Macrophage–Cryptococcus Interactions: An Update

Mansour, Michael K.; Reedy, Jennifer L.; Tam, Jenny M.; Vyas, Jatin M.

doi:10.1007/s12281-013-0165-7

Cited by 18 publications

(15 citation statements)

References 68 publications

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“…To further determine the differences of humoral immune responses between LCG exposure group and HICG exposure group, we compared the proteome between the two groups directly. As shown in Figure 5A and Table S3, Here, we found that hemocytes failed to kill C. neoformans in G. mellonella, which is in line with previous reports that C. neoformans can evade macrophage attack 32,33 35 . These changes may help C. neoformans use these phagocytes as shelters for invasion and proliferation 32,33 .…”

Section: Glabrata Exposure Triggered the Proteome Changes Of G Mesupporting

confidence: 92%

Pre-exposure to Candida glabrata protects Galleria mellonella against subsequent lethal fungal infections

Huang

Zheng

et al. 2020

Virulence

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Commensal fungi are an important part of human microbial community, among which Candida albicans and Candida glabrata are two common opportunistic pathogens. Unlike the high pathogenicity of C. albicans, C. glabrata is reported to show low pathogenicity to the host. Here, by using a Galleria mellonella infection model, we were able to confirm the much lower virulence of C. glabrata than C. albicans . Interestingly, pre-exposure to live C. glabrata (LCG) protects the larvae against subsequent various lethal fungal infections, including C. albicans, Candida tropicalis, and Cryptococcus neoformans . Inconsistently, heat-inactivated C. glabrata (HICG) pre-exposure can only protect against C. albicans or C. tropicalis re-infection, but not C. neoformans . Mechanistically, LCG or HICG pre-exposure enhanced the fungicidal activity of hemocytes against C. albicans or C. tropicalis . Meanwhile, LCG pre-exposure enhanced the humoral immunity by modulating the expression of fungal defending proteins in the cell-free hemolymph, which may contribute to the protection against C. neoformans . Together, this study suggests the important role of C. glabrata in enhancing host immunity, and demonstrates the great potential of G. mellonella model in studying the innate immune responses against infections.

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Section: Glabrata Exposure Triggered the Proteome Changes Of G Mesupporting

confidence: 92%

Pre-exposure to Candida glabrata protects Galleria mellonella against subsequent lethal fungal infections

Huang

Zheng

et al. 2020

Virulence

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“…Although no single pattern recognition receptor (PRR) has been shown to be required for binding of Cryptococcus , it is hypothesized that alveolar macrophages recognize Cryptococcus and initialize the immune response through multiple receptors such as Dectin-1, Mincle, mannose receptor, CD14, and toll-like receptors (TLRs) (Figure 1 .1) ( 27 – 30 ). The role of AMs and phagocytosis is believed to be critical during early infection, as observed in vivo imaging studies and animal models demonstrating enhanced susceptibility after AM depletion ( 31 , 32 ).…”

Section: Innate Recognitionmentioning

confidence: 99%

Immunology of Cryptococcal Infections: Developing a Rational Approach to Patient Therapy

2018

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Cryptococcal meningoencephalitis is responsible for upwards of 15% of HIV-related deaths worldwide and is currently the most common cause of non-viral meningitis in the US, affecting both previously healthy and people with immune suppression caused by cancer chemotherapy, transplantation, and biologic therapies. Despite a continued 30–50% attributable mortality, recommended therapeutic strategies have remained largely unchanged since the 1950s. Recent murine models and human studies examining the role of the immune system in both susceptibility to the infection as well as host damage have begun to influence patient care decisions. The Damage Framework Response, originally proposed in 1999, was recently used to discuss dichotomous etiologies of host damage in cryptococcal disease. These include patients suffering microbiological damage with low host immunity (especially those immunosuppressed with HIV) and those having low (live) microbiological burden but high immune-mediated damage (HIV-related immune reconstitution syndrome and non-HIV-related postinfectious inflammatory response syndrome). Cryptococcal disease in previously healthy hosts, albeit rare, has been known for a long time. Immunophenotyping and dendritic cell-T cell signaling studies on cerebral spinal fluid of these rare patients reveal immune capacity for recognition and T-cell activation pathways including increased levels of HLA-DR and CD56. However, despite effective T-cell signals, brain biopsy and autopsy specimens demonstrated an M2 alternative macrophage polarization and poor phagocytosis of fungal cells. These studies expand the paradigm for cryptococcal disease susceptibility to include a prominent role for immune-mediated damage and suggest a need for careful individual consideration of immune activation during therapy of cryptococcal disease in diverse hosts.

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“…Some particles find their way into the alveolus where the resident cells of the innate immune system attempt to clear the infection. A large body of research shows an important role for alveolar macrophages in anti-cryptococcal defense by detecting and engulfing fungal spores (Giles et al, 2009; Mansour et al, 2014). Non-professional phagocytes, such as eosinophils and mast cells (MCs) have received less attention, although one report describes effector contribution of eosinophils and interaction of MCs and C. neoformans (Feldmesser et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Cryptococcus neoformans Induces MCP-1 Release and Delays the Death of Human Mast Cells

Lopes

Stylianou

Backman

et al. 2019

Front. Cell. Infect. Microbiol.

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Cryptococcosis, caused by the basidiomycete Cryptococcus neoformans , is a life-threatening disease affecting approximately one million people per year worldwide. Infection can occur when C. neoformans cells are inhaled by immunocompromised people. In order to establish infection, the yeast must bypass recognition and clearance by immune cells guarding the tissue. Using in vitro infections, we characterized the role of mast cells (MCs) in cryptococcosis. We found that MCs recognize C. neoformans and release inflammatory mediators such as tryptase and cytokines. From the latter group MCs released mainly CCL-2/MCP-1, a strong chemoattractant for monocytic cells. We demonstrated that supernatants of infected MCs recruit monocytes but not neutrophils. During infection with C. neoformans , MCs have a limited ability to kill the yeast depending on the serotype. C. neoformans , in turn, modulates the lifespan of MCs both, by presence of its polysaccharide capsule and by secreting soluble modulators. Taken together, MCs might have important contributions to fungal clearance during early stages of cryptocococis where these cells regulate recruitment of monocytes to mucosal tissues.

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Macrophage–Cryptococcus Interactions: An Update

Cited by 18 publications

References 68 publications

Pre-exposure to Candida glabrata protects Galleria mellonella against subsequent lethal fungal infections

Pre-exposure to Candida glabrata protects Galleria mellonella against subsequent lethal fungal infections

Immunology of Cryptococcal Infections: Developing a Rational Approach to Patient Therapy

Cryptococcus neoformans Induces MCP-1 Release and Delays the Death of Human Mast Cells

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