Immune Responses to the Microbiota at the Intestinal Mucosal Surface

Duerkop, Breck A.; Vaishnava, Shipra; Hooper, Lora V.

doi:10.1016/j.immuni.2009.08.009

Cited by 357 publications

(251 citation statements)

References 79 publications

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“…The two-layered mucus organization is probably instrumental for a balanced and symbiotic relation between host and bacteria (3,50). This concept, with an inner mucus layer shielding the colon epithelial cells from bacteria, is new, and as usual in science, new concepts raise new questions.…”

Section: Summary Of Goblet Cell and Mucus Turnovermentioning

confidence: 99%

The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions

Johansson

Larsson

Hansson

2010

Proc. Natl. Acad. Sci. U.S.A.

1,079

961

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The normal intestinal microbiota inhabits the colon mucus without triggering an inflammatory response. The reason for this and how the intestinal mucus of the colon is organized have begun to be unraveled. The mucus is organized in two layers: an inner, stratified mucus layer that is firmly adherent to the epithelial cells and approximately 50 μm thick; and an outer, nonattached layer that is usually approximately 100 μm thick as measured in mouse. These mucus layers are organized around the highly glycosylated MUC2 mucin, forming a large, net-like polymer that is secreted by the goblet cells. The inner mucus layer is dense and does not allow bacteria to penetrate, thus keeping the epithelial cell surface free from bacteria. The inner mucus layer is converted into the outer layer, which is the habitat of the commensal flora. The outer mucus layer has an expanded volume due to proteolytic activities provided by the host but probably also caused by commensal bacterial proteases and glycosidases. The numerous O-glycans on the MUC2 mucin not only serve as nutrients for the bacteria but also as attachment sites and, as such, probably contribute to the selection of the species-specific colon flora. This observation that normal human individuals carry a uniform MUC2 mucin glycan array in colon may indicate such a specific selection.bacteria | intestine | goblet cell | glycoprotein | colitis

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Section: Summary Of Goblet Cell and Mucus Turnovermentioning

confidence: 99%

The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions

Johansson

Larsson

Hansson

2010

Proc. Natl. Acad. Sci. U.S.A.

1,079

961

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“…To test this possibility, we Freely available online through the PNAS open access option. 1 To whom correspondence should be addressed. E-mail: lora.hooper@utsouthwestern.…”

Section: E Faecalis V583 Produces Composite Bacteriophage Particlesmentioning

confidence: 99%

“…commensal bacteria | microbiota | enterococci | phage predation T he human gastrointestinal tract is colonized with a highly diverse population of bacteria (1). Many of these bacteria produce bacteriophage (phage), further increasing the complexity of this ecosystem.…”

mentioning

confidence: 99%

A composite bacteriophage alters colonization by an intestinal commensal bacterium

Duerkop¹,

Clements

Rollins

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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186

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The mammalian intestine is home to a dense community of bacteria and its associated bacteriophage (phage). Virtually nothing is known about how phages impact the establishment and maintenance of resident bacterial communities in the intestine. Here, we examine the phages harbored by Enterococcus faecalis, a commensal of the human intestine. We show that E. faecalis strain V583 produces a composite phage (ϕV1/7) derived from two distinct chromosomally encoded prophage elements. One prophage, prophage 1 (ϕV1), encodes the structural genes necessary for phage particle production. Another prophage, prophage 7 (ϕV7), is required for phage infection of susceptible host bacteria. Production of ϕV1/7 is controlled, in part, by nutrient availability, because ϕV1/7 particle numbers are elevated by free amino acids in culture and during growth in the mouse intestine. ϕV1/7 confers an advantage to E. faecalis V583 during competition with other E. faecalis strains in vitro and in vivo. Thus, we propose that E. faecalis V583 uses phage particles to establish and maintain dominance of its intestinal niche in the presence of closely related competing strains. Our findings indicate that bacteriophages can impact the dynamics of bacterial colonization in the mammalian intestinal ecosystem.T he human gastrointestinal tract is colonized with a highly diverse population of bacteria (1). Many of these bacteria produce bacteriophage (phage), further increasing the complexity of this ecosystem. Recent studies of human intestinal viromes have shown that these viromes are dominated by lysogenic prophages that are integrated into the chromosomes of their bacterial hosts (2). In numerous other ecological systems, phages profoundly influence ecological networks by serving as reservoirs of genetic diversity (3, 4) and acting as predators of susceptible bacterial strains (5). However, little is known about how resident phages may influence the assembly and maintenance of bacterial communities in the mammalian intestine.Enterococcus faecalis is an abundant member of the human intestinal microflora, and by adulthood, it can constitute as much as 0.5-0.9% of the total bacterial content of the intestinal tract (Table S1) (6). A Gram-positive facultative anaerobe, E. faecalis is a leading cause of antibiotic-resistant nosocomial bacteremia and endocarditis (7). Genomic sequencing has revealed a high degree of variation among E. faecalis genomes (8). Some of this variation can be attributed to an array of integrated prophage elements that encode components required for the production of phage particles.The first E. faecalis genome to be sequenced was strain V583, a clinical blood isolate that is vancomycin-resistant (9). The V583 chromosome harbors seven putative prophages designated prophages 1-7 (Fig. 1). At least two of these prophage elements seem to encode cryptic or satellite phage genomes (10) that, by themselves, do not produce functional phage particles but may encode accessory components that aid in the lytic cycle of other integrated pro...

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“…In order to contain this microbiota and fight breaches by invading microbes, the intestinal immune system deploys a complex network of lymphoid tissues and cells 2,3 . Part of this system is programmed to develop during ontogeny, such as mesenteric lymph nodes and Peyer's patches, and part of it is induced by the microbiota, such as the formation of numerous isolated lymphoid follicles (ILFs) from pre-formed cryptopatches, and the recruitment of various subsets of intestinal lymphocytes 4 .…”

Section: Introductionmentioning

confidence: 99%

“…Whereas proinflammatory cytokines, such as interferon-γ (IFN-γ), IL-17 and tumor necrosis factor (TNF), promote the elimination of intruding microbes, the anti-inflammatory cytokines IL-10 and TGF-β limit the amplitude of inflammation and favor the production and secretion of IgA, essential to mucosal immunity 2,3 . Another member of the IL-10 cytokine family, IL-22, has been shown to directly induce epithelial defense through the expression of anti-microbial peptides, such as β-defensins 8 , S100A7 (psoriasin), S100A8 (calgranulin A), S100A9 (calgranulin B) 9 , RegIIIβ and RegIIIγ 10 .…”

Section: Introductionmentioning

confidence: 99%

RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota

et al. 2011

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Immune Responses to the Microbiota at the Intestinal Mucosal Surface

Cited by 357 publications

References 79 publications

The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions

The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions

A composite bacteriophage alters colonization by an intestinal commensal bacterium

RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota

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