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Microbe-Host Interactions are Positively and Negatively Regulated by Galectin-Glycan Interactions.

Baum LG, Garner OB, Schaefer K, Lee B - Front Immunol (2014)

Bottom Line: Microbe-host interactions are complex processes that are directly and indirectly regulated by a variety of factors, including microbe presentation of specific molecular signatures on the microbial surface, as well as host cell presentation of receptors that recognize these pathogen signatures.Cell surface glycans are one important class of microbial signatures that are recognized by a variety of host cell lectins.Host cell lectins that recognize microbial glycans include members of the galectin family of lectins that recognize specific glycan ligands on viruses, bacteria, fungi, and parasites.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California Los Angeles , Los Angeles, CA , USA.

ABSTRACT
Microbe-host interactions are complex processes that are directly and indirectly regulated by a variety of factors, including microbe presentation of specific molecular signatures on the microbial surface, as well as host cell presentation of receptors that recognize these pathogen signatures. Cell surface glycans are one important class of microbial signatures that are recognized by a variety of host cell lectins. Host cell lectins that recognize microbial glycans include members of the galectin family of lectins that recognize specific glycan ligands on viruses, bacteria, fungi, and parasites. In this review, we will discuss the ways that the interactions of microbial glycans with host cell galectins positively and negatively regulate pathogen attachment, invasion, and survival, as well as regulate host responses that mitigate microbial pathogenesis.

No MeSH data available.


Related in: MedlinePlus

Host-derived galectins can positively and negatively regulate microbe–host interactions. (A) Galectins can promote microbial attachment to and infection of host cells by bridging pathogen glycans to host cell surface glycans. (B) Galectins can inhibit microbial attachment and infection by binding to host or microbial glycans and blocking molecular interactions essential for microbial binding and entry, or by binding to glycans on nascent microbes, such as budding viruses, and preventing proper structural assembly. (C) Galectins can be directly microbicidal, an effect regulated by expression of specific glycan ligands on the pathogen surface.
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Figure 1: Host-derived galectins can positively and negatively regulate microbe–host interactions. (A) Galectins can promote microbial attachment to and infection of host cells by bridging pathogen glycans to host cell surface glycans. (B) Galectins can inhibit microbial attachment and infection by binding to host or microbial glycans and blocking molecular interactions essential for microbial binding and entry, or by binding to glycans on nascent microbes, such as budding viruses, and preventing proper structural assembly. (C) Galectins can be directly microbicidal, an effect regulated by expression of specific glycan ligands on the pathogen surface.

Mentions: In many organisms, galectins have been described as participating in recognition and defense against microbial pathogens. Several recent reviews have addressed the indirect effects of galectins on microbial pathogenesis through regulation of innate and adaptive immunity, e.g., promoting dendritic cell maturation and migration, enhancing cytokine production, or initiating release of intracellular mediators such as histamine (14, 15, 19–21). In contrast, we will specifically address mechanisms by which galectins directly interact with microbial pathogens to effect three distinct outcomes – enhancement of microbial infection, blockade of microbial infection, or microbicidal activity (Figure 1).


Microbe-Host Interactions are Positively and Negatively Regulated by Galectin-Glycan Interactions.

Baum LG, Garner OB, Schaefer K, Lee B - Front Immunol (2014)

Host-derived galectins can positively and negatively regulate microbe–host interactions. (A) Galectins can promote microbial attachment to and infection of host cells by bridging pathogen glycans to host cell surface glycans. (B) Galectins can inhibit microbial attachment and infection by binding to host or microbial glycans and blocking molecular interactions essential for microbial binding and entry, or by binding to glycans on nascent microbes, such as budding viruses, and preventing proper structural assembly. (C) Galectins can be directly microbicidal, an effect regulated by expression of specific glycan ligands on the pathogen surface.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061488&req=5

Figure 1: Host-derived galectins can positively and negatively regulate microbe–host interactions. (A) Galectins can promote microbial attachment to and infection of host cells by bridging pathogen glycans to host cell surface glycans. (B) Galectins can inhibit microbial attachment and infection by binding to host or microbial glycans and blocking molecular interactions essential for microbial binding and entry, or by binding to glycans on nascent microbes, such as budding viruses, and preventing proper structural assembly. (C) Galectins can be directly microbicidal, an effect regulated by expression of specific glycan ligands on the pathogen surface.
Mentions: In many organisms, galectins have been described as participating in recognition and defense against microbial pathogens. Several recent reviews have addressed the indirect effects of galectins on microbial pathogenesis through regulation of innate and adaptive immunity, e.g., promoting dendritic cell maturation and migration, enhancing cytokine production, or initiating release of intracellular mediators such as histamine (14, 15, 19–21). In contrast, we will specifically address mechanisms by which galectins directly interact with microbial pathogens to effect three distinct outcomes – enhancement of microbial infection, blockade of microbial infection, or microbicidal activity (Figure 1).

Bottom Line: Microbe-host interactions are complex processes that are directly and indirectly regulated by a variety of factors, including microbe presentation of specific molecular signatures on the microbial surface, as well as host cell presentation of receptors that recognize these pathogen signatures.Cell surface glycans are one important class of microbial signatures that are recognized by a variety of host cell lectins.Host cell lectins that recognize microbial glycans include members of the galectin family of lectins that recognize specific glycan ligands on viruses, bacteria, fungi, and parasites.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California Los Angeles , Los Angeles, CA , USA.

ABSTRACT
Microbe-host interactions are complex processes that are directly and indirectly regulated by a variety of factors, including microbe presentation of specific molecular signatures on the microbial surface, as well as host cell presentation of receptors that recognize these pathogen signatures. Cell surface glycans are one important class of microbial signatures that are recognized by a variety of host cell lectins. Host cell lectins that recognize microbial glycans include members of the galectin family of lectins that recognize specific glycan ligands on viruses, bacteria, fungi, and parasites. In this review, we will discuss the ways that the interactions of microbial glycans with host cell galectins positively and negatively regulate pathogen attachment, invasion, and survival, as well as regulate host responses that mitigate microbial pathogenesis.

No MeSH data available.


Related in: MedlinePlus