Enhanced chemokine response in experimental acute<i>Escherichia coli</i>pyelonephritis in IL-1<i>β</i>-deficient mice

Hertting, Olof; Khalil, Adli; Jaremko, Georg; Chromek, Milan; Li, Y.-H.; Bakhiet, Moiz; Bartfai, Tamás; Tullus, Kjell; Brauner, Annelie

doi:10.1046/j.1365-2249.2003.02076.x

Cited by 37 publications

(38 citation statements)

References 42 publications

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“…The CCR2 ligand, MCP-1 (CCL-2), has been shown to be secreted in cystitis and pyelonephritis (2,12), suggesting a functional role in these infections. However, bacterial clearance from the bladders of infected CCR2-deficient mice was unchanged.…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance

Engel¹,

Dobrindt²,

Tittel³

et al. 2006

Infect Immun

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The role of dendritic cells (DC) in urinary tract infections (UTI) is unknown. These cells contribute directly to the innate defense against various viral and bacterial infections. Here, we studied their role in UTI using an experimental model induced by transurethral instillation of the uropathogenic Escherichia coli (UPEC) strain 536 into C57BL/6 mice. While few DC were found in the uninfected bladder, many had been recruited after 24 h, mostly to the submucosa and uroepithelium. They expressed markers of activation and maturation and exhibited the CD11b tumor necrosis factor alpha (TNF-␣)-and inducible nitric oxide synthase (iNOS)-producing CD11bINT DC (Tip-DC) were detected, which recently were proposed to be critical in the defense against bacterial infections. However, Tip-DC-deficient CCR2 ؊/؊ mice did not show reduced clearance of UPEC from the infected bladder. Moreover, clearance was also unimpaired in CD11c-DTR mice depleted of all DC by injection of diphtheria toxin. This may be explained by the abundance of granulocytes and of iNOS-and TNF-␣-producing non-DC that were able to replace Tip-DC functionality. These findings demonstrate that some of the abundant DC recruited in UTI contributed innate immune effector functions, which were, however, dispensable in the microenvironment of the bladder.

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Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance

Engel¹,

Dobrindt²,

Tittel³

et al. 2006

Infect Immun

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“…Moreover, there was a significant negative corre- lation between PC level and the degree of tissue pathology (r 2 ϭ Ϫ0.73, P Ͻ 0.001). During polymicrobial sepsis, chemokines including CXCL1 and CXCL2 show a progressive induction that is associated with ARF (10,11). Therefore, we examined the expression of both CXCL1 and CXCL2 in the kidneys of both sham and CLP rats.…”

Section: Endogenous Pc and Renal Pathologymentioning

confidence: 99%

Role of Protein C in Renal Dysfunction after Polymicrobial Sepsis

Gupta

Berg²,

Gerlitz³

et al. 2007

Journal of the American Society of Nephrology

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Protein C (PC) plays an important role in vascular function, and acquired deficiency during sepsis is associated with increased mortality in both animal models and in clinical studies. This study explored the consequences of PC suppression on the kidney in a cecal ligation and puncture model of polymicrobial sepsis. This study shows that a rapid drop in PC after sepsis is strongly associated with an increase in blood urea nitrogen, renal pathology, and expression of known markers of renal injury, including neutrophil gelatinase-associated lipocalin, CXCL1, and CXCL2. The endothelial PC receptor, which is required for the anti-inflammatory and antiapoptotic activity of activated PC (APC), was significantly increased after cecal ligation and puncture as well as in the microvasculature of human kidneys after injury. Treatment of septic animals with APC reduced blood urea nitrogen, renal pathology, and chemokine expression and dramatically reduced the induction of inducible nitric oxide synthase and caspase-3 activation in the kidney. The data demonstrate a clear link between acquired PC deficiency and renal dysfunction in sepsis and suggest a compensatory upregulation of the signaling receptor. Moreover, these data suggest that APC treatment may be effective in reducing inflammatory and apoptotic insult during sepsis-induced acute renal failure.

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“…Knowledge of the effects of cytokine regulation on the process of UTI has recently improved (1,2) and insights into the pathogenesis, genesis, and outcome of VUR and renal scarring also have been made (3). Many in vitro studies have shown that the expression of individual cytokines or cytokine receptors is influenced by polymorphic genotypes within regulatory regions, and that these polymorphic genotypes may play pivotal roles in the pathogenesis and progression of chronic renal diseases (4).…”

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confidence: 99%

Genetic Control of VEGF and TGF-β1 Gene Polymorphisms in Childhood Urinary Tract Infection and Vesicoureteral Reflux

et al. 2007

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ABSTRACT:We investigated whether genetic polymorphisms of vascular endothelial growth factor (VEGF) and transforming growth factor-␤1 (TGF-␤1), potential candidate genes in the pathogenesis of urinary tract infection (UTI) and vesicoureteral reflux (VUR), are associated with the susceptibility to UTI and VUR, and renal scarring. We recruited 89 controls and 86 UTI and 58 VUR children. The UTI group was subdivided into two groups according to renal scarring. Two polymorphisms of VEGF and three of TGF-␤1 genes were investigated by using PCR-restriction fragment length polymorphism analysis. In both UTI and VUR groups, there was an increase in frequency of the VEGF -460 CC (control, 4.3; UTI, 15.9; VUR, 17.8%; p Ͻ 0.05), TGF-␤1 -509 CC (control, 8.7; UTI, 34.6; VUR, 35.1%; p Ͻ 0.001), and TGF-␤1 -800 GG genotypes (control, 19.1; UTI, 40.5; VUR, 40.4%; p Ͻ 0.05). An increase in the TGF-␤1 ϩ869 CC (scar-positive, 35.4; scar-negative, 10.3%; p Ͻ 0.05) and a decrease in the ϩ869 TC genotype (scar-positive, 29.2; scarnegative, 55.2%; p Ͻ 0.05) were observed in the scar-positive subjects. There were no differences in ϩ405 VEGF genotype frequencies. The VEGF T-460C and the TGF-␤1 C-509T, G-800A, and T869C polymorphisms could be genetic markers of the process of UTI and VUR. (Pediatr Res 62: 183-187, 2007)

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Enhanced chemokine response in experimental acuteEscherichia colipyelonephritis in IL-1β-deficient mice

Cited by 37 publications

References 42 publications

Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance

Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance

Role of Protein C in Renal Dysfunction after Polymicrobial Sepsis

Genetic Control of VEGF and TGF-β1 Gene Polymorphisms in Childhood Urinary Tract Infection and Vesicoureteral Reflux

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