News | TVP23A: A Potential New Diagnostic Marker for Chronic Endometritis
Chronic endometritis (CE) is an inflammatory disorder of the endometrium often caused by infection within the uterine cavity. Although most patients have no obvious symptoms, CE is closely associated with implantation failure and miscarriage, making accurate diagnosis and timely treatment important for improving pregnancy success in assisted reproduction.
A study published in Frontiers in Medicine examined gene-expression patterns and immune-cell involvement in CE, identifying a potential diagnostic marker and providing deeper insight into its pathogenesis.
Background and significance
Histologically, CE is usually characterized by plasma-cell infiltration of the endometrial stroma. CD138 immunohistochemical staining is commonly used for clinical diagnosis, but inconsistent diagnostic thresholds for CD138-positive cells produce variable results, creating an urgent need for more reliable markers.
The study aimed to use gene-expression profiling to identify potential molecular markers associated with CE and deepen understanding of its pathophysiology.
Methods
From July 2020 to April 2021, the team recruited 190 healthy female patients and excluded those who had used antibiotics in the previous three months. CE was diagnosed using CD138 immunohistochemical staining.
For gene-expression analysis, patients were randomly selected from CE and non-CE groups for RNA sequencing, with at least 30 patients per group to improve statistical reliability. Total RNA was extracted from endometrial tissue and sequenced on the HiSeq X platform, and gene-expression levels were analyzed.
Results
Among the final eligible patients, 57 met the criteria: 24 had CE (CD138≥5) and 33 did not (CD138<5). RNA sequencing of endometrial samples from 33 CE patients and 24 non-CE patients generated 20 million paired reads.
Differential expression analysis identified 20 upregulated genes in the CE group, most associated with immunoglobulins. TVP23A was consistently upregulated in CE samples, suggesting a possible role in CE pathogenesis.
During the proliferative phase, 13 genes were upregulated in the CE group, mainly immunoglobulin genes, coiled-coil domain containing 13 (CCDC13), and marginal zone B and B1 cell-specific protein (MZB1). During the secretory phase, eight non-immunoglobulin genes were upregulated.
Immune-cell analysis found significantly more plasma cells and fewer resting CD4 memory T cells in the CE group than in the non-CE group.
Discussion and significance
The study revealed differences between CE and non-CE endometrial tissue, particularly in gene-expression patterns during the proliferative and secretory phases. TVP23A offers a novel candidate marker independent of CD138-positive cell counts. Its consistent upregulation in most CE cases makes it a potential diagnostic tool.
Changes in immune-cell populations, especially increased plasma cells and reduced CD4 memory T cells, may relate to chronic inflammation in CE tissue and may affect memory T-cell responses.
Conclusion
This study is the first to examine the molecular physiology of CE in depth using RNA sequencing. It identified multiple CE-related gene-expression changes, particularly in TVP23A, providing a new direction for early diagnosis and treatment. TVP23A may become a new CE-specific diagnostic marker and offer additional clinical support for future assisted reproductive treatment.
News | TVP23A: A Potential New Diagnostic Marker for Chronic Endometritis
News | TVP23A: A Potential New Diagnostic Marker for Chronic Endometritis
Chronic endometritis (CE) is an inflammatory disorder of the endometrium often caused by infection within the uterine cavity. Although most patients have no obvious symptoms, CE is closely associated with implantation failure and miscarriage, making accurate diagnosis and timely treatment important for improving pregnancy success in assisted reproduction.
A study published in Frontiers in Medicine examined gene-expression patterns and immune-cell involvement in CE, identifying a potential diagnostic marker and providing deeper insight into its pathogenesis.
Background and significance
Histologically, CE is usually characterized by plasma-cell infiltration of the endometrial stroma. CD138 immunohistochemical staining is commonly used for clinical diagnosis, but inconsistent diagnostic thresholds for CD138-positive cells produce variable results, creating an urgent need for more reliable markers.
The study aimed to use gene-expression profiling to identify potential molecular markers associated with CE and deepen understanding of its pathophysiology.
Methods
From July 2020 to April 2021, the team recruited 190 healthy female patients and excluded those who had used antibiotics in the previous three months. CE was diagnosed using CD138 immunohistochemical staining.
For gene-expression analysis, patients were randomly selected from CE and non-CE groups for RNA sequencing, with at least 30 patients per group to improve statistical reliability. Total RNA was extracted from endometrial tissue and sequenced on the HiSeq X platform, and gene-expression levels were analyzed.
Results
Among the final eligible patients, 57 met the criteria: 24 had CE (CD138≥5) and 33 did not (CD138<5). RNA sequencing of endometrial samples from 33 CE patients and 24 non-CE patients generated 20 million paired reads.
Differential expression analysis identified 20 upregulated genes in the CE group, most associated with immunoglobulins. TVP23A was consistently upregulated in CE samples, suggesting a possible role in CE pathogenesis.
During the proliferative phase, 13 genes were upregulated in the CE group, mainly immunoglobulin genes, coiled-coil domain containing 13 (CCDC13), and marginal zone B and B1 cell-specific protein (MZB1). During the secretory phase, eight non-immunoglobulin genes were upregulated.
Immune-cell analysis found significantly more plasma cells and fewer resting CD4 memory T cells in the CE group than in the non-CE group.
Discussion and significance
The study revealed differences between CE and non-CE endometrial tissue, particularly in gene-expression patterns during the proliferative and secretory phases. TVP23A offers a novel candidate marker independent of CD138-positive cell counts. Its consistent upregulation in most CE cases makes it a potential diagnostic tool.
Changes in immune-cell populations, especially increased plasma cells and reduced CD4 memory T cells, may relate to chronic inflammation in CE tissue and may affect memory T-cell responses.
Conclusion
This study is the first to examine the molecular physiology of CE in depth using RNA sequencing. It identified multiple CE-related gene-expression changes, particularly in TVP23A, providing a new direction for early diagnosis and treatment. TVP23A may become a new CE-specific diagnostic marker and offer additional clinical support for future assisted reproductive treatment.
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