CXCR3 and Its Ligands Participate in the Host Response to<i>Bordetella bronchiseptica</i>Infection of the Mouse Respiratory Tract but Are Not Required for Clearance of Bacteria from the Lung

Widney, Daniel P.; Hu, Yan; Foreman‐Wykert, Amy K.; Bui, Kevin; Nguyen, Tam; Liu, Bao; Gérard, Craig; Miller, Jeff F.; Smith, Jeffrey B.

doi:10.1128/iai.73.1.485-493.2005

Cited by 37 publications

(39 citation statements)

References 59 publications

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“…Previous investigations have shown that KC (3, 4), MIP-2 (5, 6), lungkine (7,8), and CXCL5 (9) are the most important chemokines to cause neutrophil accumulation in the murine lung. CXCL5 expression was also observed during pulmonary inflammation induced by gram-negative pathogens, Legionella pneumophila (22), Pseudomonas aeruginosa (23), Klebsiella pneumoniae (24), and Bordetella bronchoseptica (25). In the present study, we determined the cellular origin of CXCL5 in lung inflammation.…”

Section: Discussionmentioning

confidence: 81%

Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Jeyaseelan

Manzer

Young

et al. 2005

Am J Respir Cell Mol Biol

141

155

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Section: Discussionmentioning

confidence: 81%

Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Jeyaseelan

Manzer

Young

et al. 2005

Am J Respir Cell Mol Biol

141

155

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“…These mice have similar numbers of splenic NK cells at steady state ( [27][28][29], Fig. 6A and data not shown).…”

Section: Nk Cells Enter the Spleen Through The Marginal Zonementioning

confidence: 72%

Intrasplenic trafficking of natural killer cells is redirected by chemokines upon inflammation

et al. 2008

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The spleen is a major homing site for NK cells. How they traffic to and within this site in homeostatic or inflammatory conditions is, however, mostly unknown. Here we show that NK cells enter the spleen through the marginal sinus and home to the red pulp via a pertussis toxin-insensitive mechanism. Upon inflammation induced by poly(I:C) injection or mouse cytomegalovirus infection, many NK cells left the red pulp while others transiently entered the white pulp, predominantly the T cell area. This migration was dependent on both CXCR3 and CCL5, suggesting a synergy between CXCR3 and CCR5, and followed the path lined by fibroblastic reticular cells. Thus, the entry of NK cells in the white pulp is limited by the expression of pro-inflammatory chemokines. This phenomenon ensures the segregation of NK cells outside of the white pulp and might contribute to the control of immunopathology.Key words: Chemokines Á Migration Á Natural killer cells Á Spleen Supporting Information available online Introduction Natural killer (NK) cells are large granular lymphocytes involved in defense mechanisms against several types of microbial infections and tumors [1][2][3]. In particular in the mouse, NK cells play a critical role in the defense against mouse cytomegalovirus (MCMV) by eliminating infected cells through their cytotoxic activity [4] and by regulating the immune response through their crosstalk with dendritic cells [5,6]. Consistent with their role in immune surveillance, NK cells are widely distributed in the body. They are present in lymphoid organs as well as in non-lymphoid peripheral tissues [7]. At steady state, the spleen is the largest reservoir of mouse NK cells [8].The spleen has a complex architecture owing to its dual roles in the filtration of exhausted red blood cells and as a secondary lymphoid organ. Blood is supplied through arterioles that are FrontlineClaude GrØgoire et al. Eur. J. Immunol. 2008. 38: 2076-2084 We and others have previously reported that most NK cells are located in the red pulp area of the spleen with NK cells occasionally present in the white pulp [8,[16][17][18][19]. Moreover, previous reports have suggested that NK cell trafficking was modified in the case of inflammation [16,17], possibly by inflammatory chemokines that are known to act on NK cells [20]. However, the pattern of NK cell trafficking within the spleen is not known. In particular, the route of entry, the migration tracts, and the guidance signals that allow NK cells to enter or leave the red pulp are all issues that need to be addressed.We recently described that the cell surface expression of the activating NK cell receptor NKp46 (CD336) defines NK cells across mammalian species and that staining for NKp46 enables the unambiguous in situ visualization of NK cells in tissue sections [19]. We took advantage of this tool to analyze NK cell trafficking under steady-state and inflammatory conditions. Results NK cells enter the spleen through the marginal zoneWe sought to determine how NK cells enter the spleen and reac...

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“…This peak on day 7 after infection correlated with the beginning of reduced colonization of the lower respiratory tract by the TTSS mutant. A recent report by Widney et al (32) showed that the production of IFN-␥ in the lungs of mice infected with B. bronchiseptica peaked 2 days after infection and was not associated with reduced bacterial load. Together with our data, this suggests that that the production of systemic, and not local, IFN-␥ is important for bacterial clearance.…”

Section: Discussionmentioning

confidence: 98%

Bordetella Type III Secretion Modulates Dendritic Cell Migration Resulting in Immunosuppression and Bacterial Persistence

Skinner

Pilione

Shen

et al. 2005

The Journal of Immunology

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Chronic bacterial infection reflects a balance between the host immune response and bacterial factors that promote colonization and immune evasion. Bordetella bronchiseptica uses a type III secretion system (TTSS) to persist in the lower respiratory tract of mice. We hypothesize that colonization is facilitated by bacteria-driven modulation of dendritic cells (DCs), which leads to an immunosuppressive adaptive host response. Migration of DCs to the draining lymph nodes of the respiratory tract was significantly increased in mice infected with wild-type B. bronchiseptica compared with mice infected with TTSS mutant bacteria. Reduced colonization by TTSS-deficient bacteria was evident by 7 days after infection, whereas colonization by wild-type bacteria remained high. This decrease in colonization correlated with peak IFN-γ production by restimulated splenocytes from infected animals. Wild-type bacteria also elicited peak IFN-γ production on day 7, but the quantity was significantly lower than that elicited by TTSS mutant bacteria. Additionally, wild-type bacteria elicited higher levels of the immunosuppressive cytokine IL-10 compared with the TTSS mutant bacteria. B. bronchiseptica colonization in IL-10−/− mice was significantly reduced compared with infections in wild-type mice. These findings suggest that B. bronchiseptica use the TTSS to rapidly drive respiratory DCs to secondary lymphoid tissues where these APCs stimulate an immunosuppressive response characterized by increased IL-10 and decreased IFN-γ production that favors bacterial persistence.

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CXCR3 and Its Ligands Participate in the Host Response toBordetella bronchisepticaInfection of the Mouse Respiratory Tract but Are Not Required for Clearance of Bacteria from the Lung

Cited by 37 publications

References 59 publications

Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Intrasplenic trafficking of natural killer cells is redirected by chemokines upon inflammation

Bordetella Type III Secretion Modulates Dendritic Cell Migration Resulting in Immunosuppression and Bacterial Persistence

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