Monoclonal Antibody Detection of CD46 Clustering beneath
            <i>Neisseria gonorrhoeae</i>
            Microcolonies

Weyand, Nathan J.; Lee, Shaun W.; Higashi, Dustin L.; Cawley, Daniel B.; Yoshihara, Paul; So, Magdalene

doi:10.1128/iai.74.4.2428-2435.2006

Cited by 17 publications

(23 citation statements)

References 45 publications

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“…Further analysis by SDS-PAGE and western blotting identified β3 integrin as one of the biotinylated, thus apical proteins. The membrane cofactor CD46, which was reported to localize to the apical membrane compartment 23 , was also significantly biotinylated from the apical side, similar to β3 integrin ( to CM-stimulated 16HBE14o cells strongly reduced Ad5-muIL2 infection, whereas anti-ανβ5 integrin antibodies had no significant effects (Fig. 4e).…”

Section: Cxcl8 Mediates Apical Adenovirus Infectionmentioning

confidence: 84%

Chemotactic antiviral cytokines promote infectious apical entry of human adenovirus into polarized epithelial cells

et al. 2011

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mucosal epithelia provide strong barriers against pathogens. For instance, the outward facing apical membrane of polarized epithelial cells lacks receptors for agents, such as hepatitis C virus, herpesvirus, reovirus, poliovirus or adenovirus. In addition, macrophages eliminate pathogens from the luminal space. Here we show that human adenovirus type 5 engages an antiviral immune response to enter polarized epithelial cells. Blood-derived macrophages co-cultured apically on polarized epithelial cells facilitate epithelial infection. Infection also occurs in the absence of macrophages, if virus-conditioned macrophage-medium containing the chemotactic cytokine CXCL8 (interleukin-8), or recombinant CXCL8 are present. In polarized cells, CXCL8 activates a src-family tyrosine kinase via the apical CXCR1 and CXCR2 receptors. This activation process relocates the viral co-receptor ανβ3 integrin to the apical surface, and enables apical binding and infection with adenovirus depending on the primary adenovirus receptor CAR. This paradigm may explain how other mucosal pathogens enter epithelial cells.

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Section: Cxcl8 Mediates Apical Adenovirus Infectionmentioning

confidence: 84%

Chemotactic antiviral cytokines promote infectious apical entry of human adenovirus into polarized epithelial cells

et al. 2011

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“…The major pilin from Neisseria, PilE, was reported to hemagglutinate erythrocytes (351) and to mediate binding to host proteins on endothelial cells (110). The receptor for Neisseria pili was proposed to be CD46 (214,413), although newer evidence suggests otherwise (224).…”

Section: Adherence and Aggregationmentioning

confidence: 99%

Type IV Pilin Proteins: Versatile Molecular Modules

Giltner

Nguyen

Burrows

2012

Microbiol Mol Biol Rev

398

519

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SUMMARYType IV pili (T4P) are multifunctional protein fibers produced on the surfaces of a wide variety of bacteria and archaea. The major subunit of T4P is the type IV pilin, and structurally related proteins are found as components of the type II secretion (T2S) system, where they are called pseudopilins; of DNA uptake/competence systems in both Gram-negative and Gram-positive species; and of flagella, pili, and sugar-binding systems in the archaea. This broad distribution of a single protein family implies both a common evolutionary origin and a highly adaptable functional plan. The type IV pilin is a remarkably versatile architectural module that has been adopted widely for a variety of functions, including motility, attachment to chemically diverse surfaces, electrical conductance, acquisition of DNA, and secretion of a broad range of structurally distinct protein substrates. In this review, we consider recent advances in this research area, from structural revelations to insights into diversity, posttranslational modifications, regulation, and function.

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“…Tfp retraction recruits host cell components to the cortex beneath adhered microcolonies. These cortical plaques are enriched in cytoskeletal and signalling proteins (Edwards et al, 2000;Lee et al, 2005;Merz et al, 1999;Weyand et al, 2006), some of which have been shown to play a role in invasion (Lee et al, 2005;Shaw & Falkow, 1988). The relationship between the cortical plaque and the microcolony is dynamic.…”

Section: Introductionmentioning

confidence: 99%

Influence of type IV pilus retraction on the architecture of the Neisseria gonorrhoeae-infected cell cortex

et al. 2009

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Early in infection, Neisseria gonorrhoeae can be observed to attach to the epithelial cell surface as microcolonies and induce dramatic changes to the host cell cortex. We tested the hypothesis that type IV pili (Tfp) retraction plays a role in the ultrastructure of both the host cell cortex and the bacterial microcolony. Using serial ultrathin sectioning, transmission electron microscopy and 3D reconstruction of serial 2D images, we have obtained what we believe to be the first 3D reconstructions of the N. gonorrhoeae-host cell interface, and determined the architecture of infected cell microvilli as well as the attached microcolony. Tfp connect both wild-type (wt) and Tfp retraction-deficient bacteria with each other, and with the host cell membrane. Tfp fibres and microvilli form a lattice in the wt microcolony and at its periphery. Wt microcolonies induce microvilli formation and increases of surface area, leading to an approximately ninefold increase in the surface area of the host cell membrane at the site of attachment. In contrast, Tfp retractiondeficient microcolonies do not affect these parameters. Wt microcolonies had a symmetrical, dome-shaped structure with a circular 'footprint', while Tfp retraction-deficient microcolonies were notably less symmetrical. These findings support a major role for Tfp retraction in microvilli and microcolony architecture. They are consistent with the biophysical attributes of Tfp and the effects of Tfp retraction on epithelial cell signalling. INTRODUCTIONNeisseria gonorrhoeae (the gonococcus, or GC) remains a significant public health concern. The Gram-negative diplococcus causes a million cases of gonorrhoea annually in Western Europe and North America, and over 62 million cases worldwide (World Health Organization). Humans are the only known reservoir for GC. The exquisite tropism of GC for man and the ability of GC to establish a carrier state (Turner et al., 2002) reflect a highly evolved relationship between pathogen and host.Gonococcal attachment is promoted by type IV pili (Tfp), peritrichous fibres that are 6 nm in width and up to several micrometres in length. The Tfp filament is composed of helical polymers of pilin subunits (Craig et al., 2006;Parge et al., 1995) and minor proteins (Carbonnelle et al., 2005;Winther-Larsen et al., 2005). Tfp participate in important biological processes such as DNA uptake/genetic exchange, twitching motility, attachment, and host cell signalling (Mattick, 2002;. These activities require, or are enhanced by, the retraction of Tfp fibres (Wolfgang et al., 2000).Gonococcal Tfp retraction is an activity that requires PilT, the Tfp retraction motor subunit (Wolfgang et al., 1998). Retracting Tfp generate strong 'pull' forces, ranging from 50 picoNewtons (pN) to 1 nanoNewton (nN) (Biais et al., 2008;Opitz et al., 2009). Repeated cycles of Tfp extension, substrate attachment and Tfp retraction allow GC to crawl over surfaces and aggregate into microcolonies. Tfp retraction from bacteria in a microcolony allows the community to craw...

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Monoclonal Antibody Detection of CD46 Clustering beneath Neisseria gonorrhoeae Microcolonies

Cited by 17 publications

References 45 publications

Chemotactic antiviral cytokines promote infectious apical entry of human adenovirus into polarized epithelial cells

Chemotactic antiviral cytokines promote infectious apical entry of human adenovirus into polarized epithelial cells

Type IV Pilin Proteins: Versatile Molecular Modules

Influence of type IV pilus retraction on the architecture of the Neisseria gonorrhoeae-infected cell cortex

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