The impact of chemokine receptor CX3CR1 deficiency during respiratory infections with Mycobacterium tuberculosis or Francisella tularensis.

Abstract

Recruitment of immune cells to infection sites is a critical component of the host response to pathogens. This process is facilitated partly through interactions of chemokines with cognate receptors. Here, we examine the importance of fractalkine (CX3CL1) receptor, CX3CR1, which regulates function and trafficking of macrophages and dendritic cells, in the host's ability to control respiratory infections with Mycobacterium tuberculosis or Francisella tularensis. Following low-dose aerosol challenge with M. tuberculosis, CX3CR1(-/-) mice were no more susceptible to infection than wild-type C57BL/6 mice as measured by organ burden and survival time. Similarly, following inhalation of F. tularensis, CX3CR1(-/-) mice displayed similar organ burdens to wild-type mice. CX3CR1(-/-) mice had increased recruitment of monocytes and neutrophils in the lung; however, this did not result in increased abundance of infected monocytes or neutrophils. We conclude that CX3CR1-deficiency affects immune-cell recruitment; however, loss of CX3CR1 alone does not render the host more susceptible to M. tuberculosis or F. tularensis.

• Authors: J D Hall, S L Kurtz, N W Rigel, B M Gunn, S Taft-Benz, J P Morrison, A M Fong, D D Patel, M Braunstein, T H Kawula
• Journal: Clinical and experimental immunology (Clin Exp Immunol) Vol. 156 Issue 2 Pg. 278-84 (May 2009) ISSN: 1365-2249 [Electronic] England
• PMID: 19250281 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• CX3C Chemokine Receptor 1
• Cx3cr1 protein, mouse
• Receptors, Chemokine

Topics

• Animals
• CX3C Chemokine Receptor 1
• Dendritic Cells (immunology)
• Disease Susceptibility
• Female
• Flow Cytometry
• Francisella tularensis
• Immunophenotyping
• Lung (immunology)
• Macrophages, Alveolar (immunology)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Models, Animal
• Mycobacterium tuberculosis
• Neutrophils (immunology)
• Receptors, Chemokine (deficiency, genetics)
• Tuberculosis, Pulmonary (metabolism)
• Tularemia (immunology, metabolism)