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2016 ; 11
(5
): e0156084
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Cytokine and Chemokine Expression in Kidneys during Chronic Leptospirosis in
Reservoir and Susceptible Animal Models
#MMPMID27219334
Matsui M
; Roche L
; Geroult S
; Soupé-Gilbert ME
; Monchy D
; Huerre M
; Goarant C
PLoS One
2016[]; 11
(5
): e0156084
PMID27219334
show ga
Leptospirosis is caused by pathogenic spirochetes of the genus Leptospira. Humans
can be infected after exposure to contaminated urine of reservoir animals,
usually rodents, regarded as typical asymptomatic carriers of leptospires. In
contrast, accidental hosts may present an acute form of leptospirosis with a
range of clinical symptoms including the development of Acute Kidney Injury
(AKI). Chronic Kidney Disease (CKD) is considered as a possible AKI-residual
sequela but little is known about the renal pathophysiology consequent to
leptospirosis infection. Herein, we studied the renal morphological alterations
in relation with the regulation of inflammatory cytokines and chemokines,
comparing two experimental models of chronic leptospirosis, the golden Syrian
hamster that survived the infection, becoming carrier of virulent leptospires,
and the OF1 mouse, a usual reservoir of the bacteria. Animals were monitored
until 28 days after injection with a virulent L. borgpetersenii serogroup Ballum
to assess chronic infection. Hamsters developed morphological alterations in the
kidneys with tubulointerstitial nephritis and fibrosis. Grading of lesions
revealed higher scores in hamsters compared to the slight alterations observed in
the mouse kidneys, irrespective of the bacterial load. Interestingly,
pro-fibrotic TGF-? was downregulated in mouse kidneys. Moreover, cytokines IL-1?
and IL-10, and chemokines MIP-1?/CCL3 and IP-10/CXCL-10 were significantly
upregulated in hamster kidneys compared to mice. These results suggest a possible
maintenance of inflammatory processes in the hamster kidneys with the
infiltration of inflammatory cells in response to bacterial carriage, resulting
in alterations of renal tissues. In contrast, lower expression levels in mouse
kidneys indicated a better regulation of the inflammatory response and possible
resolution processes likely related to resistance mechanisms.