Chapter 11 : Antiadhesion Therapy

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This chapter provides a review of the various traditional approaches of antiadhesion therapy and immunity, including the usef of adhesin-based vaccines, receptor and adhesin analogs, sub-lethal concentrations of antibiotics, dietary constituents, and innate host-derived antiadhesion factors. The adhesin analog strategy is based on the assumption that the isolated adhesin molecule or its synthetic or recombinant fragment binds to the receptor and thereby competitively blocks adhesion of the bacteria. It has so far been impractical to use adhesin analogs in antiadhesion therapy because they are almost always macromolecules that must be employed in relatively high molar concentrations and they are available only in limited supply. In addition, careful consideration must be given to their toxicity and immunogenicity. Nevertheless, modern proteomics and recombinant biotechnology have permitted the development of unique types of relatively small peptides for antiadhesion therapy. The chapter talks about the studies performed to investigate the antiadhesion activities of cranberry materials. In a study it was found that cranberry extract inhibited the coaggregation between pairs of gram-negative oral bacteria more often than it did those between pairs of gram-positive bacteria. The target of the antiadhesive activity is the bacterial adhesin, not the animal cell receptors or human mucus. The most important host-derived components which potentially may provide innate immunity by inhibiting adhesion are those found associated with mucus on mucosal surfaces. The secretor or nonsecretor status of individuals is of particular interest in relation to their susceptibility to infection and the possible role of soluble adhesin receptors.

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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Image of Figure 11.1
Figure 11.1

Schematic diagram illustrating a proposed effect of antibiotic usage on the survival and spread of resistant bacteria. The proposed effect assumes that if the resistance is plasmid mediated, the rate of spread of resistance within the population will be equal to the rate of plasmid transfer within the population. The rate of conjugative plasmid transfer observed in vitro is approximately 1 in 10 bacterial cells. If the resistance is chromosomally mediated, mostly arising from point mutations, the rate of spread will be much lower, approximately 1 in 10 to 10 bacteria. Thus, assuming that an infection caused by 10 to 10 bacteria is treated with antibiotics, 1 to 10 would remain viable in chromosomal resistance population while 10 to 10 would remain viable in the plasmid-mediated resistance population. The probability that the resistant population will grow and spread to other individuals would therefore be much higher for plasmid-mediated resistance than for chromosome-mediated resistance. Continued use of the same antibiotics will inevitably result, in a relatively short period (e.g., 5 to 6 years), in infections caused mostly by resistant strains, ultimately requiring alternative antibiotic treatment.

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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Image of Figure 11.2
Figure 11.2

Schematic diagram illustrating a proposed effect of the use of antiadhesion agents on the survival and spread of resistant bacteria. The rate of spread of resistance to antiadhesion agents within the population for either plasmid- or chromosome-mediated resistance is expected to be essentially the same as that described for antibiotic resistance in Fig. 11.1 . Unlike antibiotic treatments, however, treatment with antiadhesion agents does not have a differential effect on the viability of resistant and sensitive strains. Thus, the rate of spread of resistant strains will remain low, due to the continued viability of sensitive strains. It is predicted, therefore, that over a given period, antiadhesion therapy would result in a much slower spread of resistant strains within the population than would antibiotic therapy.

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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Image of Figure 11.3
Figure 11.3

Schematic diagram and examples of receptor analog (A) and adhesin analog (B) inhibition of adhesion. (A) Adhesion mediated by a lectin on the surface of binding to sialic acid residues on host cells. Excess of sialyllactose in the reaction mixture competitively inhibits adhesion by occupying the sugar-combining sites of the bacterial lectin. A clinical study based on this type of therapy was conducted by Ukkonen et al. ( ), in which children were given synthetic sialyllactose, administered intranasally, to prevent otitis media caused mainly by and which express adhesins specific for this sugar. There was no effect on the incidence of otitis media in the experimental group compared to the placebo group. The lack of effect was postulated to be due to the presence of multiple adhesins expressed by these pathogens for distinct receptors. (B) Adhesion mediated by a protein adhesin of to its cognate receptor on the acquired pellicle on teeth. In vitro, a synthetic oligopeptide representing the binding site of the streptococcal adhesin competitively inhibited adhesion by occupying the adhesin binding site in the acquired pellicle. In a clinical study, the oligopeptide mimicking the adhesin binding site was applied directly to the tooth surfaces of four human volunteers ( ). The rate of recolonization of mutans streptococci was significantly reduced compared to that in patients given placebo, consisting of a control peptide administered in a similar fashion. The effect was specific for mutans streptococci and not for other oral bacterial genera.

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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Figure 11.4

Schematic diagram and examples of sublethal antibiotic (A) and dietary product (B) inhibition of adhesion. (A) Treatment of with subinhibitory concentrations of β-lactam antibiotics in vitro leads to lack of fimbrial expression and reduced adhesion. In a study of the effects of sublethal concentrations of penicillin on urinary tract infections, the number of CFU in urine was significantly reduced ( ). (B) Example of the inhibitory effects of dietary compounds on the adhesion of various bacteria. With respect to cranberry extract, these effects can be observed on bacteria ranging from strains of causing urinary tract infections, diarrhea, and meningitis to oral bacteria and . In two independent clinical studies, cranberry juice consumption was found to reduce significantly the incidence of urinary tract infections both in elderly ( ) and young ( ) women.

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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TABLE 11.1

Carbohydrates prevent bacterial infection in vivo

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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TABLE 11.2

Examples of probiotic bacteria inhibiting the adhesion of pathogens

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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TABLE 11.3

Glycoconjugates and saccharides from milk capable of interacting with bacteria

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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TABLE 11.4

Plant extracts containing bacterial antiadhesin activities

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
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TABLE 11.5

Examples of antiadhesion effects of juice or extracts of spp. (cranberry)

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11
Generic image for table
TABLE 11.6

Example of studies describing the interaction with mucus and effect on adhesion

Citation: Ofek I, Hasty D, Doyle R. 2003. Antiadhesion Therapy, p 157-176. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch11

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