Host-pathogen interactions in mycoplasma pathogenesis: Virulence and survival strategies of minimalist prokaryotes

Rosengarten, Renate; Citti, Christine; Glew, Michelle D.; Lischewski, A.; Droesse, Martina; Much, Peter; Winner, Florian; Brank, Marion; Spergser, Joachim

doi:10.1016/s1438-4221(00)80099-5

Cited by 108 publications

(103 citation statements)

References 46 publications

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“…This bacterium is host dependent in nature, but it can be grown in the laboratory without a host cell in a rich medium supplemented with serum (Hayflick, 1965). M. pneumoniae is the causative agent of a primary atypical pneumonia in humans (Jacobs, 1991;Principi & Esposito, 2001;Rosengarten et al, 2000;Taylor-Robinson, 1996). Epidemic outbreaks were registered in time-intervals of 3-7 years followed by endemic phases in the epidemiology of M. pneumoniae infections (Jacobs et al, 1996;Lind et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Cross-complementation between the products of the genes P1 and ORF6 of Mycoplasma pneumoniae subtypes 1 and 2

Catrein

Dumke²,

Weiner

et al. 2004

Microbiology

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The genes P1 (MPN141) and ORF6 (MPN142) are essential for the successful colonization of the human respiratory tract by Mycoplasma pneumoniae. Both genes are located in the P1 operon, which consists of three genes. The P1 gene is the second gene in the operon, followed by the ORF6 gene. The P1 gene contains two (RepMP2/3, RepMP4) and the ORF6 gene one (RepMP5) specific repetitive DNA sequence, of which seven to nine similar but not identical copies are dispersed on the genome. Despite this large potential pool for genetic variation, M. pneumoniae isolates from patients contain only one of two distinct combinations of the genes P1 and ORF6. To analyse the functions of the repetitive DNA sequences, two 'new' combinations of the genes P1 and ORF6 were constructed, keeping the P1 gene constant but exchanging RepMP5 copies of the ORF6 gene. M. pneumoniae was transformed with these constructs and the transformants were tested for their ability to grow and survive under in vitro conditions and in guinea pigs. The two transformants colonized the respiratory tract of guinea pigs and showed no obvious differences in their growth behaviour compared to M. pneumoniae isolates from patients. The results indicate that the subtype-specific combinations of the repetitive elements in the P1 and ORF6 genes are not essential for the successful adherence of M. pneumoniae to host cells and the colonization of the respiratory tract of guinea pigs.

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Section: Introductionmentioning

confidence: 99%

Cross-complementation between the products of the genes P1 and ORF6 of Mycoplasma pneumoniae subtypes 1 and 2

Catrein

Dumke²,

Weiner

et al. 2004

Microbiology

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“…However, it was 25 years ago that the human mycoplasmas, M. penetrans and M. genitalium, were first shown conclusively to enter host cells [11] and since then many others including important animal pathogens like M. gallisepticum, M. agalactiae and M. bovis have also been shown to be intracellular. It should not be too much of a surprise as it is known that the humoral host response is rarely effective in combatting mycoplasma infections; the cell mediated immune system, necessary to destroy infected cells, plays a significant role in their elimination.…”

Section: Are Mycoplasmas Intracellular?mentioning

confidence: 99%

“…The terminal organelle, shown in some but not all mycoplasmas, is thought to play a major role following intimate contact with the host cell surface possibly involving dramatic rearrangement of the cytoskeleton [11]. Recent studies with M. pulmonis, suggest that mycoplasmas may suppress host cell endosomal and autophagic systems to facilitate intracellular infection [15].…”

Section: Are Mycoplasmas Intracellular?mentioning

confidence: 99%

Mycoplasmology: the big issues

Nicholas¹,

Rosales²,

Loria³

2017

Anim Husb Dairy Vet Sci

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Important diseases like contagious bovine and caprine pleuropneumonia, avian mycoplasmosis, atypical pneumonia and contagious agalactia are caused by small degenerate wall-less organisms called mycoplasmas which evolved from gram positive bacteria about 2.5 billion years ago. The smallest of them are close to the theoretical limit for free-living existence containing less than 500 genes. However, they have acquired sophisticated means to survive both in the environment and in the host. Recent discoveries of their ability to survive as biofilms and within cells have changed our understanding of these degenerate bacteria. Despite increased knowledge over the last few decades, control of many mycoplasma infections seems further away than ever due to antibiotic resistance and our inability to develop effective vaccines. This review discusses some of the important issues confronting mycoplasmologists. New mycoplasmas, new diseases?It is not well known that some of the most important diseases of livestock are caused by mycoplasmas. Four are listed by the World Association for Animal Health (OIE) because of their socio-economic impacts and comprise: contagious bovine pleuropneumonia (CBPP), contagious agalactia, contagious caprine pleuropneumonia (CCPP) and avian mycoplasmosis. Others include enzootic pneumonia, a costly world-wide disease of pigs, bovine mycoplasmosis, which is characterised by respiratory disease, mastitis and arthritis, and community-acquired atypical pneumonia in humans. New outbreaks of mycoplasma disease in desert tortoises and big horn sheep have caused concern for the future of these endangered species.Mycoplasmas, or more correctly mollicutes, are the smallest self-replicating organisms on the planet and composed of wall-less, triple-layered membranes surrounding a matrix of nucleic acid and ribosomes. However once thought of as simple and possibly the precursors of more complex life they are actually highly sophisticated bacteria with elaborate defence mechanisms; in fact, they have undergone degenerative evolution from gram positive lactobacillusclostridial ancestors beginning some 2.5 billion years ago with the loss of the cell wall. Further huge gene loss occurred over the next few millennia until about 0.1 billion years the mycoplasma branch was created leading to the smallest of all mollicutes, the human pathogen Mycoplasma genitalium which consists of less than 500 genes: about a quarter of their original size and 1/10 th of the size of E. coli.The size of these organisms has generated interest in the minimum cell concept: "how many genes are essential for life?" with some estimating this figure at about 250. Attracted by this question, Craig Venter and his team in the USA attempted to put together a synthetic mycoplasma armed with the complete genome sequence of M. genitalium in the process discovering that at least 20% of the genes were not essential. After showing that they could successfully transplant genomes, they painstakingly assembled the genes of M. mycoides subsp cap...

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“…Other pathogenic mechanisms include production of hydrogen peroxide and superoxide radicals (Schott et al, 2014). Moreover, membrane lipoproteins, which undergo phase and size variation aid in immune evasion (Rosengarten et al, 2000). Phase and size variation of membrane lipoproteins aid in evading the host immune response (Behrens et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Effect of Mycoplasma bovis on Production of Pro-Inflammatory Cytokines by Peripheral Blood Mononuclear Cells

Valsala¹,

Rana²,

Remesh³

et al. 2017

Adv. Anim. Vet. Sci.

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| Mycoplasma bovis is an important bovine pathogen associated with calf pneumonia, mastitis, arthritis and sepicemia. It is known to persist in phagocytic and nonphagocytic cells and disseminate to various organs causing systemic infection. In this study, the effect of live M. bovis on pro-inflammatory cytokine production by bovine peripheral blood mononuclear cells was assessed by relative quantification. Temporal change in cytokine levels was assessed at 8 hourly intervals. IL-6 was upregulated (9.32 fold at 24h) by live M. bovis at MOI of 1: 10, while TNF-α levels remained unchanged over time. IL-1 and TNF-α levels were not altered by M. bovis as compared to the control group. This showed that pro-inflammatory cytokines are not much upregulated at low multiplicity of infection.

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Host-pathogen interactions in mycoplasma pathogenesis: Virulence and survival strategies of minimalist prokaryotes

Cited by 108 publications

References 46 publications

Cross-complementation between the products of the genes P1 and ORF6 of Mycoplasma pneumoniae subtypes 1 and 2

Cross-complementation between the products of the genes P1 and ORF6 of Mycoplasma pneumoniae subtypes 1 and 2

Mycoplasmology: the big issues

Effect of Mycoplasma bovis on Production of Pro-Inflammatory Cytokines by Peripheral Blood Mononuclear Cells

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