Bacterial adhesiveness and the gut.
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Adhesiveness↗
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Quantitative assessment of bacterial adhesion to eukaryotic cells of human origin.
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Bacteriological Techniques↗
Colloidal phenomena encountered in the bacterial adhesion to the tooth surface.
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Adhesiveness↗
Factors affecting adhesion of bacterial to a tooth in vitro.
The initial adhesion of oral bacteria to a tooth in vitro was examined. The organisms were grown in broth with and without sucrose, and suspensions made either in broth or a modified Ringer's solution. The tooth used was either dry or coated with natural or synthetic saliva. Adhesion was determined by counting organisms removed from the tooth surface by simple washing or by sonication. It was found that the firmest bonding occurred when a dry tooth was immersed in a suspension of bacteria in Ringer's solution; the prior growth of the organisms in the presence of sucrose did not affect adhesion. It was concluded that instantaneous irreversible adhesion of bacteria to a tooth occurs without the need for active metabolism, and that this process is inhibited by the presence of competing organic substances which probably produce a surface-conditioning film.
Corynebacterium↗
Adhesive properties of Vibrio cholerae: nature of the interaction with intact mucosal surfaces.
Two companion papers in this series have characterized the interaction between Vibrio cholerae and the surfaces of eukaryotic cells. The present paper reports studies of the association between vibrios or Salmonella enteritidis and intact slices of intestinal tissue. A significant number of differences were noted in the characteristics of bacterial adhesion in these systems. The results are interpreted to indicate the presence of at least two receptors for vibrio adhesion on the mucosal surface of the rabbit small intestine. The receptor mediating the adhesion of salmonella appeared to be distinct from these. A primary role for bacterial motility in the process of adhesion of vibrios to mucosal surfaces could not be demonstrated in the assay systems studied. Rather, loss of motility in mutant vibrios appeared to be correlated with the simultaneous loss of adhesive factors (adhesins) from the bacterial surface. The inhibition of vibrio adhesion to slices of intestinal tissues by antibody to the heat-stable antigens of V. cholerae occurred in the absence of bacterial agglutination. Agglutination in this assay system appeared to be an artifact in that it could be observed only in experiments where extremely high concentrations of vibrios were used. We speculate that such high vibrio concentrations are not likely to be present in humans at the time of infection and that agglutination in the lumen of the intestine might therefore play only a minor role in prophylactic immunity against natural cholera and other enteric infections of humans.
Agglutination↗
[The role of anaerobe adhesion in the colonization of the vaginal mucosa].
Some our previous research works on bacterial adhesion to vaginal cells in the different phases of the menstruum showed that adhesion changes depending on changing environmental conditions. We therefore considered interesting to extend our investigations to anaerobic flora, in the light of recent observations intended to attribute an important role to anaerobic flora in the pathogenesis of vaginitis. The results obtained so far indicate that the maximum adhesion capability is found in the middle of the menstruum. The very low adhesion of bacteria belonging to the Leptothrix genus remains substantially unaltered throughout the menstruum. Low adhesion is also found in sporogenic bacteria, whereas the coccoid ones have a stronger adhesion, particularly about the middle of the menstruum. With lower pH values adhesion of the anaerobic flora is enhanced, whereas in the final phase of the menstruum, with higher pH values, adhesion is reduced. Competition tests evidence a stronger adhesion of coccoid as compared to bacillar types.
Adult↗
Effects of subminimal inhibitory concentrations of ampicillin, chloramphenicol, and nitrofurantoin on the attachment of Escherichia coli to human uroepithelial cells in vitro.
An in vitro system with epithelial cells of the human urinary tract and Escherichia coli isolated from the urine of pateints with acute pyelonephritis was used for tests of the effect of antibacterial agents on bacterial adhesion. E. coli treated with subminimal inhibitory amounts of ampicillin attached less than untreated control bacteria. Subminimal inhibitory amounts of chloramphenicol and nitrofurantoin had no effect on adhesion of the 15 strains of E. coli tested. The combination of bacterial pretreatment with ampicillin and addition of antibodies to the adhesion test tube decreased adhesion more than did either treatment separately.
Adhesiveness↗
Molecular epidemiology of levofloxacin-resistant Klebsiella pneumoniae and the association of plasmid-mediated quinolone resistance genes with key biological phenotypes.
UNLABELLED: Klebsiella pneumoniae is a major opportunistic pathogen in China, yet the molecular epidemiology of quinolone resistance remains poorly characterized. This study analyzed 2,433 clinical isolates from 37 Chinese hospitals (2018-2022). The overall levofloxacin-non-susceptible (NS) rate was 53.60%, with urinary tract isolates showing higher resistance. Whole-genome sequencing identified 12 plasmid-mediated quinolone resistance (PMQR) genes. Among 1,304 NS strains, 74.54% carried at least one PMQR gene (mainly qnrS, qnrB, and aac(6')-Ib-cr), and 60.20% also had quinolone resistance-determining region (QRDR) mutations. Functional studies revealed diverse phenotypic impacts. Most PMQR genes conferred low-level resistance (minimum inhibitory concentration [MIC] = 1 mg/L), while qnrB52 and qnrB91 caused high-level resistance (MIC = 8-16 mg/L). Notably, qnrB91 reduced biofilm formation, indicating a trade-off between resistance and colonization. Growth assays showed that qnrB52, qnrB91, and qnrS1 inhibited normal growth, whereas qepA1 and qnrS1 enhanced growth under ethanol stress. Most PMQR genes (except qnrB6) attenuated bacterial adhesion. qepA1 promoted intracellular survival in macrophages, suggesting a role in chronic infection. Animal models confirmed that qnrB6, qnrB7, qnrVC6, and aac(6')-Ib-cr significantly enhanced virulence. This study is the first in China to report qnrVC6 and novel gyrA mutations (Ser83Ala/Val, Asp87Phe/His) in K. pneumoniae. It systematically reveals how PMQR genes influence infection by modulating resistance, immune evasion, and pathogenicity. These findings highlight that PMQR genes contribute not only to antibiotic resistance but also to virulence, suggesting that treatment strategies should consider specific PMQR genotypes. This research provides the largest-scale molecular epidemiological data and a theoretical basis for controlling quinolone-resistant K. pneumoniae in China. IMPORTANCE: Quinolone-resistant Klebsiella pneumoniae poses a serious threat to public health, yet the role of plasmid-mediated quinolone resistance (PMQR) genes beyond antibiotic resistance remains underexplored. In this largest-scale multicenter study in China, we analyzed 2,433 clinical isolates and discovered that PMQR genes do more than just confer drug resistance-they also influence bacterial growth, stress survival, biofilm formation, and the ability to evade or persist within host immune cells. Some PMQR genes even enhance virulence in an animal model. These findings challenge the traditional view of resistance genes as mere contributors to drug failure, revealing that they can also shape infection outcomes by altering bacterial behavior. Understanding these dual roles may guide more precise treatment strategies targeting specific PMQR genotypes.
Klebsiella pneumoniae↗
Mucosal adherence of human enteropathogenic Escherichia coli.
An in-vitro assay system has been developed to measure bacterial adhesion to the mucosa of human fetal small intestine. Two strains of Escherichia coli that are proven human enteropathogens (E.P.E.C.) have been shown to adhere in large numbers, compared with control organisms. The attachment mechanism is species specific and is not caused by common fimbriae. Mucosal adhesion may be as important as enterotoxin production or invasiveness in determining the virulence of some strains of human E.P.E.C.
Adhesiveness↗
Bordetella pertussis risA, but not risS, is required for maximal expression of Bvg-repressed genes.
Expression of virulence determinants by Bordetella pertussis, the primary etiological agent of whooping cough, is regulated by the BvgAS two-component regulatory system. The role of a second two-component regulatory system, encoded by risAS, in this process is not defined. Here, we show that mutation of B. pertussis risA does not affect Bvg-activated genes or proteins. However, mutation of risA resulted in greatly diminished expression of Bvg-repressed antigens and decreased transcription of Bvg-repressed genes. In contrast, mutation of risS had no effect on the expression of Bvg-regulated molecules. Mutation of risA also resulted in decreased bacterial invasion in a HeLa cell model. However, decreased invasion could not be attributed to the decreased expression of Bvg-repressed products, suggesting that mutation of risA may affect the expression of a variety of genes. Unlike the risAS operons in B. parapertussis and B. bronchiseptica, B. pertussis risS is a pseudogene that encodes a truncated RisS sensor. Deletion of the intact part of the B. pertussis risS gene does not affect the expression of risA-dependent, Bvg-repressed genes. These observations suggest that RisA activation occurs through cross-regulation by a heterologous system.
Bacterial Adhesion↗
Treponema pallidum fibronectin-binding proteins.
Putative adhesins were predicted by computer analysis of the Treponema pallidum genome. Two treponemal proteins, Tp0155 and Tp0483, demonstrated specific attachment to fibronectin, blocked bacterial adherence to fibronectin-coated slides, and supported attachment of fibronectin-producing mammalian cells. These results suggest Tp0155 and Tp0483 are fibronectin-binding proteins mediating T. pallidum-host interactions.
Adhesins, Bacterial↗
Studies of the pathogenesis of enteric E. coli infections in weaned pigs: bacteriological and immunofluorescent studies.
Qualitative and quantitative, bacteriological studies were performed on spontaneous cases of post weaning E. coli diarrhoea (PWD). The pigs derived from a herd, D, in which the disease had persisted for a period of almost 2 years. Orally vaccinated healthy pigs from herd D and from herds A and M without the disease were also examined. The results showed that haemolytic E. coli were frequently isolated from faecal samples which had been collected 5--7 days after weaning but seldom from samples from the same pigs collected before weaning. Haemolytic E. coli dominated the aerobic intestinal flora at 3--5 days after weaning in pigs from herd D with PWD. Oral vaccination using a formalinized vaccine delayed and suppressed the occurrence of haemolytic E. coli in pigs from herd D (Table I). Intestinal counts of the bacteria showed that the number of haemolytic E. coli present in the anterior portion of the jejunum was 10(-3)--10(-5) times higher in pigs which suffered from PWD than in weaned pigs of the same age which did not show symptoms of the disease (Table II). The lowest bacterial counts in various portions of the intestine were consistently observed in the sections obtained from the orally vaccinated healthy pigs. Pure cultures of K88-negative enteropathogenic E. coli serotype O149:K91 were consistently isolated from all the diseased pigs. Fluorescent antibody studies showed that the specific strain of bacteria adhered to the villous epithelium of the jejunum in a layer which covered the villi from the tip to the base and sometimes continued down into the crypts (Figure 1). The bacterial adhesion coincided with an intensive colonization of the jejunum with the homologous E. coli serotype and was nerve observed in apparently healthy pigs which did not have symptoms of PWD. It was concluded that characteristic intestinal colonization by adhesion may occur with enteropathogenic strains of E. coli O149:K91 which lack the K88 antigen (Figure 2).
Animals↗
[Significance of the ability of E. coli to alter capillary permeability for the reproduction of pyelonephritis in mice].
Experiments in a number of biological models showed that the cultures of E. coli isolated from the urine of children with pyelonephritis had a varied spectrum of pathogenic properties. Histologically confirmed pyelonephritis induced by intravenous infection in CBA mice, treated with 5% glucose by the method of Montgomerie et al., correlated with the bacterial adhesiveness to the epithelium and the interference with capillary permeability, registered in experiments on the pulmonary model with Evans blue used for control. The criterion for the development of pyelonephritis in mice, which was based, in the opinion of Mintogemerie et al., on the positive results, indicating the presence of the infecting agent in the culture obtained by inoculation with the samples of urine and kidney tissue, was found to be insufficient, as only 28 out of 45 cultures of E. coli isolated from the kidneys coincided with histologically confirmed cases of pyelonephritis.
Animals↗
[Simple method of detection of Fc receptor sites on cells].
A bacterial adhesion technique for identification of Fc-receptor bearing cells is based on the ability of Staphylococcus aureus, Cowan 1 strain, to form rosettes with cells previously treated with immune complexes or heat aggregated Ig G. The new technique is distinguished from other Fc-receptor detection methods by its simplicity and ease of detection of both immune complexes and aggregated IgG-binding cells.
Animals↗
Genomic, virulent and phenotypic characterization of a cerebrospinal fluid-derived ST86-KL2 hypervirulent Klebsiella pneumoniae isolate from a patient with meningitis and diabetes mellitus.
BACKGROUND: Hypervirulent Klebsiella pneumoniae (hvKP) is an important cause of invasive community-acquired infection, particularly in individuals with diabetes mellitus. However, cerebrospinal fluid (CSF)-derived hvKP isolates, especially those belonging to the ST86-KL2 lineage, remain poorly characterized at the integrated clinical, genomic, and phenotypic levels. METHODS: A K. pneumoniae isolate, designated BP9811, was recovered from the CSF of a patient with meningitis and diabetes mellitus and identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and 16 S rRNA sequencing. Antimicrobial susceptibility testing and whole-genome sequencing were performed to define its resistance, virulence, sequence type (ST), capsular type, and plasmid content. Virulence was evaluated using the Galleria mellonella infection model. In addition, interaction with human cerebral microvascular endothelial cells was preliminarily assessed using adhesion, gentamicin protection, and transmission electron microscopy assays, together with measurement of relative ompA transcription by reverse transcription-quantitative polymerase chain reaction. Comparative phylogenetic analyses were performed using publicly available CSF-derived and KL2 K. pneumoniae genomes. RESULTS: BP9811 was identified as a hypermucoviscous ST86-KL2 hvKP isolate that remained susceptible to all tested antimicrobial agents. Whole-genome sequencing revealed an IncHI1B virulence plasmid carrying canonical hvKP-associated determinants, including rmpA/rmpA2, peg-344, iucABCD, and iroBCD. In the Galleria mellonella model, BP9811 showed high virulence comparable to that of the hypervirulent reference strain NTUH-2044. In HCMEC/D3 cells, BP9811 exhibited increased adhesion and intracellular recovery under the tested conditions, and transmission electron microscopy confirmed bacterial internalization. BP9811 also showed higher ompA transcript levels than the control strain. Phylogenetic analysis indicated that BP9811 was genetically distinct from currently available CSF-derived isolates and occupied a related branch within the KL2 population. CONCLUSIONS: This study provides an integrated clinical, genomic, and phenotypic characterization of BP9811, a CSF-derived ST86-KL2 hvKP isolate recovered from a patient with meningitis and diabetes mellitus. BP9811 carried a canonical hvKP virulence plasmid, displayed marked virulence-associated phenotypes, and showed enhanced interaction with human cerebral microvascular endothelial cells in vitro under the tested conditions. These findings expand the limited isolate-level evidence on central nervous system-associated hvKP and provide a basis for future comparative and mechanistic studies.
Humans↗
Bacterial adherence: first step in pathogenesis of certain infections.
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Adhesiveness↗
Bacterial adherence to epithelial cells in the nasopharynx in children.
The presence of attached bacteria to epithelial cells from the nasopharyngeal surface of the soft palate, from the adenoid surface and from the secretions covering the adenoid was studied in 10 children undergoing adenoidectomy. Large numbers of bacteria were seen to attach to mature normal squamous epithelial cells from the soft palate and in the secretions, whereas attachment to adenoid epithelial cells was rare. Using differential interference contrast microscopy, bacteria-carrying epithelial cells were seen to have their surface covered by microridges characteristic of normal mature squamous epithelial cells. Sections of adenoid tissue showed bacterial infiltration of adenoid tissue to be virtually nonexistent in the patient group.
Adenoidectomy↗
Cytoskeletal mechanisms regulating attaching/effacing bacteria interactions with host cells: It takes a village to build the pedestal.
The actin cytoskeleton is a key cellular structure subverted by pathogens to infect and survive in or on host cells. Several pathogenic strains of Escherichia coli, such as enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC), developed a unique mechanism to remodel the actin cytoskeleton that involves the assembly of actin filament-rich pedestals beneath the bacterial attachment sites. Actin pedestal assembly is driven by bacterial effectors injected into the host cells, and this structure is important for EPEC and EHEC colonization. While the interplay between bacterial effectors and the actin polymerization machinery of host cells is well-understood, how other mechanisms of actin filament remodelling regulate pedestal assembly and bacterial attachment are poorly investigated. This review discusses the gaps in our understanding of the complexity of the actin cytoskeletal remodelling during EPEC and EHEC infection. We describe possible roles of actin depolymerizing, crosslinking and motor proteins in pedestal dynamics, and bacterial interactions with the host cells. We also discuss the biological significance of pedestal assembly for bacterial infection.
Humans↗