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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, and interested parties Long press or scan the QR code below to follow us.
There are many clinical similarities between iNatureIgG4-related sclerosing cholangitis (IgG4-SC) and primary sclerosing cholangitis (PSC).
Although the imbalance of intestinal flora has been extensively studied in PSC, the intestinal flora The role of tract flora in IgG4-SC is still unknown.
On May 25, 2021, Tang Ruqi, Ma Xiong and Lian Min from Shanghai Jiaotong University jointly published a research paper entitled "Altered faecal microbiome and metabolome in IgG4-related sclerosing cholangitis and primary sclerosing cholangitis" in Gut (IF=19.
82).
The study performed 16S rRNA gene amplicon sequencing on stool samples from 135 subjects.
These subjects were IgG4-SC (n = 34), PSC (n = 37) and healthy controls (n = 64).
A subset of samples (31 IgG4-SC, 37 PSC, and 45 controls) were also analyzed by non-targeted metabolomics.
The study found that, compared to the control, reduced alpha diversity and migration of microbial communities were observed in IgG4-SC and PSC.
These changes are accompanied by differences in the fecal metabolome.
Importantly, although there are some common changes in the composition and metabolic activity of the microbial flora, a comprehensive analysis found different host-microbe associations in IgG4-SC and PSC.
Disease-related genera and metabolites tend to be related to transaminase in IgG4-SC.
The liver inflammation of IgG4-SC may be the cause of the obvious consumption of Blautia and the increase of succinic acid.
In contrast, potential links between microbial or metabolic characteristics and cholestasis parameters were detected in PSC.
In particular, there is a consistent decrease in metabolites (including secondary bile acids) of eubacterial and microbial origin.
Interestingly, predictive models based on metabolites are more effective in distinguishing disease states than predictive models based on microorganisms.
In summary, the research data shows that IgG4-SC and PSC have different host-microbe interactions, which may be related to the pathogenesis of the disease.
These data emphasize the uniqueness of IgG4-SC.
IgG4-related sclerosing cholangitis (IgG4-SC) is the hepatobiliary phenotype of IgG4-related diseases (IgG4-RD), a multi-system fibrotic inflammatory disease, which consists of elevated serum IgG4 levels and a large number of IgG4-positive cells in the lymph Defined by plasma cell infiltration.
IgG4-SC is a progressive chronic liver disease characterized by common comorbidities of multifocal biliary stricture and inflammatory bowel disease (IBD).
The main clinical manifestations of IgG4-SC, jaundice and pruritus are similar to primary sclerosing cholangitis (PSC), so in some cases it will be misdiagnosed.
It is effective for most IgG4-SC patients, while the treatment strategy for PSC patients is limited.
The results of the two diseases are different.
Compared with IgG4-SC, the risk of liver cirrhosis, cholangiocarcinoma, and colorectal cancer is higher in PSC.
The pathogenesis of these two types of sclerosing cholangitis is still unclear.
Nevertheless, environmental exposure, especially the intestinal flora and its derivatives, has inspired recent research.
In fact, the intestinal flora of patients with PSC shows a compositional change, which is characterized by a decrease in bacterial diversity and an increase in the abundance of potential pathogenic bacteria (including Veillonella, Enterococcus and Clostridium).
Mechanism studies have found that Klebsiella pneumoniae in the intestines of PSC patients causes bacterial translocation, followed by Th17-mediated hepatitis.
In contrast, the intestinal flora in IgG4-SC has not been elucidated.
IgG4-RD is characterized by a type II immune response, and is often accompanied by a clinical history of allergies and elevated serum levels of IgE.
In view of the fact that the imbalance of intestinal flora can cause type II immune responses and allergic reactions, whether the intestinal flora plays a role in IgG4-SC needs further research.
Intestinal flora has a profound impact on host physiology, which can be mediated by small molecules produced by microorganisms.
These microbial metabolites can induce host responses in the gut and distant organs.
There is increasing evidence that microbial metabolites, such as short-chain fatty acids (SCFA), bile acids and trimethylamine, are involved in the pathogenesis of liver disease.
Fecal metabolome helps explain a large part of the difference in the composition of the gut microbiome.
Therefore, a comprehensive analysis of multi-omics data of gut microbiota, metabolome and host physiology may be the mechanism link between gut microbiota and disease Provide clues.
Here, the study performed 16S rRNA gene amplicon sequencing and non-targeted liquid chromatography-tandem mass spectrometry analysis on stool samples in a cohort consisting of IgG4-SC, PSC, and healthy controls.
Then integrate microbiome and metabolome data to characterize IgG4-SC-related and PSC-related changes in fecal microbes and metabolic profiles, as well as assess the potential functional link between the gut microbiome, metabolome, and host phenotype in the disease cohort .
The study found that, compared to the control, reduced alpha diversity and migration of microbial communities were observed in IgG4-SC and PSC.
These changes are accompanied by differences in the fecal metabolome.
Importantly, although there are some common changes in the composition and metabolic activity of the microbial flora, a comprehensive analysis found different host-microbe associations in IgG4-SC and PSC.
Disease-related genera and metabolites tend to be related to transaminase in IgG4-SC.
The liver inflammation of IgG4-SC may be the cause of the obvious consumption of Blautia and the increase of succinic acid.
In contrast, potential links between microbial or metabolic characteristics and cholestasis parameters were detected in PSC.
In particular, there is a consistent decrease in metabolites (including secondary bile acids) of eubacterial and microbial origin.
Interestingly, predictive models based on metabolites are more effective in distinguishing disease states than predictive models based on microorganisms.
In conclusion, the research data shows that IgG4-SC and PSC have different host-microbe interactions, which may be related to the pathogenesis of the disease.
These data emphasize the uniqueness of IgG4-SC.
Reference message: https://gut.
bmj.
com/content/early/2021/05/24/gutjnl-2020-323565
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, and interested parties Long press or scan the QR code below to follow us.
There are many clinical similarities between iNatureIgG4-related sclerosing cholangitis (IgG4-SC) and primary sclerosing cholangitis (PSC).
Although the imbalance of intestinal flora has been extensively studied in PSC, the intestinal flora The role of tract flora in IgG4-SC is still unknown.
On May 25, 2021, Tang Ruqi, Ma Xiong and Lian Min from Shanghai Jiaotong University jointly published a research paper entitled "Altered faecal microbiome and metabolome in IgG4-related sclerosing cholangitis and primary sclerosing cholangitis" in Gut (IF=19.
82).
The study performed 16S rRNA gene amplicon sequencing on stool samples from 135 subjects.
These subjects were IgG4-SC (n = 34), PSC (n = 37) and healthy controls (n = 64).
A subset of samples (31 IgG4-SC, 37 PSC, and 45 controls) were also analyzed by non-targeted metabolomics.
The study found that, compared to the control, reduced alpha diversity and migration of microbial communities were observed in IgG4-SC and PSC.
These changes are accompanied by differences in the fecal metabolome.
Importantly, although there are some common changes in the composition and metabolic activity of the microbial flora, a comprehensive analysis found different host-microbe associations in IgG4-SC and PSC.
Disease-related genera and metabolites tend to be related to transaminase in IgG4-SC.
The liver inflammation of IgG4-SC may be the cause of the obvious consumption of Blautia and the increase of succinic acid.
In contrast, potential links between microbial or metabolic characteristics and cholestasis parameters were detected in PSC.
In particular, there is a consistent decrease in metabolites (including secondary bile acids) of eubacterial and microbial origin.
Interestingly, predictive models based on metabolites are more effective in distinguishing disease states than predictive models based on microorganisms.
In summary, the research data shows that IgG4-SC and PSC have different host-microbe interactions, which may be related to the pathogenesis of the disease.
These data emphasize the uniqueness of IgG4-SC.
IgG4-related sclerosing cholangitis (IgG4-SC) is the hepatobiliary phenotype of IgG4-related diseases (IgG4-RD), a multi-system fibrotic inflammatory disease, which consists of elevated serum IgG4 levels and a large number of IgG4-positive cells in the lymph Defined by plasma cell infiltration.
IgG4-SC is a progressive chronic liver disease characterized by common comorbidities of multifocal biliary stricture and inflammatory bowel disease (IBD).
The main clinical manifestations of IgG4-SC, jaundice and pruritus are similar to primary sclerosing cholangitis (PSC), so in some cases it will be misdiagnosed.
It is effective for most IgG4-SC patients, while the treatment strategy for PSC patients is limited.
The results of the two diseases are different.
Compared with IgG4-SC, the risk of liver cirrhosis, cholangiocarcinoma, and colorectal cancer is higher in PSC.
The pathogenesis of these two types of sclerosing cholangitis is still unclear.
Nevertheless, environmental exposure, especially the intestinal flora and its derivatives, has inspired recent research.
In fact, the intestinal flora of patients with PSC shows a compositional change, which is characterized by a decrease in bacterial diversity and an increase in the abundance of potential pathogenic bacteria (including Veillonella, Enterococcus and Clostridium).
Mechanism studies have found that Klebsiella pneumoniae in the intestines of PSC patients causes bacterial translocation, followed by Th17-mediated hepatitis.
In contrast, the intestinal flora in IgG4-SC has not been elucidated.
IgG4-RD is characterized by a type II immune response, and is often accompanied by a clinical history of allergies and elevated serum levels of IgE.
In view of the fact that the imbalance of intestinal flora can cause type II immune responses and allergic reactions, whether the intestinal flora plays a role in IgG4-SC needs further research.
Intestinal flora has a profound impact on host physiology, which can be mediated by small molecules produced by microorganisms.
These microbial metabolites can induce host responses in the gut and distant organs.
There is increasing evidence that microbial metabolites, such as short-chain fatty acids (SCFA), bile acids and trimethylamine, are involved in the pathogenesis of liver disease.
Fecal metabolome helps explain a large part of the difference in the composition of the gut microbiome.
Therefore, a comprehensive analysis of multi-omics data of gut microbiota, metabolome and host physiology may be the mechanism link between gut microbiota and disease Provide clues.
Here, the study performed 16S rRNA gene amplicon sequencing and non-targeted liquid chromatography-tandem mass spectrometry analysis on stool samples in a cohort consisting of IgG4-SC, PSC, and healthy controls.
Then integrate microbiome and metabolome data to characterize IgG4-SC-related and PSC-related changes in fecal microbes and metabolic profiles, as well as assess the potential functional link between the gut microbiome, metabolome, and host phenotype in the disease cohort .
The study found that, compared to the control, reduced alpha diversity and migration of microbial communities were observed in IgG4-SC and PSC.
These changes are accompanied by differences in the fecal metabolome.
Importantly, although there are some common changes in the composition and metabolic activity of the microbial flora, a comprehensive analysis found different host-microbe associations in IgG4-SC and PSC.
Disease-related genera and metabolites tend to be related to transaminase in IgG4-SC.
The liver inflammation of IgG4-SC may be the cause of the obvious consumption of Blautia and the increase of succinic acid.
In contrast, potential links between microbial or metabolic characteristics and cholestasis parameters were detected in PSC.
In particular, there is a consistent decrease in metabolites (including secondary bile acids) of eubacterial and microbial origin.
Interestingly, predictive models based on metabolites are more effective in distinguishing disease states than predictive models based on microorganisms.
In conclusion, the research data shows that IgG4-SC and PSC have different host-microbe interactions, which may be related to the pathogenesis of the disease.
These data emphasize the uniqueness of IgG4-SC.
Reference message: https://gut.
bmj.
com/content/early/2021/05/24/gutjnl-2020-323565
