The Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem 9112001, Israel
Tehila Hadad
The Institute of Dental Sciences, Hebrew University School of Dental Medicine, Jerusalem 9112001, Israel
Ariella Glasner
The Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem 9112001, Israel
Chamutal Gur
The Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem 9112001, Israel
Zvi Granot
Department of Developmental Biology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem 9112001, Israel
Gilad Bachrach
The Institute of Dental Sciences, Hebrew University School of Dental Medicine, Jerusalem 9112001, Israel
Ofer Mandelboim
The Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem 9112001, Israel
Urinary tract infection (UTI) is the most common type of bacterial infection in humans. Fifty percent of all women will experience at least one UTI in their lifetime, with uropathogenic Escherichia coli (UPEC) accounting for 80% of reported cases. UTI evokes a complex, well-timed immune response that is crucial for bacterial clearance. The majority of immune cells participating in the immune response are absent from the healthy bladder, and the mechanisms used to recruit them upon UTI are not fully understood. Here, we show that immediately after UPEC infection, bladder epithelial cells secrete stromal cell-derived factor 1 (SDF-1), initiating immune cell accumulation at the site of infection. SDF-1 blockade significantly reduced immune cell migration to the infected bladder, resulting in severe exacerbation of infection. We also show that FimH, the adhesin of type 1 fimbria, one of UPEC’s virulence factors, is directly involved in the secretion of SDF-1 upon UTI.
