[Production of a factor inhibiting macrophage migration to the Candida albicans antigen in mice and their resistance to this microorganism].
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Resistance to C. albicans, an opportunistic microorganism, has been studied in CBA and C57BL/6 mice, oppositely responsive in the production of the factor inhibiting migration of macrophages to antigen obtained from this fungus. The study has shown that CBA mice, highly responsive in the macrophage migration inhibiting factor, are less resistant to C. albicans, while C57BL/6 mice with low response to this antigen are more resistant to this infective agent. Macrophages play, probably, a certain role in the generalization of the process because not all phagocytized C. albicans cells are digested.Cite
In this study we evaluated the interactions between C. albicans and either resident or Concanavalin A-activated macrophages, focusing on the ability of that pathogen to induce macrophage apoptosis and on the differential response of those macrophages to ingest and kill different strains of C. albicans. Monolayers of peritoneal murine macrophages were coincubated with strains CR1 or CR15, both isolated from HIV infected individuals, or with control strain 577, for 1 h at 37°C. Resident macrophages had a low potential to ingest all strains tested, and although the addition of serum increased significantly the percentage of phagocytosing macrophages, their potential to kill the pathogen was maintained low and presented no significant differences concerning the strain of Candida phagocytozed. The percentage of macrophages presenting nuclear condensations increased significantly after internalization of C. albicans via complement receptors, and several of those macrophages bound annexin V-FITC, which suggests that ingestion of Candida is required to trigger apoptosis. This was observed after phagocytosis of strains CR1 and CR15, but not after phagocytosis of strain 577. The ability of Con A–activated macrophages to ingest and kill strains CR1 and CR15 was significantly greater than that of resident macrophages, but no enough to prevent apoptosis of some macrophages. Since the population of macrophages is heterogeneous, containing both small and large cells, it is possible that the larger ones expressing more mannose receptors are more able to kill that pathogen, whereas the smaller ones could be better hosts for induction of apoptosis, survival and replication of Candida on their inside.
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Candida albicans is the most prevalent fungal pathogen of humans, causing a variety of diseases ranging from superficial mucosal infections to deep-seated systemic invasions. Mucus, the gel that coats all wet epithelial surfaces, accommodates C. albicans as part of the normal microbiota, where C. albicans resides asymptomatically in healthy humans. Through a series of in vitro experiments combined with gene expression analysis, we show that mucin biopolymers, the main gel-forming constituents of mucus, induce a new oval-shaped morphology in C. albicans in which a range of genes related to adhesion, filamentation, and biofilm formation are downregulated. We also show that corresponding traits are suppressed, rendering C. albicans impaired in forming biofilms on a range of different synthetic surfaces and human epithelial cells. Our data suggest that mucins can manipulate C. albicans physiology, and we hypothesize that they are key environmental signals for retaining C. albicans in the host-compatible, commensal state.The yeast Candida albicans causes both superficial infections of the mucosa and life-threatening infections upon entering the bloodstream. However, C. albicans is not always harmful and can exist as part of the normal microbiota without causing disease. Internal body surfaces that are susceptible to infection by C. albicans are coated with mucus, which we hypothesize plays an important role in preventing infections. Here, we show that the main components of mucus, mucin glycoproteins, suppress virulence attributes of C. albicans at the levels of gene expression and the corresponding morphological traits. Specifically, mucins suppress attachment to plastic surfaces and human cells, the transition to cell-penetrating hyphae, and the formation of biofilms (drug-resistant microbial communities). Additionally, exposure to mucins induces an elongated morphology that physically resembles the mating-competent opaque state but is phenotypically distinct. We suggest that mucins are potent antivirulence molecules that have therapeutic potential for suppressing C. albicans infections.
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Objective: To study function of neutrophils and macrophages in mice with mixed infection by Escherichia coli and Candida albicans. Methods:Animal models with infection by E.coli or C.albicans alone or with mixed infection by two pathogens were established. Polymyxin B was used to neutralize toxic and immunogenic effects of lipopolysaccharide. Neutrophils and macrophages were isolated from mice of different groups. Adherence and phagocytosis function of neutrophils and killing function of macrophages were examined, and TNF α level released by macrophages was detected by ELISA. Results:Adherence rate of neutrophils in mice with mixed infection of these two pathogens was significantly higher than that in mice infected by E. coli or C. albicans alone (P0.05), while phagocytosis rate was significantly lower than that in mice with either infection alone(P0.05). Killing rate of macrophges in mice with mixed infection was significantly lower than that in mice with either infection alone(P0.05). TNF α level released by macrophages in mice with mixed infection was significantly higher than that in mice with either infection alone(P0.05). Conclusions:Function of neutrophils and macrophages is depressed in mice with concurrent E. coli and C. albicans infection, and host immunity can be affected by excessive production of TNF α by macrophages.
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Candida sp are the most common fungal pathogens causing fatal health care associated infections. Among the genus of Candida, Candida albicans is the most frequent species isolated from patients. The notorious C. albicans infection is the ability of this dimorphic fungus to form biofilm. Biofilm has been pointed as a dynamic phenotypic switching in bacteria and fungi, which may result in higher morbidity and mortality in human beings. This review addresses the basic explanation of biofilm formation which is characterized by the antifungal agents resistance. The factors that influence C. albicans biofim formation and antifungal agents resistance are discussed. Key words: Candida sp – antifungal – resistance – biofilm - pathogenecity
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The dimorphic fungus Candida albicans is both a harmless commensal organism on mucosal surfaces and an opportunistic pathogen. Under certain predisposing conditions, the fungus can overgrow the mucosal microbiome and cause both superficial and life-threatening systemic infections after gaining access to the bloodstream. As the first line of defense of the innate immune response, infecting C. albicans cells face macrophages, which mediate the clearance of invading fungi by intracellular killing. However, the fungus has evolved sophisticated strategies to counteract macrophage antimicrobial activities and thus evade immune surveillance. The cytolytic peptide toxin, candidalysin, contributes to this fungal defense machinery by damaging immune cell membranes, providing an escape route from the hostile phagosome environment. Nevertheless, candidalysin also induces NLRP3 inflammasome activation, leading to an increased host-protective pro-inflammatory response in mononuclear phagocytes. Therefore, candidalysin facilitates immune evasion by acting as a classical virulence factor but also contributes to an antifungal immune response, serving as an avirulence factor. In this review, we discuss the role of candidalysin during C. albicans infections, focusing on its implications during C. albicans-macrophage interactions.
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Candida albicans is an opportunistic fungal pathogen that infects immunocompromised patients. Infection control requires phagocytosis by innate immune cells, including macrophages. Migration towards, and subsequent recognition of, C. albicans fungal cell wall components by macrophages is critical for phagocytosis. Using live-cell imaging of phagocytosis, the macrophage cell line J774.1 showed enhanced movement in response to C. albicans cell wall mutants, particularly during the first 30 min, irrespective of the infection ratio. However, phagocyte migration was reduced up to 2-fold within a C. albicans biofilm compared to planktonic fungal cells. Biofilms formed from C. albicans glycosylation mutant cells also inhibited macrophage migration to a similar extent as wildtype Candida biofilms, suggesting that the physical structure of the biofilm, rather than polysaccharide matrix composition, may hamper phagocyte migration. These data illustrate differential macrophage migratory capacities, dependent upon the form of C. albicans encountered. Impaired migration of macrophages within a C. albicans biofilm may contribute to the recalcitrant nature of clinical infections in which biofilm formation occurs.
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Hamycin is an antifungal antibiotic produced by Streptomyces pimprina Thirum. In the present study, the effect of hamycin on (a) the phagocytosis of Candida albicans by murine peritoneal macrophages and (b) the cell surface hydrophobicity (CSH) of C. albicans was investigated. Addition of hamycin to the culture of macrophages and Candida cells increased the susceptibility of Candida cells to the phagocytosis by macrophages. Pretreatment of Candida cells with hamycin increased their vulnerability to killing by macrophages. Examination of physico-chemical properties of Candida cell surface showed a significant decrease in the CSH. These findings suggest that the binding of hamycin to Candida cells induces biochemical/physico-chemical alterations of the surface, so that it becomes more susceptible to phagocytosis by murine macrophages.
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Candida albicans and Cutibacterium acnes are opportunistic pathogens that co-colonize the human body. They are involved in biofilm-related infections of implanted medical devices. The objective of this study was to evaluate the ability of these species to interact and form polymicrobial biofilms. SEM imaging and adhesion assays showed that C. acnes adhesion to C. albicans did not have a preference for a specific morphological state of C. albicans; bacteria adhered to both hyphal and yeast forms of C. albicans. C. albicans did not influence growth of C. acnes under anaerobic growth conditions, however under aerobic growth condition, C. albicans enhanced early C. acnes biofilm formation. This favorable impact of C. albicans was not mediated by secreted compounds accumulating in the medium, but required the presence of metabolically active C. albicans. The ability of these microorganisms to interact together could modulate the physiopathology of infections.
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