The chemokine receptor CXCR2 is differentially regulated on glial cellsin vivo but is not required for successful remyelination after cuprizone-induced demyelination

Glia ◽  
2008 ◽  
Vol 56 (10) ◽  
pp. 1104-1113 ◽  
Author(s):  
Maren Lindner ◽  
Corinna Trebst ◽  
Sandra Heine ◽  
Thomas Skripuletz ◽  
Paraskevi N. Koutsoudaki ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Chemokine Receptor Cxcr2

scholarly journals The role of CXC-chemokine receptor CXCR2 and suppressor of cytokine signaling-3 (SOCS-3) in renal cell carcinoma

BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Anastasios Stofas ◽  
Georgia Levidou ◽  
Christina Piperi ◽  
Christos Adamopoulos ◽  
Georgia Dalagiorgou ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Chemokine Receptor ◽  
Renal Cell ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Cxc Chemokine ◽  
Chemokine Receptor Cxcr2

048 High expression of ligands for chemokine receptor CXCR2 in Alveolar epithelial neoplasia induced by oncogenic Kras

2006 ◽  
Vol 23 (5) ◽  
pp. 535
Author(s):  
M. Wislez ◽  
F. Nobukazu ◽  
M. Burdick ◽  
I. Wistuba ◽  
R. Strieter ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
High Expression ◽  
Alveolar Epithelial ◽  
Chemokine Receptor Cxcr2

scholarly journals The Chemokine Receptor CXCR2 Controls Positioning of Oligodendrocyte Precursors in Developing Spinal Cord by Arresting Their Migration

Cell ◽  
2002 ◽  
Vol 110 (3) ◽  
pp. 373-383 ◽  
Author(s):  
Hui-Hsin Tsai ◽  
Emma Frost ◽  
Vivien To ◽  
Shenandoah Robinson ◽  
Charles ffrench-Constant ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Chemokine Receptor ◽  
Chemokine Receptor Cxcr2 ◽  
Oligodendrocyte Precursors ◽  
Developing Spinal Cord

scholarly journals Recruitment of Macrophages and Polymorphonuclear Leukocytes in Lyme Carditis

2006 ◽  
Vol 75 (2) ◽  
pp. 613-620 ◽  
Author(s):  
Ruth R. Montgomery ◽  
Carmen J. Booth ◽  
Xiaomei Wang ◽  
Victoria A. Blaho ◽  
Stephen E. Malawista ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Polymorphonuclear Leukocytes ◽  
Cellular Level ◽  
Lyme Arthritis ◽  
Compensatory Mechanisms ◽  
Lyme Carditis ◽  
Severe Arthritis ◽  
C3h Mice ◽  
Chemokine Receptor Cxcr2 ◽  
Organ Specific

ABSTRACT Lyme arthritis, caused by the spirochete Borrelia burgdorferi, can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring. A prominent difference between arthritis and carditis is the differential representation of phagocytes in these lesions: polymorphonuclear leukocytes (PMN) are more prevalent in the joint, and macrophages predominate in the heart lesion. We have previously shown differential efficiency of B. burgdorferi clearance by PMN and macrophages, and we now investigate whether these functional differences at the cellular level may contribute to the observed differences in organ-specific pathogenesis. When we infected mice lacking the neutrophil chemokine receptor (CXCR2−/− mice) with spirochetes, we detected fewer PMN in joints and less-severe arthritis. Here we have investigated the effects of the absence of the macrophage chemokine receptor CCR2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H/HeJ [C3H]) strains of mice. In B6 CCR2−/− mice, although inflammation in hearts is mild, we detected an increased burden of B. burgdorferi compared to that in wild-type (WT) mice, suggesting reduced clearance in the absence of macrophages. In contrast, C3H CCR2−/− mice have severe inflammation but a decreased B. burgdorferi burden compared to that in WT C3H mice both at peak disease and during resolution. Histopathologic examination of infected hearts revealed that infected C3H CCR2−/− animals have an increased presence of PMN, suggesting compensatory mechanisms of B. burgdorferi clearance in the hearts of infected C3H CCR2−/− mice. The more efficient clearance of B. burgdorferi from hearts by CCR2−/− versus WT C3H mice suggests a natural defect in the recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of this strain to B. burgdorferi infection.

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