Relationship between Susceptibility to Hemolytic-Uremic Syndrome and Levels of Globotriaosylceramide in Human Sera

Watarai, Shinobu; Yokota, Kenji; Tana,; Kishimoto, Takumi; Kanadani, Tomohosa; Taketa, Kazuhisa; Oguma, Keiji

doi:10.1128/jcm.39.2.798-800.2001

Cited by 8 publications

(3 citation statements)

References 14 publications

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“…Some authors also reported that female sex [108] and a higher socio-economic status [109] are associated with a higher risk of developing STEC-related disease. Genetic factors, like erythrocyte and serum Gb3 level [110,111] or presence of the platelet glycoprotein 1b alpha 145M allele [112], could also influence the susceptibility to HUS.…”

Section: Propensity To Develop Stec-husmentioning

confidence: 99%

Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

Joseph

Cointe

Kurkdjian

et al. 2020

Toxins

160

132

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The severity of human infection by one of the many Shiga toxin-producing Escherichia coli (STEC) is determined by a number of factors: the bacterial genome, the capacity of human societies to prevent foodborne epidemics, the medical condition of infected patients (in particular their hydration status, often compromised by severe diarrhea), and by our capacity to devise new therapeutic approaches, most specifically to combat the bacterial virulence factors, as opposed to our current strategies that essentially aim to palliate organ deficiencies. The last major outbreak in 2011 in Germany, which killed more than 50 people in Europe, was evidence that an effective treatment was still lacking. Herein, we review the current knowledge of STEC virulence, how societies organize the prevention of human disease, and how physicians treat (and, hopefully, will treat) its potentially fatal complications. In particular, we focus on STEC-induced hemolytic and uremic syndrome (HUS), where the intrusion of toxins inside endothelial cells results in massive cell death, activation of the coagulation within capillaries, and eventually organ failure.

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Section: Propensity To Develop Stec-husmentioning

confidence: 99%

Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

Joseph

Cointe

Kurkdjian

et al. 2020

Toxins

160

132

View full text Add to dashboard Cite

show abstract

“…91 It has also been shown that patients with HUS have lower levels of P k glycolipid in their sera compared with a healthy control group. 92 These authors propose that circulating Stx could bind to P k glycolipids in sera during infection, which may reduce the amount of Stx binding to the target cells. Consequently, patients with low serum levels of P k would have a higher susceptibility to EHEC infections.…”

Section: Bacteriamentioning

confidence: 99%

P1PK: The blood group system that changed its name and expanded

et al. 2013

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The antigens in the P1PK blood group system are carried on glycosphingolipids. The system currently includes three different antigens, P1, Pk, and NOR. The P1 antigen was disovered in 1927 by Landsteiner and Levine, and Pkand NOR were described in 1951 and 1982, respectively. As in the ABO system, naturally occurring antibodies of the immunoglobulin (Ig) M or IgG class, against the missing carbohydrate structures, can be present in the sera of people lacking the corresponding antigen. Anti-P1 is generally a weak and cold-reactive antibody not implicated in hemolytic transfusion reaction (HTR) or hemolytic disease of the fetus and newborn while Pkantibodies can cause HTR, and anti-NOR is regarded as a polyagglutinin. A higher frequency of miscarriage is seen in women with the rare phenotypes p, P1 k, and P2 k. Furthermore, the Pkand P1 antigens have wide tissue distributions and can act as host receptors for various pathogens and toxins. Why p individuals lack not only Pkand P expression but also P1 has been a longstanding enigma. Recently, it was shown that the same A4GALT-encoded galactosyltransferase synthesizes both the P1 and Pkantigens and that a polymorphism in a new exon in this gene predicts the P1and P2phenotypes. Immunohematology 2013;29:25–33.

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“…It possesses large pores and provides a large surface area and, hence, favorable prerequisites for the absorption of distinct molecules providing harm to the vertebrate host. AC has long been used as an antidote for the treatment of intoxications [22] and of infectious enteritis caused by Escherichia coli, Vibrio cholerae, and Cryptosporidium species [22][23][24][25]. In clinical studies, AC was shown to mitigate diarrhea caused by antibiotic and chemotherapeutic agents [26][27][28] and to alleviate symptoms of patients diagnosed with irritable bowel syndrome [29,30].…”

Section: Introductionmentioning

confidence: 99%

Prophylactic Oral Application of Activated Charcoal Mitigates Acute Campylobacteriosis in Human Gut Microbiota-Associated IL-10−/− Mice

Heimesaat,

Schabbel,

Langfeld

et al. 2024

Biomolecules

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The incidence of human Campylobacter jejuni infections is increasing worldwide. It is highly desirable to prevent campylobacteriosis in individuals at risk for severe disease with antibiotics-independent non-toxic compounds. Activated charcoal (AC) has long been used as an anti-diarrheal remedy. Here, we tested the disease-mitigating effects of oral AC versus placebo in human gut microbiota-associated (hma) IL-10−/− mice starting a week prior to C. jejuni infection. On day 6 post-infection, the gastrointestinal C. jejuni loads were comparable in both infected cohorts, whereas campylobacteriosis symptoms such as wasting and bloody diarrhea were mitigated upon AC prophylaxis. Furthermore, AC application resulted in less pronounced C. jejuni-induced colonic epithelial cell apoptosis and in dampened innate and adaptive immune cell responses in the colon that were accompanied by basal concentrations of pro-inflammatory mediators including IL-6, TNF-α, IFN-γ, and nitric oxide measured in colonic explants from AC treated mice on day 6 post-infection. Furthermore, C. jejuni infection resulted in distinct fecal microbiota shift towards higher enterobacterial numbers and lower loads of obligate anaerobic species in hma mice that were AC-independent. In conclusion, our pre-clinical placebo-controlled intervention study provides evidence that prophylactic oral AC application mitigates acute murine campylobacteriosis.

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Relationship between Susceptibility to Hemolytic-Uremic Syndrome and Levels of Globotriaosylceramide in Human Sera

Cited by 8 publications

References 14 publications

Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

P1PK: The blood group system that changed its name and expanded

Prophylactic Oral Application of Activated Charcoal Mitigates Acute Campylobacteriosis in Human Gut Microbiota-Associated IL-10−/− Mice

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