Circulating Granulocyte Colony-Stimulating Factor, C-X-C, and C-C Chemokines in Children with Escherichia Coli O157:H7 Associated Hemolytic Uremic Syndrome

Proulx, Francesca

doi:10.1203/01.pdr.0000034233.75228.0b

Cited by 7 publications

(4 citation statements)

References 12 publications

(15 reference statements)

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“…However, it also leaks into the circulation and it can be detected in the serum of normal individuals at very low levels, and at increased levels in patients with infections. [27][28][29][30] Systemic effects include inhibition of proliferation of haematopoietic stem cells, 31 and a non-aggregating variant of MIP-1a has been tested in patients for its ability to protect stem cells during chemotherapy. 32 It also mobilises dendritic cell precursors and haematopoietic stem cells into the circulation.…”

Section: Discussionmentioning

confidence: 99%

Systemic administration of the chemokine macrophage inflammatory protein 1 exacerbates inflammatory bowel disease in a mouse model

Pender

Chance²,

Whiting³

et al. 2005

Gut

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Introduction: Exacerbations of inflammatory bowel disease are thought to be related to concurrent infections. As infections are associated with elevated local and serum concentrations of chemokines, we have determined whether systemic administration of the CC chemokine macrophage inflammatory protein 1a (MIP-1a) exacerbates colitis in a mouse model. Methods: Colitis was induced in Balb/c mice using trinitrobenzene sulfonic acid (TNBS). Starting four days later, animals received daily intraperitoneal injections of recombinant MIP-1a. On day 7, mice were killed and pieces of colon taken for immunohistology and polymerase chain reaction analysis. The direct effects of MIP-1a on mucosal T cells and fibroblasts in vitro were also investigated. Results: Systemic administration of MIP-1a markedly enhanced colitis with mice developing large transmural ulcers filled with granulation tissue. Treatment resulted in increased numbers of CD4 cells infiltrating the colonic lamina propria, increased interferon c (IFN-c) levels, and increased transcripts for tumour necrosis factor a (TNF-a) and matrix metalloproteinase 3 (MMP3). Isolated lamina propria lymphocytes from mice with TNBS colitis contained increased numbers of IFN-c and TNF-a transcripts when stimulated with MIP-1a in vitro. Colonic lamina propria fibroblasts also responded to MIP-1a with increased proliferation and decreased collagen 1 synthesis but fibroblast proliferation was not seen in vivo. Conclusions: These experiments show that increasing serum concentrations of a chemokine, MIP-1a, exacerbates immune mediated colitis. The effect seems to be due to the ability of MIP-1a to boost Th1 responses in the gut wall. Our findings also suggest a potential pathway by which peripheral infections can exacerbate inflammatory bowel disease.

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Section: Discussionmentioning

confidence: 99%

Systemic administration of the chemokine macrophage inflammatory protein 1 exacerbates inflammatory bowel disease in a mouse model

Pender

Chance²,

Whiting³

et al. 2005

Gut

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“…Various laboratory parameters associated with inflammatory responses have been examined as indicators of EHEC‐induced HUS severity, including the number of white blood cells, decreases in serum sodium and total protein, and increased serum alanine aminotransferase . Recent reports have also highlighted the potential applications of various cytokines and chemokines as biomarkers of disease activity in EHEC‐induced HUS (Table ).…”

Section: Clinical Application Of Serum Cytokine Profiles In Hemolyticmentioning

confidence: 99%

“…Various laboratory parameters associated with inflammatory responses have been examined as indicators of EHEC-induced HUS severity, including the number of white blood cells, decreases in serum sodium and total protein, and increased serum alanine aminotransferase. 62,63 Recent reports have also highlighted the potential applications of various cytokines and chemokines as biomarkers of disease activity in EHEC-induced HUS [5][6][7][8][9][10][11][12][13][14][15][16][17][18]61,[64][65][66] (Table 2). TNF, tumor necrosis factor; sTNFR, soluble tumor necrosis factor receptor; IL, interleukin; sST2, soluble ST2; SDF, stromal cell-derived factor; G-CSF, granulocyte-colony stimulating factor; CXCL, C-X-C motif chemokine ligand.…”

Section: Clinical Application Of Serum Cytokine Profiles In Hemolyticmentioning

confidence: 99%

Pathogenic functions and diagnostic utility of cytokines/chemokines in EHEC‐HUS

Shimizu

2020

Pediatrics International

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Hemolytic − uremic syndrome (HUS) is a severe complication of infection by Shiga toxin (STx)‐producing enterohemorrhagic Escherichia coli. Hemolytic − uremic syndrome is defined clinically as a triad of non‐immune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injuries. Neurologic complications such as acute encephalopathy are also observed. In humans, endothelial cells, proximal tubular epithelial cells, mesangial cells, podocytes, intestinal epithelial cells, and monocytes / macrophages are susceptible to STx‐mediated injury. Shiga toxin induces the secretion of inflammatory cytokines and chemokines from susceptible cells, including tumor necrosis factor‐α interleukin (IL)‐1, IL‐6, and IL‐8. These cytokines and chemokines contribute to the pathogenesis of HUS and encephalopathy by enhancing STx‐induced cytotoxicity and inducing inflammatory cell infiltration. Serum cytokine/chemokine levels are therefore useful as indicators of disease activity and predictors of progression from acute kidney injury to chronic kidney disease. Anti‐inflammation therapy combined with apheresis to remove excessive cytokines / chemokines and methylprednisolone pulse therapy to suppress cytokine/chemokine production may be an effective treatment regimen for severe E. coli‐associated HUS. However, this regimen requires careful monitoring of potential side effects, such as infections, thrombus formation, and hypertension.

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“…Thus, multiple cell types may release potent inflammatory mediators and enzymes. Furthermore, cytokines, chemokines, soluble adhesion molecules, growth factors, cytokine receptors and acute-phase response proteins are elevated in EHEC-associated HUS patients [78,[119][120][121][122][123][124][125][126][127][128][129][130] and may contribute to the progression of renal damage particularly as elevated cytokine levels have been demonstrated in the urine of patients with HUS [121]. The chemokine receptor CXCR4/CXCR7/stromal cell-derived factor 1 pathway is also activated in vivo, and in vitro by Shiga toxin, thus also contributing to renal damage [131].…”

Section: Renal Failurementioning

confidence: 99%

Haemolytic uraemic syndrome

et al. 2016

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Abstract. Karpman D, Loos S, Tati R, Arvidsson I (Clinical Sciences Lund, Lund University, Lund, Sweden). Haemolytic uraemic syndrome (Review). J Intern Med 2017; 281: 123-148.Haemolytic uraemic syndrome (HUS) is defined by the simultaneous occurrence of nonimmune haemolytic anaemia, thrombocytopenia and acute renal failure. This leads to the pathological lesion termed thrombotic microangiopathy, which mainly affects the kidney, as well as other organs. HUS is associated with endothelial cell injury and platelet activation, although the underlying cause may differ. Most cases of HUS are associated with gastrointestinal infection with Shiga toxin-producing enterohaemorrhagic Escherichia coli (EHEC) strains. Atypical HUS (aHUS) is associated with complement dysregulation due to mutations or autoantibodies. In this review, we will describe the causes of HUS. In addition, we will review the clinical, pathological, haematological and biochemical features, epidemiology and pathogenetic mechanisms as well as the biochemical, microbiological, immunological and genetic investigations leading to diagnosis. Understanding the underlying mechanisms of the different subtypes of HUS enables tailoring of appropriate treatment and management. To date, there is no specific treatment for EHEC-associated HUS but patients benefit from supportive care, whereas patients with aHUS are effectively treated with anti-C5 antibody to prevent recurrences, both before and after renal transplantation.

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Circulating Granulocyte Colony-Stimulating Factor, C-X-C, and C-C Chemokines in Children with Escherichia Coli O157:H7 Associated Hemolytic Uremic Syndrome

Cited by 7 publications

References 12 publications

Systemic administration of the chemokine macrophage inflammatory protein 1 exacerbates inflammatory bowel disease in a mouse model

Systemic administration of the chemokine macrophage inflammatory protein 1 exacerbates inflammatory bowel disease in a mouse model

Pathogenic functions and diagnostic utility of cytokines/chemokines in EHEC‐HUS

Haemolytic uraemic syndrome

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