Candida Biofilms And Their Role In Infection – Periodontal disease depends on the presence of microorganisms in the oral cavity, which may enable them to survive under adverse conditions or facilitate further colonization of host tissues, as they form a multispecies biofilm community during colonization of oral tissues. Numerous species of bacteria are involved in the biofilm complex structure, but not only fungi, Candida albicans, in particular, live in large numbers in the mouth. C. albicans utilizes a virulent arsenal that enables successful bacterial coexistence to colonize the host and infect the host. In this article, Early colonizers in the oral cavity; A variety of aspects are highlighted that may facilitate cooperation with associated bacterial representatives of hybrid species and late colonizers. “Red complex” species. in particular, We also present the presence of candidal cell surface proteins—primary cytosolic “moonlight” proteins that perform a novel function on the cell surface and within biofilm structures—typical fungal bodies. Another group of virulence factors considered include secreted aspartic proteases (Sap) and other secreted hydrolytic enzymes. Equally important and discussed is the specific structure of the candidal cell wall, which dynamically changes during morphological transitions of fungi that favor biofilm formation. Non-protein biofilm assembly factors also show dynamic change upon exposure to bacteria, and their biosynthesis processes may be involved in the stability of mixed biofilms. This review focuses on biofilm-related changes in microbial communication systems using different quorum sensing molecules of both fungal and bacterial cells. All the factors discussed about virulence involved in the formation of mixed biofilms pose new challenges and influence the successful design of new diagnostic methods and the application of appropriate therapies for periodontal diseases.
Dental diseases are the most common worldwide and cause major consequences for human health, cardiovascular diseases, diabetes insulin resistance; Gastrointestinal cancer; respiratory tract infection; Alzheimer’s disease Adverse pregnancy outcomes (Kassebaum et al., 2014; Whitmore and Lamont, 2014; Hajishengallis, 2015; Sonti and Fleury, 2015; Vamos et al., 2015; Bui et al., 2019; Do et al., 2019; Liu et al., 2019). et al., 2021). The etiology of periodontal diseases is based on the composition of the polymicrobial community living in the subgingival compartment, which depends on the potential for infection, characterized by synergistic reactions in the community or nososymbiocity (Hajishengallis and Lamont, 2012; Hajishengallis, 2016 and Lamont; ) Mutual microbial coexistence based on frequent metabolic co-adaptations is a specialization of microbial activity. and can cause changes in the properties of community members from large to pathogenic ( Wright et al., 2013; Lamont and Hajishengallis, 2015).
Candida Biofilms And Their Role In Infection
The simplest taxonomy of bacteria involved in the development of periodontal disease identifies mucosal and saliva-coated tissues as containing primarily Gram-positive facultative anaerobes such as Streptococcus spp. (S. gordonii, S. mitis, S. oralis, and S. sanguinis) and Actinomyces spp. (Socransky et al., 1998). They dominate the local environment and cooperate with secondary colonizers such as Fusobacterium nucleatum and late colonizers such as Porphyromonas gingivalis, which act as bridging compounds for aggregation. A combination of Tannerella forsythia and Treponema denticola; ” These species are considered the main causative agents of periodontal diseases (Suzuki et al., 2013). Such microbial succession is triggered by changes in local habitats, including changes in pH and redox potential, or decreases in oxygen levels. Another factor that favors colonizer survival involves tight intercellular interactions with microbial surface acids (Kolenbrander et al., 2006). However, The model of successive colonization has evolved since the development of microarray techniques, showing that infection progression is a more complex process.
Biofilm Disruptors: Clinical Insight For Gut Health
P. gingivalis has been proposed to play a key anti-inflammatory role in regulating inflammation by remodeling the microbiota from benign to dysbiotic, even at low levels of host colonization (Hajishengallis and Lamont, 2016). The physical interaction and diffusion of soluble factors can modulate viral gene expression and microbial virulence (Frias-Lopez and Duran-Pinedo, 2012). Coordination usually involves providing an attachment layer—S. gordonii and P. gingivalis dual-species biofilm (Kuboniwa et al., 2006); Cross-nutrient feeding identified for S. gordonii metabolism; (L-lactate) promotes the pathogenicity of A. actinomycetemcomitans (Ramsey et al., 2011) and finds a synergistic metabolic cross-talk for P. gingivalis and T. denticola that stimulates isobutyric acid production by P. gingivalis. denticola growth and the secretion of T. denticola succinate affect P. gingivalis cell development (see review by Miller et al., 2019). Such manipulation can increase the pathogenicity of the entire microbial community ( Hajishengallis and Lamont, 2012 ; Hajishengallis et al., 2012 ).
In addition, The state of the host immune system, modified by disorders or medical treatments, can strongly influence polymicrobial dysbiosis and subsequent diseases by itself (Hajishengallis and Lamont, 2021). major stone pathogen (Hajishengallis, 2014); P. gingivalis can modulate the Toll-like receptor response and facilitate the survival of the entire microbial community (Darveau, 2010). P. gingivalis suppresses interleukin-8 production by gingival epithelial cells and delays neutrophil recruitment to the site of infection ( Darveau et al., 1998 ; Hasegawa et al., 2008 ; Hajishengallis and Lamont, 2014 ). Finally, Exposed or secreted cysteine proteins (gingipains) can evade detection of surface microbiota to activate or degrade complement factors C3 and C5 (Hajishengallis and Lamont, 2012; Hussain et al., 2015).
These findings should extend the analysis of mixed-species community formation between bacteria belonging to the Candida genus and possible commensal fungal species to early, Bridging and major renal diseases of periodontal disease initiate severe caries in vivo (Wu et al., 2015; Hwang et al., 2017; Kim et al., 2017; Sztukowska et al., 2018; Bartnicka et al., 2019; Bartnicka et al., 2020). ).
C. albicans is the most common yeast in the oral cavity of healthy individuals (Ghannoum et al., 2010; Baumgardner, 2019). A preliminary hypothesis that this fungus may be involved in the development of chronic periodontal disease was based on analysis of samples from supragingival and subgingival sites of patients with chronic kidney disease, which showed high rates of C. albicans colonization compared to healthy individuals. Urzúa et al., 2008). In addition, The importance of this fungus is emphasized by the recent finding that C. albicans is a prominent keystone in the oral cavity capable of forming heterogeneous networks with different bacteria (Diaz et al., 2014; Janus et al., 2016; De-La-Torre et al., 2018; Krüger et al., 2019; Young et al., 2020; Jabri et al., 2021). Changes in biofilm composition in shared ecological niches with fungi may promote cooperation among fungal species for the benefit of all interacting partners, such as evasion of the host immune system or enhancement of biofilm properties (Figure 1 ). The biological consequences of biofilm interactions in periodontitis for both specific microorganisms and the host remain largely unclear.
Selective Photoinactivation Of Candida Albicans In The Non Vertebrate Host Infection Model Galleria Mellonella
Figure 1 Influence of oral bacteria on virulence and pathogenesis of Candida albicans. The interaction of C. albicans with oral bacteria occurs through several mechanisms and can either reduce or increase the incidence of fungal infections. For some bacteria, Published preliminary analyzes have not conclusively determined the nature of the bacterial influence on the prevalence of mixed infections with C. albicans . AI-2, autoinducer 2; Ah, Aggregatibacteria actinomycetemcomitans.
For the early colonizing group, including S. sanguinis, S. oralis, S. mitis, and S. gordonii; The outcome of interactions with fungi is not well understood; Available reports often contradict each other. However, All of these species have been shown to coexist with clinical isolates of C. albicans (Jenkinson et al., 1990). In the case of S. sanguinis; One of the first reports suggested that bacterial-derived regions depend on the conditions of specific fields. Prior oral exposure to S. sanguinis , an oral isolate of C. albicans isolated from healthy and HIV-infected individuals, inhibited or promoted germ tube formation ( Nair et al., 2001 ). Further, in vitro analyzes showed that the addition of S. sanguinis and S. mitis cells to C. albicans ATCC 18804 cells to promote initial fungal adhesion significantly reduced the mixed fungal biofilm CFU compared to a single fungal species biofilm. S. mitis but not S. sanguinis reduced C. albicans filamentation (do Rosário Palma et al., 2019). A biofilm formation study on saliva flow showed that C. albicans strain ATCC SC5314 showed better biofilm formation ability than S. sanguinis and S. gordonii (Diaz et al., 2012). Therefore, It is questionable whether a group of early colonizers modify fungal biofilm formation to influence oral health or pathogenicity in the host organism. In addition, Studies using Galleria mellonella as a surrogate model of mixed bacterial fungal infection;
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