Bacterial Capsules and Evasion of Immune Responses

Merino, Susana; Jm, Tomás

doi:10.1002/9780470015902.a0000957.pub3

Cited by 14 publications

(11 citation statements)

References 30 publications

(18 reference statements)

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“…Pathogens often resist recognition and subsequent complement activation owing to their surface capsular polysaccharide, which masks underlying structures and by itself activates complement poorly (5)(6)(7). In addition, secretion of the exopolysaccharide colanic acid protects UPEC from complement-mediated killing (8).…”

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confidence: 99%

Phenotypic Heterogeneity Enables Uropathogenic Escherichia coli To Evade Killing by Antibiotics and Serum Complement

et al. 2015

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Uropathogenic strains of Escherichia coli (UPEC) are the major cause of bacteremic urinary tract infections. Survival in the bloodstream is associated with different mechanisms that help to resist serum complement-mediated killing. While the phenotypic heterogeneity of bacteria has been shown to influence antibiotic tolerance, the possibility that it makes cells refractory to killing by the immune system has not been experimentally tested. In the present study we sought to determine whether the heterogeneity of bacterial cultures is relevant to bacterial targeting by the serum complement system. We monitored cell divisions in the UPEC strain CFT073 with fluorescent reporter protein. T he immune system has several pathways for recognizing and killing pathogenic bacteria. However, some pathogenic bacteria can maintain infection in mammalian hosts despite inflammation, specific antimicrobial mechanisms, and a robust adaptive immune response and can therefore give rise to persistent infection (1). Uropathogenic Escherichia coli (UPEC) causes recurrent urinary tract infections that can progress from the lower to the upper urinary tract and can lead to the dissemination of bacteria into the bloodstream.The complement system is part of the defense against invading pathogens, with an essential role in both innate and adaptive immunity (2). It is composed of more than 40 plasma and membrane proteins. It can be activated via three distinct routes: the classical (antibody dependent), lectin, and alternative pathways. Activation of complement cascades leads to the formation of the key component C3b on the bacterial surface, which stimulates phagocytosis. Late complement components (C5 to C9 proteins) are also activated via C3b, resulting in the formation of the membrane attack complex (MAC) causing cell lysis (2). The primary source of complement is blood, but complement proteins are also synthesized by a variety of other cell types and tissues (3).Bacterial resistance to serum complement killing depends on the presence or absence of antigenic outer membrane proteins (4). Pathogens often resist recognition and subsequent complement activation owing to their surface capsular polysaccharide, which masks underlying structures and by itself activates complement poorly (5-7). In addition, secretion of the exopolysaccharide colanic acid protects UPEC from complement-mediated killing (8). Modification of lipopolysaccharide (LPS) is also important for complement evasion (9, 10). It has been shown that serum sensitivity depends on the bacterial growth phase; cells are more readily killed by serum during early logarithmic phase (11)(12)(13)(14). However, there are examples showing that exponential-phase cells are more resistant to complement-mediated killing than stationary-phase cells (15,16). That phenomenon is largely explained by the growth-phase-dependent expression of antigens, capsule, and LPS modification (14, 15). Cell size can also be an important determinant of complement-mediated killing, since larger or aggregated cells ...

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confidence: 99%

Phenotypic Heterogeneity Enables Uropathogenic Escherichia coli To Evade Killing by Antibiotics and Serum Complement

et al. 2015

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“…It is appreciated that one function of bacterial capsules is to shield immunogenic structures present on the surface of the microorganisms (14). Indeed, attenuated strains of Francisella lacking capsule triggered even higher pro-inflammatory responses than encapsulated wild type strains (24, 25).…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial capsules are generally thought to contribute to evasion of host defenses by cloaking immunostimulatory structures present on the bacterial surface, providing resistance to complement mediated killing, and limiting phagocytosis by host cells [as reviewed, (14)]. However, there is some data suggesting that capsular material may take a more active role in modulating the immune response by suppressing the ability of host cells to mount protective inflammatory responses (15).…”

Section: Introductionmentioning

confidence: 99%

Metabolic Reprogramming of Host Cells by Virulent Francisella tularensis for Optimal Replication and Modulation of Inflammation

Wyatt

Diaz

Griffin

et al. 2016

The Journal of Immunology

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A shift in macrophage metabolism from oxidative phosphorylation to aerobic glycolysis is a requirement for activation to effectively combat invading pathogens. Francisella tularensis is a facultative intracellular bacterium that causes an acute, fatal disease called tularemia. Its primary mechanism of virulence is its ability to evade and suppress inflammatory responses while replicating in the cytosol of macrophages. The means by which F. tularensis modulates macrophage activation are not fully elucidated. Here we demonstrate that virulent F. tularensis impairs production of inflammatory cytokines in primary macrophages by preventing their shift to aerobic glycolysis, as evidenced by the down regulation of HIF-1α, and failure to upregulate pfkfb3. We also uncover that Francisella capsule is required for this process. In addition to modulating inflammatory responses, inhibition of glycolysis in host cells is also required for early replication of virulent Francisella. Together our data demonstrate that metabolic reprogramming of host cells by F. tularensis is a key component of both inhibition of host defense mechanisms and replication of the bacterium.

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“…The bacterial sEPS was first studied and characterized in pathogens, where such macromolecules play a crucial role as a virulence factor in the interaction of the bacterium with its host through modulation of the immune system [65]. …”

Section: Intestinal Functionmentioning

confidence: 99%

Diversity, ecology and intestinal function of bifidobacteria

et al. 2014

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The human gastrointestinal tract represents an environment which is a densely populated home for a microbiota that has evolved to positively contribute to host health. At birth the essentially sterile gastrointestinal tract (GIT) is rapidly colonized by microorganisms that originate from the mother and the surrounding environment. Within a short timeframe a microbiota establishes within the (breastfed) infant's GIT where bifidobacteria are among the dominant members, although their numerical dominance disappears following weaning. The numerous health benefits associated with bifidobacteria, and the consequent commercial relevance resulting from their incorporation into functional foods, has led to intensified research aimed at the molecular understanding of claimed probiotic attributes of this genus. In this review we provide the current status on the diversity and ecology of bifidobacteria. In addition, we will discuss the molecular mechanisms that allow this intriguing group of bacteria to colonize and persist in the GIT, so as to facilitate interaction with its host.

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Bacterial Capsules and Evasion of Immune Responses

Cited by 14 publications

References 30 publications

Phenotypic Heterogeneity Enables Uropathogenic Escherichia coli To Evade Killing by Antibiotics and Serum Complement

Phenotypic Heterogeneity Enables Uropathogenic Escherichia coli To Evade Killing by Antibiotics and Serum Complement

Metabolic Reprogramming of Host Cells by Virulent Francisella tularensis for Optimal Replication and Modulation of Inflammation

Diversity, ecology and intestinal function of bifidobacteria

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