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Abstract

Melanins are enigmatic pigments that are produced by a wide variety of microorganisms including several species of pathogenic bacteria, fungi and helminths. The study of melanin is difficult because these pigments defy complete biochemical and structural analysis. Nevertheless, the availability of new reagents in the form of monoclonal antibodies and melanin-binding peptides, combined with the application of various physical techniques, has provided insights into the process of melanization. Melanization is important in microbial pathogenesis because it has been associated with virulence in many microorganisms. Melanin appears to contribute to virulence by reducing the susceptibility of melanized microbes to host defence mechanisms. However, the interaction of melanized microbes and the host is complex and includes immune responses to melanin-related antigens. Production of melanin has also been linked to protection against environmental insults. Interference with melanization is a potential strategy for antimicrobial drug and pesticide development. The process of melanization poses fascinating problems in cell biology and provides a type of pathogenic strategy that is common to highly diverse pathogens.

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A role for excreted quinones in extracellular electron transfer.

D K Newman, R Kolter (2000)

Respiratory processes in bacteria are remarkable because of their ability to use a variety of compounds, including insoluble minerals, as terminal electron acceptors. Although much is known about microbial electron transport to soluble electron acceptors, little is understood about electron transport to insoluble compounds such as ferric oxides. In anaerobic environments, humic substances can serve as electron acceptors and also as electron shuttles to ferric oxides. To explore this process, we identified mutants in Shewanella putrefaciens that are unable to respire on humic substances. Here we show that these mutants contain disruptions in a gene that is involved in the biosynthesis of menaquinone. During growth, the wild type releases a menaquinone-related redox-active small molecule into the medium that complements the mutants. This finding raises the possibility that electron transfer to a variety of oxidants, including poorly soluble minerals, may be mediated by microbially excreted quinones that have yet to be identified.

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Cryptococcus neoformans interactions with amoebae suggest an explanation for its virulence and intracellular pathogenic strategy in macrophages.

Judith Steenbergen, H Shuman, A. Casadevall (2001)

Cryptococcus neoformans (Cn) is a soil fungus that causes life-threatening meningitis in immunocompromised patients and is a facultative intracellular pathogen capable of replication inside macrophages. The mechanism by which environmental fungi acquire and maintain virulence for mammalian hosts is unknown. We hypothesized that the survival strategies for Cn after ingestion by macrophages and amoebae were similar. Microscopy, fungal and amoebae killing assays, and phagocytosis assays revealed that Cn is phagocytosed by and replicates in Acanthamoeba castellanii, which leads to death of amoebae. An acapsular strain of Cn did not survive when incubated with amoebae, but melanization protected these cells against killing by amoebae. A phospholipase mutant had a decreased replication rate in amoebae compared with isogenic strains. These observations suggest that cryptococcal characteristics that contribute to mammalian virulence also promote fungal survival in amoebae. Intracellular replication was accompanied by the accumulation of polysaccharide containing vesicles similar to those described in Cn-infected macrophages. The results suggest that the virulence of Cn for mammalian cells is a consequence of adaptations that have evolved for protection against environmental predators such as amoebae and provide an explanation for the broad host range of this pathogenic fungus.

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Breaking and entering: host penetration by the fungal rice blast pathogen Magnaporthe grisea.

R J Howard, B Valent (1996)

Fungal plant pathogens have evolved diverse mechanisms for penetrating into host plant tissue, ranging from entry through natural plant openings to various mechanisms of direct penetration through the outer surface. The filamentous fungus Magnaporthe grisea can cause disease on many species of the grass (Poaceae) family. The disease on rice, Rice Blast, is of enormous economic importance and biological interest. The mechanism used by this pathogen for breaching the formidable host surface barriers has been studied cytologically and genetically as a model for plant pathology, and represents a remarkably sophisticated achievement of nature. The single-celled appressorium of M. grisea acts as a vessel for the generation and application of perhaps the highest turgor pressures known. The fungus requires and utilizes melanin-derived, osmotically generated pressures estimated at 80 bars to drive an actin-rich cellular protuberance through the surface of a rice leaf or plastic coverslip.

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PubMed ID:: 12675679

DOI:: 10.1046/J.1462-5814.2003.00268.X

ScienceOpen disciplines: Chemistry

Keywords: Animals,Bacteria,metabolism,pathogenicity,Fungi,Helminths,Humans,Laccase,Melanins,Oxidoreductases,Phagocytosis,physiology,Virulence

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ScienceOpen disciplines: Chemistry

Keywords: Animals, Bacteria, metabolism, pathogenicity, Fungi, Helminths, Humans, Laccase, Melanins, Oxidoreductases, Phagocytosis, physiology, Virulence

The contribution of melanin to microbial pathogenesis.

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Microbiology Independent Research Journal (MIR Journal)

Most cited references 128

A role for excreted quinones in extracellular electron transfer.

Cryptococcus neoformans interactions with amoebae suggest an explanation for its virulence and intracellular pathogenic strategy in macrophages.

Breaking and entering: host penetration by the fungal rice blast pathogen Magnaporthe grisea.

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