Role of type 1 fimbriae in the pathogenesis of ascending urinary tract infection induced by escherichia coli in mice

Iwahi, Tomoyuki; Abe, Yutaro; Nakao, Makoto; Imada, Akira; Tsuchiya, Kanji

doi:10.1128/iai.39.3.1307-1315.1983

Cited by 104 publications

(40 citation statements)

References 31 publications

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“…37,39 Attachment to and colonization of the mucosal surface of the GIT is aided by the presence of fimbriae, the most common being type 1 and type 3 fimbriae. 42 In addition, the KPF-28 fimbriae, has also been recognized to be involved in adhesion as demonstrated by in vitro experiments on human carcinoma and intestinal cell lines. 43 Apart from adhesion, the fimbriae is also involved in biofilm formation which increases the virulence of the bacteria by enabling the enclosure of bacteria within a dense polysaccharide matrix, thus shielding it from the host immune responses and digestive enzymes secreted within the GIT.…”

Section: Pathogenic Mechanisms and Virulence Factors Of K Pneumoniae Imentioning

confidence: 99%

Impact of Klebsiella pneumoniae in lower gastrointestinal tract diseases

Kaur

Vadivelu

Samudi

2018

J of Digest Diseases

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The 2016 Global Burden of Disease report by WHO revealed that diseases of the gastrointestinal tract (GIT) had one of the highest incidence rates worldwide. The plethora of factors that contribute to the development of GIT-related illnesses can be divided into genetic, environmental and lifestyle factors. Apart from that, the role that infectious agents play in the development of GIT diseases has piqued the interest of researchers worldwide. The human gut harbors approximately 10 bacteria in it with increasing concentration toward the lower GIT. Among the various microbiota that colonize the human gut, Gram-negative bacteria have been most notoriously linked to GIT-related diseases such as inflammatory bowel disease (IBD) including Crohn's disease and ulcerative colitis and colorectal cancer (CRC). Some of the notable culprits that have been attributed to these diseases are Bacteroides fragilis, Fusobacterium nucleatum, Escherichia coli and Helicobacter pylori. However, studies in recent years are beginning to recognize a new player, Klebsiella pneumoniae (K. pneumoniae) in the causation and progression of GIT diseases. Once synonymous with infections and diseases of the upper respiratory tract, K. pneumoniae has now emerged as one of the pathogens commonly isolated from patients with GIT diseases. However, extensive studies attributing K. pneumoniae to GIT diseases, particularly that of CRC are scanty. Therefore, this review intends to shed light on the association of K. pneumoniae in gastrointestinal diseases such as Crohn's disease, ulcerative colitis as well as CRC.

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Section: Pathogenic Mechanisms and Virulence Factors Of K Pneumoniae Imentioning

confidence: 99%

Impact of Klebsiella pneumoniae in lower gastrointestinal tract diseases

Kaur

Vadivelu

Samudi

2018

J of Digest Diseases

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“…1). Iwahi et al (1983) demonstrated that the binding of uropathogenic Escherichia coli to mouse bladder cells is mediated by type 1 fimbriae (10). Having established the presence of type 1 fimbriae on strain V and type 1 and type 3 fimbriae on strain A an investigation was carried out to determine their role in the adherence of S. enteritidis to the host epithelial cells.…”

Section: Ld50mentioning

confidence: 99%

Role of Type 1 and Type 3 Fimbriae on the Adherence and Pathogenesis of Salmonella enteritidis in Mice

Aslanzadeh

Paulissen

1992

Microbiology and Immunology

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Through hemagglutination tests two isogenic strains of Salmonella enteritidis were shown to possess type 1 fimbriae (strain V) and type 1 and type 3 fimbriae (strain A). The two strains bound to human buccal and mouse small intestine epithelial cells. Strain A attached to the epithelial cells more readily and in larger numbers in comparison to strain V. Adherence of both strains were sensitive to the presence of D-mannose and pretreatment of the epithelial cells with tannic acid did not promote D-mannose resistant type binding of strain A S. enteritidis to human buccal and mouse small intestine epithelial cells. Furthermore, results from LD50 study indicated that, when the tests were carried out through oral inoculation of the mice the highly fimbriated stain A appeared to be more virulent. However, when the tests were carried out through intraperitoneal inoculation strain V was more virulent. These results indicate that adherence is a major contributing factor to the virulence of S. enteritidis and both type 1 and type 3 fimbriae contribute to this phenomenon.

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“…In another approach, the infectivity of pairs of bacterial variants or phenotypes, only one of which expresses the type 1 fimbrial lectin, were examined. This approach was used in studies of gastrointestinal infection induced by S. typhimurium in mice [33], as well as of urinary tract infection induced by K. pneumoniae in rats [29] or by E. coli in mice [34]. In all cases, the infectivity of the fimbriated phenotype was several times higher than that of the non-fimbriated one.…”

Section: Initiation Of Infectionmentioning

confidence: 99%

Bacterial lectins, cell‐cell recognition and infectious disease

1987

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Numerous bacterial strains produce surface lectins, commonly in the form of fimbriae that are filamentous assemblies of protein subunits. Among the best characterized of these are the type 1 (mannose specific) fimbrial lectins of Escherichia coli that consist almost exclusively of one class of subunit with a molecular mass of 17 kDa. They possess an extended combining site corresponding to a trisaccharide and preferentially bind carbohydrate units of oligomannose or hybrid type. Type 1 fimbriae also possess a hydrophobic region close to the carbohydrate-binding site, since aromatic a-mannosides inhibit strongly (up to lOOO-times more than methyl a-mannoside) the agglutination of yeasts by the bacteria and the adherence of the latter to pig ileal epithelial cells. The combining sites of type 1 fimbriae of the salmonellae and of other enteric bacteria are different from those of E. coli in that they are smaller and do not possess a hydrophobic region. The various bacterial surface lectins appear to function primarily in the initiation of infection by mediating bacterial adherence to epithelial cells, e.g. in the urinary and gastrointestinal tracts. The mannose specific lectins also act as recognition molecules in lectinophagocytosis (i.e. phagocytosis of the bacteria in the absence of opsonins) by mouse, rat and human peritoneal macrophages, and human polymorphonuclear leukocytes. Affinity chromatography of membrane lysates from human polymorphonuclear leukocytes on immobilized type 1 fimbrial lectin, using methyl u-mannoside as eluent, showed that glycoproteins with apparent molecular masses of 7&80, 100 and 150 kDa act as receptors for the bacteria. Inhibition experiments with monoclonal antibodies suggest that the glycoprotein bands of 100 and 150 kDa may be identical with the a and /l subunits of leukocyte complement receptors and adhesion glycoproteins involved in complement-mediated opsonophagocytosis. The systems described serve as a fine illustration for the biological role of lectin-carbohydrate interactions. Further studies of these systems will lead to a deeper understanding of the molecular basis of infectious diseases, and perhaps also to new approaches for their prevention.

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Role of type 1 fimbriae in the pathogenesis of ascending urinary tract infection induced by escherichia coli in mice

Cited by 104 publications

References 31 publications

Impact of Klebsiella pneumoniae in lower gastrointestinal tract diseases

Impact of Klebsiella pneumoniae in lower gastrointestinal tract diseases

Role of Type 1 and Type 3 Fimbriae on the Adherence and Pathogenesis of Salmonella enteritidis in Mice

Bacterial lectins, cell‐cell recognition and infectious disease

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