[HTML][HTML] Toll-like receptor-4: renal cells and bone marrow cells signal for neutrophil recruitment during pyelonephritis

PS Patole, S Schubert, K Hildinger, S Khandoga… - Kidney international, 2005 - Elsevier
PS Patole, S Schubert, K Hildinger, S Khandoga, A Khandoga, S Segerer, A Henger…
Kidney international, 2005Elsevier
Toll-like receptor-4: Renal cells and bone marrow cells signal for neutrophil recruitment
during pyelonephritis. Background The molecular mechanisms of pathogen recognition that
initiate infective pyelonephritis are poorly understood. Toll-like receptor-4 (TLR4) mutant
mice infected with uropathogenicEscherichia coli lack renal CXCL2 mRNA expression,
subsequent neutrophil recruitment, and renal abscess formation. Methods We used a bone
marrow transplant approach in order to investigate the contribution of TLR4 in intrinsic renal …
Toll-like receptor-4: Renal cells and bone marrow cells signal for neutrophil recruitment during pyelonephritis.
Background
The molecular mechanisms of pathogen recognition that initiate infective pyelonephritis are poorly understood. Toll-like receptor-4 (TLR4) mutant mice infected with uropathogenicEscherichia coli lack renal CXCL2 mRNA expression, subsequent neutrophil recruitment, and renal abscess formation.
Methods
We used a bone marrow transplant approach in order to investigate the contribution of TLR4 in intrinsic renal cells or bone-marrow-derived immune cells to neutrophil recruitment during infective pyelonephritis.
Results
Both chimera either expressing mutanttlr4 in intrinsic renal cells and wild-typetlr4 in bone marrow-derived cells or vice versa showed an impaired response to uropathogenicE. coli infection in terms of leukocyturia and renal abscess formation when compared totlr4 wild-type mice with congenic bone marrow transplants.
Conclusion
These data suggest that TLR4 is required on both intrinsic renal cells (e.g., tubular epithelial cells) and bone marrow-derived immune cells for the control of ascending uropathogenicE. coli infection by initiating chemokine-driven renal neutrophil recruitment.
Elsevier