Local innate host response and filamentous fungi in patients with cystic fibrosis

Roilides, Emmanuel; Simitsopoulou, Maria

doi:10.3109/13693786.2010.511286

Cited by 16 publications

(9 citation statements)

References 69 publications

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“…Phagocytes are especially important effector cells in the control (or attempted control) of systemic mycoses, and serve a fundamental role in innate immunity through internalisation of the fungus. 24 , 38 In this context, the presence of a-glucans on the S. apiospermum conidial surface was demonstrated to be important for phagocytosis by peritoneal macrophages and for the activation of these cells. 39 …”

Section: Resultsmentioning

confidence: 99%

Ultrastructural viewpoints on the interaction events of Scedosporium apiospermum conidia with lung and macrophage cells

Aor

Mello

Sangenito

et al. 2018

Mem. Inst. Oswaldo Cruz

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BACKGROUND Scedosporium apiospermum is a ubiquitous, emerging and multidrug-resistant fungal pathogen with still rather unknown virulence mechanisms.OBJECTIVES/METHODS The cellular basis of the in vitro interaction between fungi and host cells/tissues is the determinant factor for the development of a successful in vivo infection. Herein, we evaluated the interaction of S. apiospermum conidia with lung epithelial (A549), lung fibroblast (MRC-5) and RAW 264.7 macrophages by light and scanning/transmission electron microscopy.FINDINGS After 4 h of fungi-host cell contact, the percentage of infected mammalian cells and the number of fungi per infected cell was measured by light microscopy, and the following association indexes were calculated for A549, MRC-5 and macrophage cells: 73.2 ± 25.9, 69.7 ± 22.5 and 59.7 ± 11.1, respectively. Both conidia and germinated conidia were regularly observed interacting with the evaluated cells, with a higher prevalence of non-germinated conidia. Interestingly, nests of germinated conidia were evidenced at the surface of lung cells by scanning electron microscopy. Some germination projections and hyphae were seen penetrating/evading the mammalian cells. Furthermore, internalised conidia were seen within vacuoles as visualised by transmission electron microscopy.MAIN CONCLUSIONS The present study contributes to a better understanding of S. apiospermum pathogenesis by demonstrating the first steps of the infection process of this opportunistic fungus.

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Section: Resultsmentioning

confidence: 99%

Ultrastructural viewpoints on the interaction events of Scedosporium apiospermum conidia with lung and macrophage cells

Aor

Mello

Sangenito

et al. 2018

Mem. Inst. Oswaldo Cruz

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“…are frequently isolated from the respiratory tract of patients with CF (88), where it causes typical biofilms and may be associated with deterioration of lung function, invasive infection, or allergic bronchopulmonary aspergillosis. Host defenses against Aspergillus in the respiratory tract of CF patients have been reviewed (89,90). Like all biofilms, Aspergillus biofilms are quite resistant to the antifungal activity of PMNs and macrophages, the two major airway phagocytes.…”

Section: Other Organismsmentioning

confidence: 99%

How Biofilms Evade Host Defenses

et al. 2015

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The steps involved during the biofilm growth cycle include attachment to a substrate followed by more permanent adherence of the microorganisms, microcolony arrangement, and cell detachment required for the dissemination of single or clustered cells to other organ systems. Various methods have been developed for biofilm detection and quantitation. Biofilm-producing microorganisms can be detected in tissue culture plates, using silicone tubes and staining methods, and by visual assessment using scanning electron microscopy or confocal scanning laser microscopy. Quantitative measurement of biofilm growth is determined by using methods that include dry cell weight assays, colony-forming-unit counting, DNA quantification, or XTT 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium hydroxide reduction assay. Upon infection, innate immune defense strategies are able to establish an immediate response through effector mechanisms mediated by immune cells, receptors, and several humoral factors. We present an overview of the life cycle of biofilms and their diversity, detection methods for biofilm development, and host immune responses to pathogens. We then focus on current concepts in bacterial and fungal biofilm immune evasion mechanisms. This appears to be of particular importance because the use of host immune responses may represent a novel therapeutic approach against biofilms.

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“…There are different ‘ Aspergillus ‐related diseases’ effecting the human body. In individuals with altered lung function such as asthma and cystic fibrosis, Aspergillus can cause allergic bronchopulmonary aspergillosis, a hypersensitive response to fungal components 2 . Aspergillomas may form following exposure to conidia in preexisting lung cavities such as healed lesions in tuberculosis patients.…”

Section: Introductionmentioning

confidence: 99%

Minireview: host defence in invasive aspergillosis

Lass‐Flörl

Roilides

Löffler

et al. 2013

Mycoses

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Aspergillus is a saprophytic fungus, which mainly becomes pathogenic in immunosuppressed hosts. A failure of host defences results in a diverse set of illnesses, ranging from chronic colonisation, aspergilloma, invasive disease and hypersensitivity. A key concept in immune responses to Aspergillus species is that host susceptibility determines the morphological form, antigenic structure and physical location of the fungus. Traditionally, innate immunity has been considered as a first line of defence and activates adaptive immune mechanisms by the provision of specific signals; innate and adaptive immune responses are intimately linked. The T-helper cell (TH 1) response is associated with increased production of inflammatory cytokines IFN-γ, IL-2 and IL-12 and stimulation of antifungal effector cells. Alternatively, TH 2-type responses are associated with suppression of antifungal effector cell activity, decreased production of IFN-γ and increased concentrations of IL-4 and IL-10, which promote humoral responses to Aspergillus. The host's defensive capacity is defined by the sum of resistance and tolerance. Resistance displays the ability to limit fungal burden and elimination of the pathogen, and tolerance means the ability to limit host damage caused by immune response.

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Local innate host response and filamentous fungi in patients with cystic fibrosis

Cited by 16 publications

References 69 publications

Ultrastructural viewpoints on the interaction events of Scedosporium apiospermum conidia with lung and macrophage cells

Ultrastructural viewpoints on the interaction events of Scedosporium apiospermum conidia with lung and macrophage cells

How Biofilms Evade Host Defenses

Minireview: host defence in invasive aspergillosis

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