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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Am+Soc+Nephrol
2016 ; 27
(3
): 792-803
Nephropedia Template TP
gab.com Text
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English Wikipedia
Ly6Chigh Monocytes Protect against Kidney Damage during Sepsis via a
CX3CR1-Dependent Adhesion Mechanism
#MMPMID26160897
Chousterman BG
; Boissonnas A
; Poupel L
; Baudesson de Chanville C
; Adam J
; Tabibzadeh N
; Licata F
; Lukaszewicz AC
; Lombès A
; Deterre P
; Payen D
; Combadière C
J Am Soc Nephrol
2016[Mar]; 27
(3
): 792-803
PMID26160897
show ga
Monocytes have a crucial role in both proinflammatory and anti-inflammatory
phenomena occurring during sepsis. Monocyte recruitment and activation are
orchestrated by the chemokine receptors CX3CR1 and CCR2 and their cognate
ligands. However, little is known about the roles of these cells and chemokines
during the acute phase of inflammation in sepsis. Using intravital microscopy in
a murine model of polymicrobial sepsis, we showed that inflammatory Ly6C(high)
monocytes infiltrated kidneys, exhibited altered motility, and adhered strongly
to the renal vascular wall in a chemokine receptor CX3CR1-dependent manner.
Adoptive transfer of Cx3cr1-proficient monocyte-enriched bone marrow cells into
septic Cx3cr1-depleted mice prevented kidney damage and promoted mouse survival.
Modulation of CX3CR1 activation in septic mice controlled monocyte adhesion,
regulated proinflammatory and anti-inflammatory cytokine expression, and was
associated with the extent of kidney lesions such that the number of lesions
decreased when CX3CR1 activity increased. Consistent with these results, the
pro-adhesive I249 CX3CR1 allele in humans was associated with a lower incidence
of AKI in patients with sepsis. These data show that inflammatory monocytes have
a protective effect during sepsis via a CX3CR1-dependent adhesion mechanism. This
receptor might be a new therapeutic target for kidney injury during sepsis.
|*Cell Adhesion/genetics
[MESH]
|Acute Kidney Injury/etiology/pathology/*prevention & control
[MESH]