Induction of protective immunity after escherichia coli bladder infection in primates. Dependence of the globoside-specific P-fimbrial tip adhesin and its cognate receptor.

Söderhäll, Mats; Normark, Staffan; Ishikawa, Kiyohito; Karlsson, Karl Anders; Teneberg, Susann; Winberg, Jan; Möllby, R.

doi:10.1172/jci119542

Cited by 25 publications

(10 citation statements)

References 40 publications

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“…In addition, the decrease in pIgR mRNA and protein did not depend on an intact TLR-4 signaling. One of the key roles of IgA previously described is the blocking of bacterial binding to epithelia, thereby interfering with the receptor:adhesin interaction (17). We propose a working hypothesis that P fimbriated E. coli associated with acute pyelonephritis evolved to exploit this system after binding and signal the host to decrease pIgR-mediated transport of IgA into the urine, therefore evading one of the key protective systems involved in the anti-adherence response.…”

Section: Regulation Of Pigr Rna and Protein Expression In The Kidney mentioning

confidence: 90%

“…Although the exact roles of S-IgA antibodies and free SC (FSC) in pyelonephritis have not been fully elucidated, several studies suggest that S-Ig are important in protecting the urinary tract mucosa. S-IgA excretion rates are elevated during acute pyelonephritis in normal patients (15), depressed in girls with recurrent UTI compared with normal girls (16), and associated with a protective immune response to P-fimbriated E. coli UTI in a primate model (17). However, the question of whether E. coli that express P fimbriae interact with renal epithelial cells and affect the local secretory antibody immune response have not been elucidated.…”

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confidence: 99%

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Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Rice¹,

Peng²,

Spence³

et al. 2005

Journal of the American Society of Nephrology

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P fimbriae are proteinaceous appendages on the surface of Escherichia coli bacteria that mediate adherence to uroepithelial cells. E. coli that express P fimbriae account for the majority of ascending urinary tract infections in women with normal urinary tracts. The hypothesis that P fimbriae on uropathic E. coli attach to renal epithelia and may regulate the immune response to establish infection was investigated. The polymeric Ig receptor (pIgR), produced by renal epithelia, transports IgA into the urinary space. Kidney pIgR and urine IgA levels were analyzed in a mouse model of ascending pyelonephritis, using E. coli with (P؉) and without (P؊) P fimbriae, to determine whether P(؉) E. coli regulate epithelial pIgR expression and IgA transport into the urine. (P؉) E. coli establish infection and persist to a greater amount than P(؊) E. coli. P(؉)-infected mice downregulate pIgR mRNA and protein levels compared with P(؊)-infected or PBS controls at >48 h. The decrease in pIgR was associated with decreased urinary IgA levels in the P(؉)-infected group at 48 h. pIgR mRNA and protein also decline in P(؉) E. coli-infected LPS-hyporesponsive mice. These studies identify a novel virulence mechanism of E. coli that express P fimbriae. It is proposed that P fimbriae decrease pIgR expression in the kidney and consequently decrease IgA transport into the urinary space. This may explain, in part, how E. coli that bear P fimbriae exploit the immune system of human hosts to establish ascending pyelonephritis. Escherichia coli that express P fimbriae are the most common cause for upper urinary tract infections (UTI) or pyelonephritis (1). The P fimbriae mediate adherence to uroepithelial cells by binding to the Gal␣(1 to 4)Gal disaccharide on the apical surface of renal epithelial cells, glomeruli, and endothelia (2). The expression of P fimbriae on E. coli is important in establishing pyelonephritis, as P fimbriae-specific antibodies prevent the adherence of bacteria to uroepithelial cells in vitro (3) and protect animals from ascending E. coli pyelonephritis in vivo (4). Although P fimbriae are not the sole virulence factor on uropathic E. coli, pyelonephritis with P(ϩ) E. coli strains are more often associated with kidney histopathology than P(Ϫ) E. coli (5). In addition to its role as an adhesin, E. coli that express P fimbriae may determine the pattern of the local immune response via interaction with its P-specific glycosphingolipid receptors present on uroepithelial cells (6) and/or by signaling via inflammatory cytokines (7).The secretions that protect the mucosal surface of renal epithelia contain an array of host defense factors, including secretory immunoglobulins, of which IgA is the major class. The polymeric Ig receptor (pIgR) is responsible for transporting these secretory immunoglobulins (S-Ig) in vesicles from the basolateral to the apical surface of epithelial cells (8 -10), including renal tubule cells. The extracellular portion of the pIgR, termed secretory component (SC), is cleaved at the apical surface ...

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Section: Regulation Of Pigr Rna and Protein Expression In The Kidney mentioning

confidence: 90%

mentioning

confidence: 99%

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Rice¹,

Peng²,

Spence³

et al. 2005

Journal of the American Society of Nephrology

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“…(f) The presence of acquired immunity (e.g. Soderhall et al, 1997;Frost et al, 2005) in rural populations is relevant to the comparison of risk of infection from bathing waters and PWS. This would be expected to reduce infection risk for people drinking private water but not for bathers -because the bathing cohort would have a higher proportion of children and city dwellers that are unlikely to have been exposed to E. coli O157 previously.…”

Section: Discussionmentioning

confidence: 99%

Microbial pollution of water by livestock: approaches to risk assessment and mitigation

Vinten¹,

Potts

Avery³

et al. 2009

Animal

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In this study, we investigate the extent to which the incidence of Escherichia coli O157:H7 can be predicted in human faeces, from human intake and infection via water contaminated by livestock and carrying this zoonotic pathogen in North-East (NE) and South-West (SW) regions of Scotland. In SW Scotland, there is a risk of coastal recreational waters failing EU standards for faecal indicator organisms, and this is assumed to be the main potential waterborne route of infection. In NE Scotland, the main waterborne route is assumed to be the many private drinking water supplies; these are mainly derived from shallow groundwater and surveys show that there is potential for significant levels of microbial contamination from livestock. The risk to human health from these sources has been assessed using a combination of process models, epidemiological risk-assessment methods and survey data. A key assumption in the calculations is the amount of mixing of pathogenic and non-pathogenic E. coli between animal faecal sources and contaminated water intake by humans. Using the probability distributions of the E. coli O157 content of individual faecal pat material (which would imply no mixing between source and human intake), based on three recent surveys of animal faeces in Scotland, led to predicted annual risks of infection slightly higher than observed human infection incidence. Using the geometric mean to represent partial mixing (which theoretically may over-or underestimate incidence with a concave dose-response curve) gave infection rates similar to those observed for two of the three faecal surveys. Using the arithmetic mean led to over-prediction of risk. This is to be expected if the true dose-response curve is (such as the Beta-Poisson curve used here) concave. Other factors that may lead to over-prediction of incidence are discussed, including under-reporting, loss of infectivity as a result of environmental exposure, immunity and the appropriateness of the Beta-Poisson curve. It is concluded that better epidemiological data for calibration of the dose-response curve, better knowledge of the degree of mixing and understanding of immunity are key requirements for progress in process model-based predictions of infection rate. The paper also explores the potential of improved farm and catchment scale management to deliver cost-effective mitigation of pollution of bathing and drinking water by livestock zoonoses.

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“…A high level of protection against P fimbriae has been developed too in a primate model (Soderhall et al, 1997). Molecular microbiology of bacterial pathogenesis and new technologies show favorable expectations concerning discoveries of new vaccines against bacterial infectious diseases (Moingeon et al, 2003;Sasakawa & Hacker, 2006;Westerlund-Wikström & Korhonen, 2005).…”

Section: Experiences Against Fimbrial Adhesionmentioning

confidence: 99%

Antiadhesive Effect of Plant Compounds in Bacteria

Guirado¹,

Barreto²

2012

Phytochemicals as Nutraceuticals - Global Approaches to Their Role in Nutrition and Health

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Induction of protective immunity after escherichia coli bladder infection in primates. Dependence of the globoside-specific P-fimbrial tip adhesin and its cognate receptor.

Cited by 25 publications

References 40 publications

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Microbial pollution of water by livestock: approaches to risk assessment and mitigation

Antiadhesive Effect of Plant Compounds in Bacteria

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