Capsular polysaccharide of Cryptococcus neoformans induces proinflammatory cytokine release by human neutrophils

Retini, Cinzia; Vecchiarelli, Anna; Monari, Claudia; Tascini, Carlo; Bistoni, Francesco; Kozel, Thomas R.

doi:10.1128/iai.64.8.2897-2903.1996

Cited by 127 publications

(48 citation statements)

References 31 publications

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“…Direct interaction of GXM with PMN has been reported as a regulator of tumor necrosis factor receptor expression and L-selectin shedding, which may prevent accumulation of neutrophils in infected tissues (7). Additional data on the interaction of GXM with human neutrophils, probably mediated by complement activation, have been provided by our group (34). Using an in vitro experimental system we found that encapsulated C. neoformans or purified GXM induced proinflammatory cytokine release by human PMN.…”

mentioning

confidence: 63%

Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material ofCryptococcus neoformans

et al. 1998

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In a previous paper we demonstrated that human polymorphonuclear cells (PMN) in the presence of normal human serum (NHS) secrete proinflammatory cytokines in response to Cryptococcus neoformans or its major capsular component, glucuronoxylomannan (GXM). The hypothesis that activation of the complement system could be responsible for the observed phenomenon is supported by the fact that encapsulated and acapsular C. neoformans isolates are activators of the complement system and, in particular, large encapsulated isolates are powerful activators. In the present study we demonstrate that (i) interleukin-8 (IL-8) release in response to acapsular or encapsulated strains of C. neoformans is significantly reduced in the presence of heatinactivated serum rather than NHS and is completely abrogated in the absence of human serum; (ii) GXMinduced IL-8 release is strictly dependent on the presence of NHS, is inhibited by specific antibodies to either C3a and C5 complement components, and is completely abrogated by the combined use of these antibodies; (iii) the addition of purified C3a and C5a directly stimulates IL-8 release by PMN; and (iv) monoclonal antibody to GXM in combination with GXM or encapsulated C. neoformans potentiates IL-8 release by PMN. These data shed light on the mechanism involved in GXM-induced IL-8 secretion by PMN, provide an additional potential role for complement in the control of C. neoformans infections, and suggest a complex interplay between the complement system, humoral immunity, and cytokine regulation.

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mentioning

confidence: 63%

Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material ofCryptococcus neoformans

et al. 1998

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“…Essentially, the initial (up to 5-6 h) release of chemokines derives from a direct (transcriptional) effect of LPS, whereas the second delayed phase is mainly mediated by the endogenous production of TNF-a in an autocrine/paracrine manner; LPS-stimulated IL-1b also serves as endogenous mediator, acting synergistically with TNF-a (40). Interestingly, other experimental conditions have been reported to have analogies with the above-described network, for instance in the case of neutrophils stimulated with Cryptococcus neoformans (43) or with Toxoplasma gondii antigen (44). However, the autocrine role of endogenous TNF-a in mediating neutrophil-derived chemokine expression and production does not apply to all situations.…”

Section: Cytokine Network Regulating Neutrophil-derived Chemokinesmentioning

confidence: 93%

The neutrophil as a cellular source of chemokines

Scapini

Lapinet-Vera

Gasperini

et al. 2000

Immunological Reviews

692

538

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Neutrophils are known to play an important role in inflammatory responses by virtue of their ability to perform a series of effector functions that collectively represent a major mechanism of innate immunity against injury and infection. In recent years, however, it has become obvious that the contribution of neutrophils to host defence and natural immunity extends well beyond their traditional role as professional phagocytes. Indeed, neutrophils can be induced to express a number of genes whose products lie at the core of inflammatory and immune responses. These include not only Fc receptors, complement components, cationic antimicrobial and NADPH oxidase proteins, but also a variety of cytokines (including tumour necrosis factor-alpha, interleukin (IL)-1beta, IL-1R alpha, IL-12 and vascular endothelial growth factor), and chemokines such as IL-8, growth-related gene product, macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, interferon-gamma-inducible protein of 10 kDa and monokine induced by interferon-gamma. Because these chemokines are primarily chemotactic for neutrophils, monocytes, immature dendritic cells and T-lymphocyte subsets, a potential role for neutrophils in orchestrating the sequential recruitment of distinct leukocyte types to the inflamed tissue is likely to occur. The purpose of this review is to summarize the essential features of the production of chemokines by polymorphonuclear neutrophil leukocytes and the contribution that we have made to characterize some aspects of this newly discovered crucial function of neutrophils.

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“…Tissue GXM levels correlated with the cfu determinations and the capsular size of the yeast in the respective tissues. Although GXM can be cleared from serum over several days (Lendvai et al, 1998), deposition in organs and the presence of GXM in serum has diverse adverse effects on immune cell function (Retini et al, 1996), including downregulation of T-cell responses (Vecchiarelli, 2007), inhibition of neutrophil chemotaxis (Dong and Murphy, 1996;Monari et al, 2002) and impared macrophage killing (Monari et al, 2003).…”

Section: Figurementioning

confidence: 99%

Cryptococcus neoformans responds to mannitol by increasing capsule size in vitro and in vivo

Guimarães¹,

Frasés²,

Cordero³

et al. 2010

Cellular Microbiology

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SummaryThe polysaccharide capsule of the fungus Cryptococcus neoformans is its main virulence factor. In this study, we determined the effects of mannitol and glucose on the capsule and exopolysaccharide production. Growth in mannitol significantly increased capsular volume compared with cultivation in glucose. However, cells grown in glucose concentrations higher than 62.5 mM produced more exopolysaccharide than cells grown in mannitol. The fibre lengths and glycosyl composition of capsular polysaccharide from yeast grown in mannitol was structurally different from that of yeast grown in glucose. Furthermore, mannitol treatment of mice infected intratracheally with C. neoformans resulted in fungal cells with significantly larger capsules and the mice had reduced fungal dissemination to the brain. Our results demonstrate the capacity of carbohydrate source and concentration to modify the expression of a major virulence factor of C. neoformans. These findings may impact the clinical management of cryptococcosis. Introductionc mi_1430 740..753

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Capsular polysaccharide of Cryptococcus neoformans induces proinflammatory cytokine release by human neutrophils

Cited by 127 publications

References 31 publications

Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material ofCryptococcus neoformans

Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material ofCryptococcus neoformans

The neutrophil as a cellular source of chemokines

Cryptococcus neoformans responds to mannitol by increasing capsule size in vitro and in vivo

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