ArticleNature communications2024
Host response during unresolved urinary tract infection alters female mammary tissue homeostasis through collagen deposition and TIMP1.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Urogenital immune signatures are associated with birth outcomes after maternal urinary tract infection.Science translational medicine · 2026Article
- Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.Nature communications · 2025Article
- MaGNet: A Network-Based Method for Quantitative Analysis of the Mammary Ductal Tree in Developing Female Mice.Journal of mammary gland biology and neoplasia · 2025Article
- Defining breast epithelial cell types in the single-cell era.Developmental cell · 2025Review
- Distinct maternofetal immune signatures delineate preterm birth onset following urinary tract infection.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Exposure to pathogens throughout a lifetime influences immunity and organ function. Here, we explore how the systemic host-response to bacterial urinary tract infection (UTI) induces tissue-specific alterations to the mammary gland. Utilizing a combination of histological tissue analysis, single cell transcriptomics, and flow cytometry, we identify that mammary tissue from UTI-bearing mice displays collagen deposition, enlarged ductal structures, ductal hyperplasia with atypical epithelial transcriptomes and altered immune composition. Bacterial cells are absent in the mammary tissue and blood of UTI-bearing mice, therefore, alterations to the distal mammary tissue are mediated by the systemic host response to local infection. Furthermore, broad spectrum antibiotic treatment resolves the infection and restores mammary cellular and tissue homeostasis. Systemically, unresolved UTI correlates with increased plasma levels of the metalloproteinase inhibitor, TIMP1, which controls extracellular matrix remodeling and neutrophil function. Treatment of nulliparous and post-lactation UTI-bearing female mice with a TIMP1 neutralizing antibody, restores mammary tissue normal homeostasis, thus providing evidence for a link between the systemic host response during UTI and mammary gland alterations.
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Registered trials
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