cirrhosis, compared to controls. Patients with cirrhosis have impaired salivary defenses and worse inflammation. Salivary dysbiosis was greater in patients with cirrhosis who developed 90-day hospitalizations. These findings could represent a global mucosal-immune interface change in cirrhosis. SN - 1527-3350 UR - https://www.unboundmedicine.com/medline/citation/25820757/Salivary_microbiota_reflects_changes_in_gut_microbiota_in_cirrhosis_with_hepatic_encephalopathy_ L2 - https://doi.org/10.1002/hep.27819 DB - PRIME DP - Unbound Medicine ER -