4 results on '"Ouafae Karimi"'
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2. Interruption of CXCL13-CXCR5 axis increases upper genital tract pathology and activation of NKT cells following chlamydial genital infection.
- Author
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Janina Jiang, Ouafae Karimi, Sander Ouburg, Cheryl I Champion, Archana Khurana, Guangchao Liu, Amanda Freed, Jolein Pleijster, Nora Rozengurt, Jolande A Land, Helja-Marja Surcel, Aila' Tiitinen, Jorma Paavonen, Mitchell Kronenberg, Servaas A Morré, and Kathleen A Kelly
- Subjects
Medicine ,Science - Abstract
BackgroundRegulation of immune responses is critical for controlling inflammation and disruption of this process can lead to tissue damage. We reported that CXCL13 was induced in fallopian tube tissue following C. trachomatis infection. Here, we examined the influence of the CXCL13-CXCR5 axis in chlamydial genital infection.Methodology and principal findingsDisruption of the CXCL13-CXCR5 axis by injecting anti-CXCL13 Ab to BALB/c mice or using Cxcr5-/- mice increased chronic inflammation in the upper genital tract (UGT; uterine horns and oviducts) after Chlamydia muridarum genital infection (GT). Further studies in Cxcr5-/- mice showed an elevation in bacterial burden in the GT and increased numbers of neutrophils, activated DCs and activated NKT cells early after infection. After resolution, we noted increased fibrosis and the accumulation of a variety of T cells subsets (CD4-IFNγ, CD4-IL-17, CD4-IL-10 & CD8-TNFα) in the oviducts. NKT cell depletion in vitro reduced IL-17α and various cytokines and chemokines, suggesting that activated NKT cells modulate neutrophils and DCs through cytokine/chemokine secretion. Further, chlamydial glycolipids directly activated two distinct types of NKT cell hybridomas in a cell-free CD1d presentation assay and genital infection of Cd1d-/- mice showed reduced oviduct inflammation compared to WT mice. CXCR5 involvement in pathology was also noted using single-nucleotide polymorphism analysis in C. trachomatis infected women attending a sub-fertility clinic. Women who developed tubal pathology after a C. trachomatis infection had a decrease in the frequency of CXCR5 SNP +10950 T>C (rs3922).Conclusions/significanceThese experiments indicate that disruption of the CXCL13-CXCR5 axis permits increased activation of NKT cells by type I and type II glycolipids of Chlamydia muridarum and results in UGT pathology potentially through increased numbers of neutrophils and T cell subsets associated with UGT pathology. In addition, CXCR5 appears to contribute to inter-individual differences in human tubal pathology following C. trachomatis infection.
- Published
- 2012
- Full Text
- View/download PDF
3. Interruption of CXCL13-CXCR5 Axis Increases Upper Genital Tract Pathology and Activation of NKT Cells following Chlamydial Genital Infection
- Author
-
Janina Jiang, Ouafae Karimi, Sander Ouburg, Cheryl I. Champion, Archana Khurana, Guangchao Liu, Amanda Freed, Jolein Pleijster, Nora Rozengurt, Jolande A. Land, Helja-Marja Surcel, Aila' Tiitinen, Jorma Paavonen, Mitchell Kronenberg, Servaas A. Morré, and Kathleen A. Kelly
- Subjects
Multidisciplinary ,Science ,lcsh:R ,lcsh:Medicine ,Correction ,03 medical and health sciences ,0302 clinical medicine ,030220 oncology & carcinogenesis ,Medicine ,lcsh:Q ,lcsh:Science ,030217 neurology & neurosurgery - Published
- 2013
4. Interruption of CXCL13-CXCR5 Axis Increases Upper Genital Tract Pathology and Activation of NKT Cells following Chlamydial Genital Infection
- Author
-
Jolande A. Land, Amanda Freed, Guangchao Liu, Sander Ouburg, Heljä-Marja Surcel, Janina Jiang, Servaas A. Morré, Jolein Pleijster, Nora Rozengurt, Jorma Paavonen, Aila Tiitinen, Archana Khurana, Cheryl I. Champion, Kathleen A. Kelly, Ouafae Karimi, Mitchell Kronenberg, Reproductive Origins of Adult Health and Disease (ROAHD), Clinicum, Department of Obstetrics and Gynecology, HUS Gynecology and Obstetrics, Medical Microbiology and Infection Prevention, CCA - Immuno-pathogenesis, RS: CAPHRI School for Public Health and Primary Care, RS: GROW - School for Oncology and Reproduction, Gynaecologie en Obstetrie, and Institute for Public Health Genomics
- Subjects
Pathology ,Chemokine ,SUBSETS ,MURIDARUM INFECTION ,medicine.disease_cause ,Lymphocyte Activation ,Reproductive Tract Infections ,Cohort Studies ,Mice ,0302 clinical medicine ,3123 Gynaecology and paediatrics ,T-Lymphocyte Subsets ,Pelvic inflammatory disease ,TRACHOMATIS INFECTION ,IMMUNE-RESPONSE ,Chlamydia ,Immune Response ,0303 health sciences ,Multidisciplinary ,biology ,Natural killer T cell ,CD1D ,3. Good health ,Bacterial Pathogens ,medicine.anatomical_structure ,Infectious Diseases ,Chemokine secretion ,Medicine ,Cytokines ,Female ,Research Article ,EXPRESSION ,Receptors, CXCR5 ,medicine.medical_specialty ,Chlamydia muridarum ,T cell ,Science ,education ,Immunology ,Sexually Transmitted Diseases ,Immunopathology ,Microbiology ,Polymorphism, Single Nucleotide ,White People ,03 medical and health sciences ,medicine ,ANTIGEN PRESENTATION ,Genetics ,Animals ,Humans ,Biology ,030304 developmental biology ,Inflammation ,KILLER T-CELLS ,Immunity ,Human Genetics ,Reproductive Immunology ,PELVIC INFLAMMATORY DISEASE ,Immunologic Subspecialties ,Chlamydia Infections ,biology.organism_classification ,medicine.disease ,Chemokine CXCL13 ,Disease Models, Animal ,biology.protein ,Natural Killer T-Cells ,Antigens, CD1d ,Chlamydia trachomatis ,030215 immunology - Abstract
Background: Regulation of immune responses is critical for controlling inflammation and disruption of this process can lead to tissue damage. We reported that CXCL13 was induced in fallopian tube tissue following C. trachomatis infection. Here, we examined the influence of the CXCL13-CXCR5 axis in chlamydial genital infection.Methodology and Principal Findings: Disruption of the CXCL13-CXCR5 axis by injecting anti-CXCL13 Ab to BALB/c mice or using Cxcr5-/- mice increased chronic inflammation in the upper genital tract (UGT; uterine horns and oviducts) after Chlamydia muridarum genital infection (GT). Further studies in Cxcr5-/- mice showed an elevation in bacterial burden in the GT and increased numbers of neutrophils, activated DCs and activated NKT cells early after infection. After resolution, we noted increased fibrosis and the accumulation of a variety of T cells subsets (CD4-IFN gamma, CD4-IL-17, CD4-IL-10 & CD8-TNF alpha) in the oviducts. NKT cell depletion in vitro reduced IL-17 alpha and various cytokines and chemokines, suggesting that activated NKT cells modulate neutrophils and DCs through cytokine/chemokine secretion. Further, chlamydial glycolipids directly activated two distinct types of NKT cell hybridomas in a cell-free CD1d presentation assay and genital infection of Cd1d-/- mice showed reduced oviduct inflammation compared to WT mice. CXCR5 involvement in pathology was also noted using single-nucleotide polymorphism analysis in C. trachomatis infected women attending a sub-fertility clinic. Women who developed tubal pathology after a C. trachomatis infection had a decrease in the frequency of CXCR5 SNP +10950 T>C (rs3922).Conclusions/Significance: These experiments indicate that disruption of the CXCL13-CXCR5 axis permits increased activation of NKT cells by type I and type II glycolipids of Chlamydia muridarum and results in UGT pathology potentially through increased numbers of neutrophils and T cell subsets associated with UGT pathology. In addition, CXCR5 appears to contribute to inter-individual differences in human tubal pathology following C. trachomatis infection.
- Published
- 2012
- Full Text
- View/download PDF
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