ArticleInfection and immunity2005
CXCR3 and its ligands participate in the host response to Bordetella bronchiseptica infection of the mouse respiratory tract but are not required for clearance of bacteria from the lung.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed.
- IgA-producing B cells in lung homeostasis and disease.Frontiers in immunology · 2023Review
- Bordetella pertussis-infected innate immune cells drive the anti-pertussis response of human airway epithelium.Scientific reports · 2022Article
- Recruited and Tissue-Resident Natural Killer Cells in the Lung During Infection and Cancer.Frontiers in immunology · 2022Review
- Involvement of chemokine receptor CXCR3 in the defense mechanism againstFrontiers in microbiology · 2022Article
- Evaluating the role of chemokines and chemokine receptors involved in coronavirus infection.Expert review of clinical immunology · 2022Article
- Natural Killer Cell Recruitment to the Lung During Influenza A Virus Infection Is Dependent on CXCR3, CCR5, and Virus Exposure Dose.Frontiers in immunology · 2018Article
- Chemokines and NK cells: regulators of development, trafficking and functions.Immunology letters · 2012Review
- Resident Corneal Cells Communicate with Neutrophils Leading to the Production of IP-10 during the Primary Inflammatory Response to HSV-1 Infection.International journal of inflammation · 2012Article
- Organ-specific features of natural killer cells.Nature reviews. Immunology · 2011Review
- Article
- CXCR2-dependent mucosal neutrophil influx protects against colitis-associated diarrhea caused by an attaching/effacing lesion-forming bacterial pathogen.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Neutrophil recruitment to the lungs during bacterial pneumonia.Infection and immunity · 2009Review
- The trafficking of natural killer cells.Immunological reviews · 2007Review
- A role for natural killer cells in intestinal inflammation caused by infection with Salmonella enterica serovar Typhimurium.FEMS immunology and medical microbiology · 2007Article
- CXCL16 regulates cell-mediated immunity to Salmonella enterica serovar Enteritidis via promotion of gamma interferon production.Infection and immunity · 2006Article
- CXCR3 and IFN protein-10 in Pneumocystis pneumonia.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- gammadelta T cells regulate the early inflammatory response to bordetella pertussis infection in the murine respiratory tract.Infection and immunity · 2006Article
- Functional diversity of chemokines and chemokine receptors in response to viral infection of the central nervous system.Current topics in microbiology and immunology · 2006Review
- Interferon-inducible protein 10, but not monokine induced by gamma interferon, promotes protective type 1 immunity in murine Klebsiella pneumoniae pneumonia.Infection and immunity · 2005Article
- Bordetella bronchiseptica flagellin is a proinflammatory determinant for airway epithelial cells.Infection and immunity · 2005Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Intranasal inoculation of mice with Bordetella bronchiseptica produces a transient pneumonia that is cleared over several weeks in a process known to require both neutrophils and lymphocytes. In this study, we evaluated the roles of the chemokines MIG (CXCL9), IP-10 (CXCL10), and I-TAC (CXCL11) and their common receptor, CXCR3. Following bacterial inoculation, message expression of interleukin-1 (IL-1), IL-6, and the neutrophil-attracting chemokines KC, LIX, and MIP-2 was rapidly induced, with maximal expression found at 6 h. In contrast, message expression of gamma interferon, MIG, IP-10, and I-TAC peaked at 2 days. Expression of all of these chemokines and cytokines returned to near baseline by 5 days, despite the persistence of high levels of live bacteria at this time. Induced MIG, IP-10, and I-TAC protein expression was localized in areas of inflammation at 2 to 3 days and was temporally associated with increased levels of CXCR3(+) lymphocytes in bronchoalveolar lavage fluid. There was no increase in mortality in mice lacking CXCR3. However, the clearance of bacteria from the lung and trachea was delayed, and the recruitment of lymphocytes and NK cells was slightly decreased, for CXCR3(-/-) mice relative to CXCR3(+/+) mice. We conclude that the CXCR3 receptor-ligand system contributes to pulmonary host defense in B. bronchiseptica infection by recruiting lymphocytes and NK cells into the lung.
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