Influence of cigarette smoke condensate on cariogenic and candidal biofilm formation on orthodontic materials

Baboni, Fernanda Brasil; Filho, Odilon Guariza; Moreno, Andréa Novais; Rosa, Edvaldo Antônio Ribeiro

doi:10.1016/j.ajodo.2009.05.023

Cited by 42 publications

(40 citation statements)

References 29 publications

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“…This adhesion may be increased in the presence of cigarette smoke, as demonstrated in the present study, in which CSC-pretreated C. albicans adhered better to gingival fibroblast monolayers than did CSC-untreated C. albicans . CSC has been shown to favor the adhesion of S mutans to dental materials [49] and of C albicans on various materials [49]. We thus demonstrate, for the first time, the significant adhesion of C. albicans to gingival fibroblasts following contact with CSC.…”

Section: Discussionsupporting

confidence: 55%

Cigarette Smoke-ExposedCandida albicansIncreased Chitin Production and Modulated Human Fibroblast Cell Responses

Alanazi

Semlali

Perraud

et al. 2014

BioMed Research International

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The predisposition of cigarette smokers for development of respiratory and oral bacterial infections is well documented. Cigarette smoke can also contribute to yeast infection. The aim of this study was to investigate the effect of cigarette smoke condensate (CSC) on C. albicans transition, chitin content, and response to environmental stress and to examine the interaction between CSC-pretreated C. albicans and normal human gingival fibroblasts. Following exposure to CSC, C. albicans transition from blastospore to hyphal form increased. CSC-pretreated yeast cells became significantly (P < 0.01) sensitive to oxidation but significantly (P < 0.01) resistant to both osmotic and heat stress. CSC-pretreated C. albicans expressed high levels of chitin, with 2- to 8-fold recorded under hyphal conditions. CSC-pretreated C. albicans adhered better to the gingival fibroblasts, proliferated almost three times more and adapted into hyphae, while the gingival fibroblasts recorded a significantly (P < 0.01) slow growth rate but a significantly higher level of IL-1β when in contact with CSC-pretreated C. albicans. CSC was thus able to modulate both C. albicans transition through the cell wall chitin content and the interaction between C. albicans and normal human gingival fibroblasts. These findings may be relevant to fungal infections in the oral cavity in smokers.

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Section: Discussionsupporting

confidence: 55%

Cigarette Smoke-ExposedCandida albicansIncreased Chitin Production and Modulated Human Fibroblast Cell Responses

Alanazi

Semlali

Perraud

et al. 2014

BioMed Research International

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“…Nonetheless, several other groups have recently reported on the effects of cigarette smoke exposure on biofilm formation by various microbial pathogens. BABONI et al [7] reported that exposure of both Streptococcus mutans and Candida albicans to CSC increased the adherence of these oral pathogens to orthodontic material in the setting of increased biofilm formation [7], while BAGAITKAR et al [8] also observed increased biofilm formation following exposure of another oral pathogen, Porphyromonas gingivalis, to CSC. Even more recently, GOLDSTEIN-DARUACH et al [9] reported that exposure of a range of bacterial pathogens, isolated from the sinonasal cavities of smokers, to smoke generated by combustion of five reference cigarettes resulted in activation of biofilm formation [9].…”

Section: Discussionmentioning

confidence: 99%

Effects of cigarette smoke condensate on pneumococcal biofilm formation and pneumolysin

et al. 2012

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Although the well-recognised predisposition of cigarette smokers to the development of severe pneumococcal disease may be attributable to impairment of local host defences, less is known about the direct effects of smoke exposure on airway pathogens, or their virulence factors. In the current study, we have investigated the effects of cigarette smoke condensate (CSC) on biofilm formation by Streptococcus pneumoniae, and on the pore-forming activity of its major toxin, pneumolysin.Biofilm formation following exposure of the pneumococcus to CSC (20-160 mg?mL -1 ) was measured using a crystal violet-based spectrophotometric procedure, while the pore-forming activity of recombinant pneumolysin was determined by a fura-2/acetoxymethyl ester-based spectrofluorimetric procedure to monitor the uptake of extracellular Ca 2+ by isolated human neutrophils. Exposure of the pneumococcus or pneumolysin to CSC resulted in significant dose-related augmentation of biofilm formation (pf0.05 at 80 and 160 mg?mL -1 ) and substantial attenuation of the pore-forming interactions of pneumolysin, respectively. Augmentation of biofilm formation and inactivation of pneumolysin as a consequence of smoking are likely to favour microbial colonisation and persistence, both being essential precursors of pneumococcal disease.

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“…Zonuz et al (2008) reported that the growth of Streptococcus mutans and Streptococcus sanguis is accelerated in the vicinity of CSC. CSC has also been reported to interfere with the adhesion and biofilm formation in contact with Streptococcus mutans and Candida albicans cells (Baboni et al 2010). However, there have been few studies to date reporting results about the destruction of bacterial flora by swallowed CSC together with saliva and during smoking and biological activity correlating between CSC and intestinal bacterial flora.…”

Section: Introductionmentioning

confidence: 99%

“…The water containing CSC was filtered through a pore membrane (0.44 mm, Millipore) immediately after the cigarettes were burned (Baboni et al 2010). A final concentration of 0.45 mg TPM/mL was determined in the filtrate.…”

Section: Cigarette Smoke Condensatementioning

confidence: 99%

Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

Wei

Sun

et al. 2015

An. Acad. Bras. Ciênc.

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The aim of the study was to investigate the effect of cigarette smoke on the production and characterization of exopolysaccharides (EPSs) produced by Bifidobacterium. Cigarettes of Shanhua brand (nicotine: 1.1 mg, tar: 11 mg) were utilized to prepare a cigarette smoke condensate (CSC). The standard strain of Bifidobacterium animalis was cultured in MRS media under anaerobic addition of CSC. The results showed that CSC significantly decreased the growth of B. animalis as well as EPSs and acetic acid production. Furthermore, two EPSs fractions (Fr-I and Fr-II) were isolated and purified for chemical and molecular determination. By comparison with control, CSC was found to be of great impact on EPSs carbohydrate composition. The molecular weight mass of Fr-I changed from 3.33×10 5 g/mol (without CSC) to 2.99×10 5 (with CSC). In conclusion, in vitro studies revealed that CSC was directly able to affect the production of metabolites for B. animalis, which could be an essential factor in certain pathological disorders.

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Influence of cigarette smoke condensate on cariogenic and candidal biofilm formation on orthodontic materials

Cited by 42 publications

References 29 publications

Cigarette Smoke-ExposedCandida albicansIncreased Chitin Production and Modulated Human Fibroblast Cell Responses

Cigarette Smoke-ExposedCandida albicansIncreased Chitin Production and Modulated Human Fibroblast Cell Responses

Effects of cigarette smoke condensate on pneumococcal biofilm formation and pneumolysin

Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

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