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AuthorNovember A basic feature of the immune system is the ability to form memories of previously encountered threats, thereby enhancing the ability to respond to subsequent challenges
.
However, more and more evidence shows that the components of the innate immune system may also be affected by inflammation or infection.
This phenomenon is called "training immunity" [1]
.
However, it is not clear how the mother's infection experience at different developmental stages affects the immune system of the offspring
.
In order to uncover the answer to this question, the Yasmine Belkaid research group of the National Institutes of Health (NIH) published a paper in Science titled Prenatal maternal infection promotes tissue-specific immunity and inflammation in offspring, and found that the maternal infection promotes tissue-specific immunity and inflammation in offspring.
Immunity of offspring is improved, revealing the basic development window of the immune system and the host immune imprinting and epigenetic changes caused by infection
.
To this end, the authors used a food-borne strain called Yersinia pseudotuberculosis (Yersinia pseudotuberculosis) to feed the mice at 10.
5 days of pregnancy, this time point is considered to be fetal mouse immunity The key developmental stage of the system, when blood stem cells appear and hematopoietic function begins [2]
.
The female mouse will then excrete the strain from the body and cause only a small degree of infection.
Therefore, Yersinia pseudotuberculosis is a very mild and maternal-specific infection model
.
After establishing a suitable model, the authors compared and tested the lymphocyte composition of the offspring of the infected mother and the offspring of the non-infected mother.
The authors were surprised to find that the TH17 cells expressing RORγt CD4+ T cells showed obvious signs after infection.
Increase (Figure 1), and this increase is mainly located in the intestine
.
By changing the feeding method of the control group, the authors found that this "immune memory" was not caused by changes in the maternal microbiota after delivery or lactation.
The intestinal TH17 cell response caused by maternal infection was acquired in the uterus
.
Figure 1 TH17 cells are significantly increased after infection.
A variety of soluble factors including cytokines can cross the placental barrier [3].
Therefore, the authors want to know whether the impact of maternal infection on fetal immune memory is through the regulation of soluble factors Content
.
By detecting the increase of cytokines in the offspring of maternal infection, the authors found that there are four cytokines interleukins IL-6, IFN-γ, G-CSF, and TNF-α
.
But only in vitro injection of IL-6 and not other cytokines can increase the number of TH17 cells in the offspring
.
Neutralization by injection of IL-6 antibody after maternal infection will significantly reduce the number of TH17 cells in the offspring
.
Therefore, the authors found that IL-6 is sufficient and necessary for the effect of maternal pathogen infection on the immunity of offspring
.
Figure 2 Changes in cytokines in the offspring of maternal infection So, how does the increased level of IL-6 after infection affect the "immune memory" of the offspring of the fetus? In order to uncover the answer to this question, the authors tested the effects of IL-6 on the fetal intestine
.
The authors found that the genome accessibility of many genes related to cell fate determination in intestinal epithelial cells, that is, the openness, has increased significantly.
Fetal intestinal epithelial cells are enriched with transcription factor binding motifs.
These motifs interact with the intestinal tract.
Development, differentiation of intestinal epithelial cells and establishment of intestinal epithelial cell identity are closely related [4]
.
Injection of IL-6 to the fetus during pregnancy will also cause a significant increase in chromatin accessibility in the fetal intestinal epithelial cells.
Compared with the control, there are only 4 areas with significant openness compared to the numbness of IL-6 injection The accessibility of 2118 areas in the offspring was significantly increased
.
Moreover, the authors found that the exposure of IL-6 before the birth of the fetus will also have a significant impact on the chromatin accessibility and transcriptome of intestinal epithelial stem cells.
This phenomenon directly affects the function of the offspring’s intestinal epithelial cells
.
Maternal infection or IL-6 injection will promote the protective immunity of the offspring of the fetus.
For example, the antibacterial defense ability of the offspring against acute Salmonella typhimurium is significantly increased
.
However, in the context of maternal colitis, increasing the maternal IL-6 exposure during pregnancy will increase the effect of inflammation
.
This result shows that after infection with the maternal pathogen, the "immune memory" can be written into the offspring's fetus by changing the accessibility of the genome, but if the mother has its own disease, the offspring's fetus will have a stronger inflammatory response
.
Figure 3 Working model In general, this work found that minor infections encountered during the prenatal development of the fetus can lead to lasting changes in intestinal epithelial stem cells, resulting in enhanced resistance to intestinal infections
.
The impact of maternal infection is tissue-specific, mainly mediated by the cytokine interleukin IL-6, which acts on intestinal epithelial stem cells during fetal development
.
Maternal infection changes the immunity of the offspring at the expense of increased susceptibility to inflammation of the intestinal mucosa
.
Therefore, the infection of maternal pathogens propped up a protective umbrella written into "immune memory" for the fetus
.
Original link: https://doi.
org/10.
1126/science.
abf3002 Platemaker: Eleven References 1 Netea, MG et al.
Defining trained immunity and its role in health and disease.
Nature reviews.
Immunology 20, 375-388 , doi:10.
1038/s41577-020-0285-6 (2020).
2 McGrath, KE et al.
Distinct Sources of Hematopoietic Progenitors Emerge before HSCs and Provide Functional Blood Cells in the Mammalian Embryo.
Cell reports 11, 1892-1904, doi :10.
1016/j.
celrep.
2015.
05.
036 (2015).
3 Ganal-Vonarburg, SC, Hornef, MW & Macpherson, AJ Microbial-host molecular exchange and its functional consequences in early mammalian life.
Science (New York, NY) 368 , 604-607, doi:10.
1126/science.
aba0478 (2020).
4 Francis, R.
et al.
Gastrointestinal transcription factors drive lineage-specific developmental programs in organ specification and cancer.
Science advances 5, eaax8898, doi:10.
1126/sciadv .
aax8898 (2019).
Reprinting instructions [Original Articles] BioArt original articles, personal sharing is welcome, reprinting is prohibited without permission, the copyrights of all published works are owned by BioArt
.
BioArt reserves all statutory rights and offenders must be investigated
.
.
However, more and more evidence shows that the components of the innate immune system may also be affected by inflammation or infection.
This phenomenon is called "training immunity" [1]
.
However, it is not clear how the mother's infection experience at different developmental stages affects the immune system of the offspring
.
In order to uncover the answer to this question, the Yasmine Belkaid research group of the National Institutes of Health (NIH) published a paper in Science titled Prenatal maternal infection promotes tissue-specific immunity and inflammation in offspring, and found that the maternal infection promotes tissue-specific immunity and inflammation in offspring.
Immunity of offspring is improved, revealing the basic development window of the immune system and the host immune imprinting and epigenetic changes caused by infection
.
To this end, the authors used a food-borne strain called Yersinia pseudotuberculosis (Yersinia pseudotuberculosis) to feed the mice at 10.
5 days of pregnancy, this time point is considered to be fetal mouse immunity The key developmental stage of the system, when blood stem cells appear and hematopoietic function begins [2]
.
The female mouse will then excrete the strain from the body and cause only a small degree of infection.
Therefore, Yersinia pseudotuberculosis is a very mild and maternal-specific infection model
.
After establishing a suitable model, the authors compared and tested the lymphocyte composition of the offspring of the infected mother and the offspring of the non-infected mother.
The authors were surprised to find that the TH17 cells expressing RORγt CD4+ T cells showed obvious signs after infection.
Increase (Figure 1), and this increase is mainly located in the intestine
.
By changing the feeding method of the control group, the authors found that this "immune memory" was not caused by changes in the maternal microbiota after delivery or lactation.
The intestinal TH17 cell response caused by maternal infection was acquired in the uterus
.
Figure 1 TH17 cells are significantly increased after infection.
A variety of soluble factors including cytokines can cross the placental barrier [3].
Therefore, the authors want to know whether the impact of maternal infection on fetal immune memory is through the regulation of soluble factors Content
.
By detecting the increase of cytokines in the offspring of maternal infection, the authors found that there are four cytokines interleukins IL-6, IFN-γ, G-CSF, and TNF-α
.
But only in vitro injection of IL-6 and not other cytokines can increase the number of TH17 cells in the offspring
.
Neutralization by injection of IL-6 antibody after maternal infection will significantly reduce the number of TH17 cells in the offspring
.
Therefore, the authors found that IL-6 is sufficient and necessary for the effect of maternal pathogen infection on the immunity of offspring
.
Figure 2 Changes in cytokines in the offspring of maternal infection So, how does the increased level of IL-6 after infection affect the "immune memory" of the offspring of the fetus? In order to uncover the answer to this question, the authors tested the effects of IL-6 on the fetal intestine
.
The authors found that the genome accessibility of many genes related to cell fate determination in intestinal epithelial cells, that is, the openness, has increased significantly.
Fetal intestinal epithelial cells are enriched with transcription factor binding motifs.
These motifs interact with the intestinal tract.
Development, differentiation of intestinal epithelial cells and establishment of intestinal epithelial cell identity are closely related [4]
.
Injection of IL-6 to the fetus during pregnancy will also cause a significant increase in chromatin accessibility in the fetal intestinal epithelial cells.
Compared with the control, there are only 4 areas with significant openness compared to the numbness of IL-6 injection The accessibility of 2118 areas in the offspring was significantly increased
.
Moreover, the authors found that the exposure of IL-6 before the birth of the fetus will also have a significant impact on the chromatin accessibility and transcriptome of intestinal epithelial stem cells.
This phenomenon directly affects the function of the offspring’s intestinal epithelial cells
.
Maternal infection or IL-6 injection will promote the protective immunity of the offspring of the fetus.
For example, the antibacterial defense ability of the offspring against acute Salmonella typhimurium is significantly increased
.
However, in the context of maternal colitis, increasing the maternal IL-6 exposure during pregnancy will increase the effect of inflammation
.
This result shows that after infection with the maternal pathogen, the "immune memory" can be written into the offspring's fetus by changing the accessibility of the genome, but if the mother has its own disease, the offspring's fetus will have a stronger inflammatory response
.
Figure 3 Working model In general, this work found that minor infections encountered during the prenatal development of the fetus can lead to lasting changes in intestinal epithelial stem cells, resulting in enhanced resistance to intestinal infections
.
The impact of maternal infection is tissue-specific, mainly mediated by the cytokine interleukin IL-6, which acts on intestinal epithelial stem cells during fetal development
.
Maternal infection changes the immunity of the offspring at the expense of increased susceptibility to inflammation of the intestinal mucosa
.
Therefore, the infection of maternal pathogens propped up a protective umbrella written into "immune memory" for the fetus
.
Original link: https://doi.
org/10.
1126/science.
abf3002 Platemaker: Eleven References 1 Netea, MG et al.
Defining trained immunity and its role in health and disease.
Nature reviews.
Immunology 20, 375-388 , doi:10.
1038/s41577-020-0285-6 (2020).
2 McGrath, KE et al.
Distinct Sources of Hematopoietic Progenitors Emerge before HSCs and Provide Functional Blood Cells in the Mammalian Embryo.
Cell reports 11, 1892-1904, doi :10.
1016/j.
celrep.
2015.
05.
036 (2015).
3 Ganal-Vonarburg, SC, Hornef, MW & Macpherson, AJ Microbial-host molecular exchange and its functional consequences in early mammalian life.
Science (New York, NY) 368 , 604-607, doi:10.
1126/science.
aba0478 (2020).
4 Francis, R.
et al.
Gastrointestinal transcription factors drive lineage-specific developmental programs in organ specification and cancer.
Science advances 5, eaax8898, doi:10.
1126/sciadv .
aax8898 (2019).
Reprinting instructions [Original Articles] BioArt original articles, personal sharing is welcome, reprinting is prohibited without permission, the copyrights of all published works are owned by BioArt
.
BioArt reserves all statutory rights and offenders must be investigated
.
