Tumor necrosis factor prevents Candida albicans biofilm formation

Rocha, Francisco Airton Castro da; Alves, Anelise Maria Costa Vasconcelos; Rocha, Marcos Fábio Gadelha; Cordeiro, Rossana de Aguiar; Brilhante, Raimunda Sâmia Nogueira; Pinto, Ana Carolina Matias Dinelly; Nunes, Rodolfo de Melo; Girão-Carmona, Virgínia Cláudia Carneiro; Sidrim, José Júlio Costa

doi:10.1038/s41598-017-01400-4

Cited by 24 publications

(14 citation statements)

References 21 publications

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“…TNF-α inhibits synthesis of structural components such as type I collagen and induces production of stromal collagenases [56]. These cytokines released by fibroblasts after recognition of C. albicans are important to the host defense against candidiasis [57]. Recognition of C. albicans by gingival fibroblast could drive a balanced proinflammatory cytokine production that collaborate to Th17 and/or Th1 protective immune responses and killing fungal pathogen [58].…”

Section: Discussionmentioning

confidence: 99%

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

et al. 2018

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Recent evidence indicates that nonprofessional immune cells such as epithelial cells, endothelial cells, and fibroblasts also contribute to innate immunity via secretion of cytokines. Fibroblasts are the principal type of cell found in the periodontal connective tissues and they are involved in the immune response during periodontal disease. The role of fibroblasts in the recognition of pathogens via Toll-like receptors (TLRs) has been established; however, few studies have been conducted concerning the involvement of innate immune receptors in the recognition of Candida albicans by gingival fibroblast. In the current study, we investigate the functional activity of TLR2, cluster of differentiation 14 (CD14), and myeloid differentiation primary response gene 88 (MyD88) molecules in the recognition of C. albicans by gingival fibroblast. First, we identified that gingival fibroblasts expressed TLR2, TLR3, and TLR4. Our results showed that TLR agonists had no effect on these receptors’ expression by TLR2, MyD88, and CD14-deficient cells. Notably, C. albicans and a synthetic triacylated lipoprotein (Pam3CSK4) induced a remarkable increase of TLR3 expression on MyD88-deficient gingival fibroblasts. TLR4 expression levels were lower than TLR2 and TLR3 levels and remained unchanged after TLR agonist stimulation. Gingival fibroblasts presented morphological similarities; however, TLR2 deficiency on these cells leads to a lower proliferative response, whereas the deficiency on CD14 expression resulted in lower levels of type I collagen by these cells. In addition, the recognition of C. albicans by gingival fibroblasts had an effect on the secretion of cytokines and it was dependent on a specific recognition molecule. Specifically, tumor necrosis factor-α (TNF-α ) production after the recognition of C. albicans was dependent on MyD88, CD14, and TLR2 molecules, whereas the production of interleukin-1β (IL-1β ) and IL-13 was dependent on TLR2. These findings are the first to describe a role of gingival fibroblast in the recognition of C. albicans and the pathways involved in this process. An understanding of these pathways may lead to alternative treatments for patients with periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

et al. 2018

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“…In addition, C. albicans cells growing in conventional biofilms are capable of altering the cytokine profile of attacking mononuclear cells [108]. For example, the presence of a conventional biofilm leads to the downregulation of TNF-α, a pro-inflammatory cytokine produced by mononuclear leukocytes that would normally suppress biofilm formation [103,108,109]. Intriguingly, conventional biofilms that are grown in the presence of mononuclear leukocytes form thicker biofilms, a phenomenon that is thought to be mediated by an unknown soluble factor that is present when the two are co-cultured [108].…”

Section: Properties Of Conventional and Sexual Biofilms Comparedmentioning

confidence: 99%

Unraveling How Candida albicans Forms Sexual Biofilms

Perry

Hernday

Nobile

2020

JoF

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Biofilms, structured and densely packed communities of microbial cells attached to surfaces, are considered to be the natural growth state for a vast majority of microorganisms. The ability to form biofilms is an important virulence factor for most pathogens, including the opportunistic human fungal pathogen Candida albicans. C. albicans is one of the most prevalent fungal species of the human microbiota that asymptomatically colonizes healthy individuals. However, C. albicans can also cause severe and life-threatening infections when host conditions permit (e.g., through alterations in the host immune system, pH, and resident microbiota). Like many other pathogens, this ability to cause infections depends, in part, on the ability to form biofilms. Once formed, C. albicans biofilms are often resistant to antifungal agents and the host immune response, and can act as reservoirs to maintain persistent infections as well as to seed new infections in a host. The majority of C. albicans clinical isolates are heterozygous (a/α) at the mating type-like (MTL) locus, which defines Candida mating types, and are capable of forming robust biofilms when cultured in vitro. These “conventional” biofilms, formed by MTL-heterozygous (a/α) cells, have been the primary focus of C. albicans biofilm research to date. Recent work in the field, however, has uncovered novel mechanisms through which biofilms are generated by C. albicans cells that are homozygous or hemizygous (a/a, a/Δ, α/α, or α/Δ) at the MTL locus. In these studies, the addition of pheromones of the opposite mating type can induce the formation of specialized “sexual” biofilms, either through the addition of synthetic peptide pheromones to the culture, or in response to co-culturing of cells of the opposite mating types. Although sexual biofilms are generally less robust than conventional biofilms, they could serve as a protective niche to support genetic exchange between mating-competent cells, and thus may represent an adaptive mechanism to increase population diversity in dynamic environments. Although conventional and sexual biofilms appear functionally distinct, both types of biofilms are structurally similar, containing yeast, pseudohyphal, and hyphal cells surrounded by an extracellular matrix. Despite their structural similarities, conventional and sexual biofilms appear to be governed by distinct transcriptional networks and signaling pathways, suggesting that they may be adapted for, and responsive to, distinct environmental conditions. Here we review sexual biofilms and compare and contrast them to conventional biofilms of C. albicans.

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“…Not only is this predicted to impact phagocyte function in the host but the alteration in production of TNF-α may also have a direct impact on the biofilm. Application of exogenous TNF-α has been shown to prevent C. albicans biofilm formation, through a TNF receptor-independent pathway ( 104 ). Furthermore, this activity is blocked by preincubation of TNF-α with N , N ′-diacetylchitobiose, a major carbohydrate component of C. albicans cell wall ( 104 ).…”

Section: Candida Biofilmsmentioning

confidence: 99%

“…Application of exogenous TNF-α has been shown to prevent C. albicans biofilm formation, through a TNF receptor-independent pathway ( 104 ). Furthermore, this activity is blocked by preincubation of TNF-α with N , N ′-diacetylchitobiose, a major carbohydrate component of C. albicans cell wall ( 104 ). Therefore, inhibition of TNF-α by biofilms may represent an evolutionary adaption and mechanism of immune evasion.…”

Section: Candida Biofilmsmentioning

confidence: 99%

The Interface between Fungal Biofilms and Innate Immunity

et al. 2018

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Fungal biofilms are communities of adherent cells surrounded by an extracellular matrix. These biofilms are commonly found during infection caused by a variety of fungal pathogens. Clinically, biofilm infections can be extremely difficult to eradicate due to their resistance to antifungals and host defenses. Biofilm formation can protect fungal pathogens from many aspects of the innate immune system, including killing by neutrophils and monocytes. Altered immune recognition during this phase of growth is also evident by changes in the cytokine profiles of monocytes and macrophages exposed to biofilm. In this manuscript, we review the host response to fungal biofilms, focusing on how these structures are recognized by the innate immune system. Biofilms formed by Candida, Aspergillus, and Cryptococcus have received the most attention and are highlighted. We describe common themes involved in the resilience of fungal biofilms to host immunity and give examples of biofilm defenses that are pathogen-specific.

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Tumor necrosis factor prevents Candida albicans biofilm formation

Cited by 24 publications

References 21 publications

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

Unraveling How Candida albicans Forms Sexual Biofilms

The Interface between Fungal Biofilms and Innate Immunity

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