Genetic Mechanisms of Surface Variation

Yogev, David; Browning, Glenn F.; Wise, Kim S.

doi:10.1007/0-306-47606-1_19

Cited by 38 publications

(50 citation statements)

References 86 publications

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“…MALP-404, like other lipoproteins from Mycoplasma, is an immune dominant Ag (22). It is likely that this high immunogenicity arises from the covalently linked lipid moiety, which acts as a danger signal (1-3) by stimulating the innate immune system via the pattern recognition receptor TLR 2/6.…”

Section: Discussionmentioning

confidence: 99%

The Mucosal Adjuvant Macrophage-Activating Lipopeptide-2 Directly Stimulates B Lymphocytes via the TLR2 without the Need of Accessory Cells

Borsutzky

Kretschmer

Becker

et al. 2005

The Journal of Immunology

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The macrophage-activating lipopeptide-2 (MALP-2) is an agonist of the TLR heterodimer 2/6, which exhibits potent activity as mucosal adjuvant, promoting strong humoral and cellular responses. Although B cells expressing TLR2/6 are potential targets, very little is known about the effect of MALP-2 on B cells. Studies were performed using total spleen cells or purified B cells from WT mice or animals deficient in TLR2, T cells, B cells, or specific subpopulations of B cells. They demonstrated that MALP-2 promotes a T cell-independent activation and maturation of B cells (mainly follicular but also B-1a and marginal zone B cells) via TLR2. MALP-2 also increased the frequency of IgM- and IgG-secreting cells, but bystander cells were required for IgA secretion. Activated B cells exhibited increased expression of activation markers and ligands that are critical for cross-talk with T cells (CD19, CD25, CD80, CD86, MHC I, MHC II, and CD40). Immunization of mice lacking T cells showed that MALP-2-mediated stimulation of TLR2/6 was unable to circumvent the need of T cell help for efficient Ag-specific B cell activation. Immunization of mice lacking B cells demonstrated that B cells are critical for MALP-2-dependent improvement of T cell responses. The knowledge emerging from this work suggests that MALP-2-mediated activation of B cells through TLR2/6 is critical for adjuvanticity. B cell stimulation by pattern recognition receptors seems to be a basic mechanism that can be exploited to improve the immunogenicity of vaccine formulations.

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Section: Discussionmentioning

confidence: 99%

The Mucosal Adjuvant Macrophage-Activating Lipopeptide-2 Directly Stimulates B Lymphocytes via the TLR2 without the Need of Accessory Cells

Borsutzky

Kretschmer

Becker

et al. 2005

The Journal of Immunology

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“…It also increases the risk of their dissemination by the hands of the milker (Al-Momani et al 2008). The mollicutes can adapt themselves to different hosts, and mutations have been reported as a survival mechanism (Yogev et al 2002).…”

Section: Resultsmentioning

confidence: 99%

Assessment of cow and farm level risk factors associated with Ureaplasma diversum in pasture-based dairy systems - A field study

Nascimento-Rocha¹,

Filho

Arnhold

et al. 2017

An. Acad. Bras. Ciênc.

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Potential risk factors for Ureaplasma diversum in the vaginal mucus of 1,238 dairy cows were included in a multivariate logistic regression model, based on the cow level (i.e., granular vulvovaginitis [+GVV], yearly milk production [4500 kg or more], pregnancy, predominance of Bos taurus [+Bos Taurus], score of corporal condition [at least 2.5], concomitant positivity for Escherichia coli [+E.coli]), and farm level i.e., milking room hygiene (-Milking room), dunghill location, and replacement female). Ureaplasma diversum was present in 41.1% of the samples. Independent risk factors for U. diversum were +GVV (odds ratio [OR], 1.31); +Mycoplasma spp (OR, 5.67); yearly milk production (4500 kg or more) (OR, 1.99); +Bos taurus (OR, 1.68); +E. coli (OR, 4.96); -milking room (OR, 2.31); and replacement females (OR, 1.89). Ureaplasma diversum vaginal colonization was strongly associated with Mycoplasma spp., E. coli, and number of pregnant cows.

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“…The molecular mechanisms responsible for this immune evasion are not fully understood; however, a number of recent studies have suggested probable mechanisms for continuous infection of mycoplasmas; these include molecular mimicry of host cell components (Jacobs et al, 1995), modulation of host immunity by mycoplasmal cell components (Rottem, 2003), invasion of host cells and generation of surface antigen variants of mycoplasmas (Denison et al, 2005;Rosengarten et al, 2000). Among these strategies, surface antigenic variation is a commonly observed phenomenon in many mycoplasma species (Citti et al, 2005;Yogev et al, 2002). Surface variations may play important roles in interaction between mycoplasmas and host cells during Abbreviations: Tsr, tyrosine site-specific recombinase; Ap, ampicillin; Cm, chloramphenicol; Gm, gentamicin; Km, kanamycin; Sp, spectinomycin; IR, inverted repeat.…”

Section: Introductionmentioning

confidence: 99%

Identification of a site-specific tyrosine recombinase that mediates promoter inversions of phase-variable mpl lipoprotein genes in Mycoplasma penetrans

et al. 2009

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Mycoplasma penetrans has the ability to change its surface lipoprotein profiles frequently. The P35 family lipoproteins encoded by the mpl genes are key players in this profile variation. The M. penetrans HF-2 genome has 38 mpl genes that form three gene clusters. Most of these mpl genes have an invertible promoter sequence that is responsible for the ON/OFF switching of individual mpl gene expression. Here, we identified the recombinase that catalyses inversions of the mpl gene promoters. We focused on two open reading frames of the M. penetrans HF-2 genome, namely MYPE2900 and MYPE8180, which show significant homology to the tyrosine site-specific recombinase (Tsr) family proteins. Since genetic tools for M. penetrans are still not developed, we cloned the MYPE2900 and MYPE8180 genes and expressed them in Mycoplasma pneumoniae and Escherichia coli. The promoter regions of the mpl genes [p35 (MYPE6810) or p42 (MYPE6630) genes] were also introduced into M. pneumoniae and E. coli cells expressing MYPE2900 or MYPE8180. Inversion of these promoters occurred in the presence of the MYPE2900 gene but not in the presence of the MYPE8180 gene, indicating that the MYPE2900 gene product is the recombinase that catalyses mpl gene promoter inversions. We used a PCR-based method to detect mpl promoter inversion. This method also enabled us to detect inversions of 10 mpl gene promoters in M. penetrans HF-2 cells. All these promoter inversions occurred at the 12 bp inverted repeat (IR) sequences flanking the promoter sequence. The consensus sequence of these IRs was proposed as TAAYNNNDATTA (Y5C or T; D5A, G or T). INTRODUCTIONMycoplasmas belong to a group of bacteria with no cell wall and have the minimum range of genome sizes that are necessary for self-replication. Their small genomes (580-1350 kb) sequenced to date lack numerous genes required for biosynthetic pathways, thus reflecting their parasitic lifestyle with a dependence on host organisms for nutrient acquisition. Mycoplasmas usually inhabit the mucosal tissues of specific host organisms. Almost 200 mycoplasma species have been isolated from a wide range of host organisms, including humans. Several of these species are well recognized as pathogens (Sasaki, 2006;Waites et al., 2005). As parasitic bacteria, mycoplasmas can continue to colonize their host even in the presence of specific immune responses. The molecular mechanisms responsible for this immune evasion are not fully understood; however, a number of recent studies have suggested probable mechanisms for continuous infection of mycoplasmas; these include molecular mimicry of host cell components (Jacobs et al., 1995), modulation of host immunity by mycoplasmal cell components (Rottem, 2003), invasion of host cells and generation of surface antigen variants of mycoplasmas (Denison et al., 2005;Rosengarten et al., 2000). Among these strategies, surface antigenic variation is a commonly observed phenomenon in many mycoplasma species (Citti et al., 2005;Yogev et al., 2002). Surface variations may play important...

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Genetic Mechanisms of Surface Variation

Cited by 38 publications

References 86 publications

The Mucosal Adjuvant Macrophage-Activating Lipopeptide-2 Directly Stimulates B Lymphocytes via the TLR2 without the Need of Accessory Cells

The Mucosal Adjuvant Macrophage-Activating Lipopeptide-2 Directly Stimulates B Lymphocytes via the TLR2 without the Need of Accessory Cells

Assessment of cow and farm level risk factors associated with Ureaplasma diversum in pasture-based dairy systems - A field study

Identification of a site-specific tyrosine recombinase that mediates promoter inversions of phase-variable mpl lipoprotein genes in Mycoplasma penetrans

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