Salivary Microbiota Reflects Changes in Gut Microbiota in Cirrhosis with Hepatic Encephalopathy
Identifieur interne : 000D33 ( Main/Exploration ); précédent : 000D32; suivant : 000D34Salivary Microbiota Reflects Changes in Gut Microbiota in Cirrhosis with Hepatic Encephalopathy
Auteurs : Jasmohan S. Bajaj [États-Unis] ; Naga S. Betrapally [États-Unis] ; Phillip B. Hylemon [États-Unis] ; Douglas M. Heuman [États-Unis] ; Kalyani Daita [États-Unis] ; Melanie B. White [États-Unis] ; Ariel Unser [États-Unis] ; Leroy R. Thacker [États-Unis] ; Arun J. Sanyal [États-Unis] ; Dae Joong Kang [États-Unis] ; Masoumeh Sikaroodi [États-Unis] ; Patrick M. Gillevet [États-Unis]Source :
- Hepatology (Baltimore, Md.) [ 0270-9139 ] ; 2015.
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.
Evaluate the oral microbiome in cirrhosis and compare with stool microbiome.
Cirrhotic outpatients [with/without hepatic encephalopathy (HE)] and controls underwent stool/saliva microbiome analysis (for composition and function) and also systemic inflammatory evaluation. 90-day liver-related hospitalizations were recorded. Salivary inflammation was studied using Th1 cytokines/secretory IgA, histatins and lysozyme in a subsequent group.
102 cirrhotics (43 prior-HE) and 32 age-matched controls were included. On PCO, stool and saliva microbiome clustered far apart showing differences between sites as a whole.
With prior-HE, relative abundance of autochthonous families decreased while potentially pathogenic ones (
Relative autochthonous taxa abundance reduced in prior-HE, along with increased
38 patients were hospitalized within 90 days. Their salivary dysbiosis was significantly worse and predicted this outcome independent of cirrhosis severity.
was studied in an additional 86 age-matched subjects (43 controls/43 cirrhotics); significantly higher IL-6/IL-1β, secretory IgA and lower lysozyme, and histatins 1 and 5 were found in cirrhotics compared to controls.
Dysbiosis, represented by reduction in autochthonous bacteria, is present in both saliva and stool in cirrhosis patients compared to controls. Cirrhotic patients have impaired salivary defenses and worse inflammation. Salivary dysbiosis was greater in cirrhotics who developed 90-day hospitalizations. These findings could represent a global mucosal-immune interface change in cirrhosis.
Url:
DOI: 10.1002/hep.27819
PubMed: 25820757
PubMed Central: 4587995
Affiliations:
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<author><name sortKey="Daita, Kalyani" sort="Daita, Kalyani" uniqKey="Daita K" first="Kalyani" last="Daita">Kalyani Daita</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Unser, Ariel" sort="Unser, Ariel" uniqKey="Unser A" first="Ariel" last="Unser">Ariel Unser</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, Virginia</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Virginie</region>
</placeName>
<wicri:cityArea> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond</wicri:cityArea>
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<author><name sortKey="Thacker, Leroy R" sort="Thacker, Leroy R" uniqKey="Thacker L" first="Leroy R" last="Thacker">Leroy R. Thacker</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Virginie</region>
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<author><name sortKey="Sanyal, Arun J" sort="Sanyal, Arun J" uniqKey="Sanyal A" first="Arun J" last="Sanyal">Arun J. Sanyal</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, Virginia</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Virginie</region>
</placeName>
<wicri:cityArea> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond</wicri:cityArea>
</affiliation>
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<author><name sortKey="Kang, Dae Joong" sort="Kang, Dae Joong" uniqKey="Kang D" first="Dae Joong" last="Kang">Dae Joong Kang</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond, Virginia</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Virginie</region>
</placeName>
<wicri:cityArea> Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire VA Medical Center, Richmond</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Sikaroodi, Masoumeh" sort="Sikaroodi, Masoumeh" uniqKey="Sikaroodi M" first="Masoumeh" last="Sikaroodi">Masoumeh Sikaroodi</name>
<affiliation wicri:level="2"><nlm:aff id="A4">Microbiome Analysis Center, George Mason University, Manassas, Virginia</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Virginie</region>
</placeName>
<wicri:cityArea>Microbiome Analysis Center, George Mason University, Manassas</wicri:cityArea>
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<author><name sortKey="Gillevet, Patrick M" sort="Gillevet, Patrick M" uniqKey="Gillevet P" first="Patrick M" last="Gillevet">Patrick M. Gillevet</name>
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<country xml:lang="fr">États-Unis</country>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">Altered gut microbiome is associated with systemic inflammation and cirrhosis decompensation. However, the correlation of the oral microbiome with inflammation in cirrhosis is unclear.</p>
</sec>
<sec id="S2"><title>Aim</title>
<p id="P2">Evaluate the oral microbiome in cirrhosis and compare with stool microbiome.</p>
</sec>
<sec id="S3"><title>Methods</title>
<p id="P3">Cirrhotic outpatients [with/without hepatic encephalopathy (HE)] and controls underwent stool/saliva microbiome analysis (for composition and function) and also systemic inflammatory evaluation. 90-day liver-related hospitalizations were recorded. Salivary inflammation was studied using Th1 cytokines/secretory IgA, histatins and lysozyme in a subsequent group.</p>
</sec>
<sec id="S4"><title>Results</title>
<p id="P4">102 cirrhotics (43 prior-HE) and 32 age-matched controls were included. On PCO, stool and saliva microbiome clustered far apart showing differences between sites as a whole.</p>
<sec id="S5"><title>Salivary microbiome</title>
<p id="P5">With prior-HE, relative abundance of autochthonous families decreased while potentially pathogenic ones (<italic>Enterobacteriaceae</italic>
, <italic>Enterococcaceae</italic>
) increased in saliva. Endotoxin-related predicted functions were significantly higher in cirrhotic saliva.</p>
</sec>
<sec id="S6"><title>Stool microbiome</title>
<p id="P6">Relative autochthonous taxa abundance reduced in prior-HE, along with increased <italic>Enterobacteriaceae</italic>
and <italic>Enterococcaceae.</italic>
Cirrhotic stool microbiota demonstrated a significantly higher correlation with systemic inflammation compared to saliva microbiota on correlation networks.</p>
</sec>
<sec id="S7"><title>Outcomes</title>
<p id="P7">38 patients were hospitalized within 90 days. Their salivary dysbiosis was significantly worse and predicted this outcome independent of cirrhosis severity.</p>
</sec>
<sec id="S8"><title>Salivary inflammation</title>
<p id="P8">was studied in an additional 86 age-matched subjects (43 controls/43 cirrhotics); significantly higher IL-6/IL-1β, secretory IgA and lower lysozyme, and histatins 1 and 5 were found in cirrhotics compared to controls.</p>
</sec>
</sec>
<sec id="S9"><title>Conclusions</title>
<p id="P9">Dysbiosis, represented by reduction in autochthonous bacteria, is present in both saliva and stool in cirrhosis patients compared to controls. Cirrhotic patients have impaired salivary defenses and worse inflammation. Salivary dysbiosis was greater in cirrhotics who developed 90-day hospitalizations. These findings could represent a global mucosal-immune interface change in cirrhosis.</p>
</sec>
</div>
</front>
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<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Virginie</li>
</region>
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<tree><country name="États-Unis"><region name="Virginie"><name sortKey="Bajaj, Jasmohan S" sort="Bajaj, Jasmohan S" uniqKey="Bajaj J" first="Jasmohan S" last="Bajaj">Jasmohan S. Bajaj</name>
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<name sortKey="Betrapally, Naga S" sort="Betrapally, Naga S" uniqKey="Betrapally N" first="Naga S" last="Betrapally">Naga S. Betrapally</name>
<name sortKey="Daita, Kalyani" sort="Daita, Kalyani" uniqKey="Daita K" first="Kalyani" last="Daita">Kalyani Daita</name>
<name sortKey="Gillevet, Patrick M" sort="Gillevet, Patrick M" uniqKey="Gillevet P" first="Patrick M" last="Gillevet">Patrick M. Gillevet</name>
<name sortKey="Heuman, Douglas M" sort="Heuman, Douglas M" uniqKey="Heuman D" first="Douglas M" last="Heuman">Douglas M. Heuman</name>
<name sortKey="Hylemon, Phillip B" sort="Hylemon, Phillip B" uniqKey="Hylemon P" first="Phillip B" last="Hylemon">Phillip B. Hylemon</name>
<name sortKey="Kang, Dae Joong" sort="Kang, Dae Joong" uniqKey="Kang D" first="Dae Joong" last="Kang">Dae Joong Kang</name>
<name sortKey="Sanyal, Arun J" sort="Sanyal, Arun J" uniqKey="Sanyal A" first="Arun J" last="Sanyal">Arun J. Sanyal</name>
<name sortKey="Sikaroodi, Masoumeh" sort="Sikaroodi, Masoumeh" uniqKey="Sikaroodi M" first="Masoumeh" last="Sikaroodi">Masoumeh Sikaroodi</name>
<name sortKey="Thacker, Leroy R" sort="Thacker, Leroy R" uniqKey="Thacker L" first="Leroy R" last="Thacker">Leroy R. Thacker</name>
<name sortKey="Unser, Ariel" sort="Unser, Ariel" uniqKey="Unser A" first="Ariel" last="Unser">Ariel Unser</name>
<name sortKey="White, Melanie B" sort="White, Melanie B" uniqKey="White M" first="Melanie B" last="White">Melanie B. White</name>
</country>
</tree>
</affiliations>
</record>
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