Differences in susceptibility of inbred and outbred infant mice to enterotoxigenic Escherichia coli of bovine, porcine and human origin

Duchet-Suchaux, Marion; Maitre, Christine L. Le; Bertin, Aline

doi:10.1099/00222615-31-3-185

Cited by 30 publications

(33 citation statements)

References 22 publications

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“…ETEC fimbria is host-specific (27,28,30), and we have also found that neither K99 ϩ nor CFA/I ϩ ETEC is able to infect adult mice (data not shown), presumably, because of the unavailability of host receptors on the murine intestinal epithelium, confirming what has been reported previously (11). Rather, the Salmonella vaccine vector has the ability to target host mucosal inductive sites, e.g., Peyer's patches (52), therefore enabling the vaccine to reach these sites.…”

supporting

confidence: 90%

“…Although a shift in the type of Th cells elicited as a consequence of K99 fimbrial expression, immune IgA and IgG anti-K99 fimbria antibodies were still produced. To assess whether these differences could impact protective immunity, a Duchet-Suchaux neonatal ETEC challenge model was employed (1,10,11). Groups of CD-1 female mice were orally immunized with one of the Salmonella-K99 constructs or with vector (strain H647) only; they were subsequently mated, and pups were allowed to come to parturition.…”

Section: Resultsmentioning

confidence: 99%

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Partially Assembled K99 Fimbriae Are Required for Protection

et al. 2005

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Antibodies to K99 fimbriae afford protection to F5؉ bovine enterotoxigenic Escherichia coli (ETEC). Previous studies show that murine dams immunized with Salmonella vaccine vectors stably expressing K99 fimbriae confer protection to ETEC-challenged neonatal pups. To begin to address adaptation of the K99 scaffold to display heterologous B-and T-cell epitopes, studies were conducted to determine how much of the assembled K99 fimbria is required to maintain protective immunity. Sequential deletions in the K99 gene clusters were made, resulting in diminished localization of the K99 fimbrial subunit in the outer membrane. As placement of the K99 fimbrial subunit became progressively contained within the vaccine vector, diminished immunoglobulin A (IgA) and IgG1 antibody titers, as well as diminished Th2-type cytokine responses, were observed in orally immunized mice. Deletion of fanGH, which greatly reduced the export of the fimbrial subunit to the outer membrane, showed only partial reduction in protective immunity. By contrast, deletion of fanDEFGH, which also reduced the export of the fimbrial subunit to the outer membrane but retained more subunit in the cytoplasm, resulted in protective immunity being dramatically reduced. Thus, these studies showed that retention of K99 fimbrial subunit as native fimbriae or with the deletion of fanGH is sufficient to confer protection.

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confidence: 90%

Section: Resultsmentioning

confidence: 99%

Partially Assembled K99 Fimbriae Are Required for Protection

et al. 2005

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“…One explanation for this phenomenon may be that the mice used in our experiments were genetically heterogenous outbred animals, making some variation in susceptibility to ETEC likely. Studies of infant mice have shown that there is considerable phenotypic variation with respect to susceptibility to ETEC or its toxins among different inbred strains of mice (3,17,18), indicating that host genetic factors may play a significant role in the acquisition of ETEC infections.…”

Section: Discussionmentioning

confidence: 99%

Importance of Heat-Labile Enterotoxin in Colonization of the Adult Mouse Small Intestine by Human EnterotoxigenicEscherichia coliStrains

Allen¹,

Randolph²,

2006

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Enterotoxigenic Escherichia coli (ETEC) infections are a significant cause of diarrheal disease and infant mortality in developing countries. Studies of ETEC pathogenesis relevant to vaccine development have been greatly hampered by the lack of a suitable small-animal model of infection with human ETEC strains. Here, we demonstrate that adult immunocompetent outbred mice can be effectively colonized with the prototypical human ETEC H10407 strain (colonization factor antigen I; heat-labile and heat-stable enterotoxin positive) and that production of heat-labile holotoxin provides a significant advantage in colonization of the small intestine in this model.Enterotoxigenic Escherichia coli (ETEC) infections are a significant cause of diarrheal disease worldwide. Infections caused by this heterogeneous group of pathogens remain major causes of diarrheal morbidity and infant mortality in developing countries (11,33,61), are perennially associated with disease in travelers (4, 7, 43) and in soldiers deployed to developing countries (8, 32), and have recently been associated with large outbreaks in developed countries, including the United States (1, 13).In the presently accepted paradigm for ETEC pathogenesis, fimbrial (or fibrillar) colonization factors (CFs) (10,22,27) mediate colonization of the small intestine, where organisms elaborate heat-labile enterotoxin (LT) and/or heat-stable enterotoxin (ST) (21, 68). Vaccine development has largely focused on the CFs; however, development of a broadly protective ETEC vaccine has been hampered due to the considerable heterogeneity of the known CFs (6,52,58,62).While a number of other surface antigens of ETEC have been described (20,25,51), their utility as potential vaccine candidates has not been effectively explored, largely due to the lack of a suitable animal model for testing. Animal models that have been used in previous studies of ETEC include infant (3, 16-18, 28, 47) and adult (9) mice, rats (34, 35), and rabbits (19,46,51). All of these models have inherent difficulties in utilization or require anesthesia and/or significant surgical manipulation. Some of the models have not been thoroughly evaluated.We sought to develop a murine model of small-intestinal colonization with human ETEC isolates using adult immunocompetent mice. Here, we report our initial use of this model using the prototypical human ETEC H10407 strain. Furthermore, similar to recent studies of porcine ETEC infection of gnotobiotic piglets (2), we demonstrate that elaboration of the heat-labile toxin provides a distinct advantage to the organism in establishing early colonization of the small-intestinal mucosa.

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“…Data obtained from infant mice, a model for K99-positive ETEC infection, indicate that differences in susceptibility depend on the parental murine strain, and suggest that resistance is inherited as a dominant trait (Duchet-Suchaux et al, 1990). In piglets, it has not been possible to get an insight into the transmission of susceptibility/resistance.…”

Section: Discussionmentioning

confidence: 99%

Adhesion of K99 fimbriated Escherichia coli to pig intestinal epithelium: correlation of adhesive and non-adhesive phenotypes with the sialoglycolipid content

Seignole¹,

Mouricout²,

Duval-Iflah

et al. 1991

Journal of General Microbiology

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Evidence for the existence of two phenotypes of piglets born to experimental herds was obtained based on the susceptibility of intestinal brush borders to adhesion of K99-positive Escherichia cofi. The enterocytes of the K99-receptive piglets displayed a characteristic sialoglycolipid pattern, with a higher content of the monosialoglycolipids I13NeuGc-LacCer (GM~Gc), IV3NeuGc-nLcOse4Cer (SPGGc) and IV3NeuAc-nLcOse4Cer (SPG) and the oligosialogangliosides IV3NeuAc,I13NeuAc-GgOse,Cer (GDla), I13(NeuAc),-GgOse,Cer (GD2), I13(NeuAc)z-GgOse4Cer (GD1 b) and IV3NeuAc,I13(NeuAc)2-GgOse4Cer (GTlb) when compared to the gangliosides of non-receptive piglets. The gangliosides from enterocytes of the non-receptive piglets were mainly the monosialogangliosides 113 NeuAc-GgOse,Cer (GM2) and I13NeuAc-LacCer (GM3), only traces of the other sialoglycolipids being detected. Adhesion of 4C-labelled K99-positive E. cofi cells to the piglet small intestinal sialoglycolipids, as tested by the thin-layer chromatogram overlay assay, revealed that the receptive enterocyte membrane was richer in glycolipids containing K99 receptor structures than the non-receptive enterocyte.Adhesion of K99-positive E. cofi correlated with the degree of sialylation of the brush border glycolipids.

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Differences in susceptibility of inbred and outbred infant mice to enterotoxigenic Escherichia coli of bovine, porcine and human origin

Cited by 30 publications

References 22 publications

Partially Assembled K99 Fimbriae Are Required for Protection

Partially Assembled K99 Fimbriae Are Required for Protection

Importance of Heat-Labile Enterotoxin in Colonization of the Adult Mouse Small Intestine by Human EnterotoxigenicEscherichia coliStrains

Adhesion of K99 fimbriated Escherichia coli to pig intestinal epithelium: correlation of adhesive and non-adhesive phenotypes with the sialoglycolipid content

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