Nutritional Profiles of Neisseria gonorrhoeae, Neisseria meningitidis, and Neisseria lactamica in Chemically Defined Media and the Use of Growth Requirements for Gonococcal Typing

Catlin, B. Wesley

doi:10.1093/infdis/128.2.178

Cited by 298 publications

(10 citation statements)

References 42 publications

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“…Contrary to α522, the growth of MC58 was slightly suppressed by these two amino acids. The ability of MC58 but not α522 to grow in the absence of Cys and Gln indicates strain specific differences in the respective metabolic pathways, and the requirement of some meningococcal strains for Cys and its growth inhibiting effect on others has already been reported [60]. In parallel with these phenotypic differences, genome comparisons revealed also striking differences in Cys and Gln biosynthesis genes that might contribute to the phenotypic finding, although the repertoire of enzymes required for the biosynthesis of amino acids is otherwise highly conserved in both genomes.…”

Section: Resultsmentioning

confidence: 94%

Transcriptomic buffering of cryptic genetic variation contributes to meningococcal virulence

et al. 2017

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BackgroundCommensal bacteria like Neisseria meningitidis sometimes cause serious disease. However, genomic comparison of hyperinvasive and apathogenic lineages did not reveal unambiguous hints towards indispensable virulence factors. Here, in a systems biological approach we compared gene expression of the invasive strain MC58 and the carriage strain α522 under different ex vivo conditions mimicking commensal and virulence compartments to assess the strain-specific impact of gene regulation on meningococcal virulence.ResultsDespite indistinguishable ex vivo phenotypes, both strains differed in the expression of over 500 genes under infection mimicking conditions. These differences comprised in particular metabolic and information processing genes as well as genes known to be involved in host-damage such as the nitrite reductase and numerous LOS biosynthesis genes. A model based analysis of the transcriptomic differences in human blood suggested ensuing metabolic flux differences in energy, glutamine and cysteine metabolic pathways along with differences in the activation of the stringent response in both strains. In support of the computational findings, experimental analyses revealed differences in cysteine and glutamine auxotrophy in both strains as well as a strain and condition dependent essentiality of the (p)ppGpp synthetase gene relA and of a short non-coding AT-rich repeat element in its promoter region.ConclusionsOur data suggest that meningococcal virulence is linked to transcriptional buffering of cryptic genetic variation in metabolic genes including global stress responses. They further highlight the role of regulatory elements for bacterial virulence and the limitations of model strain approaches when studying such genetically diverse species as N. meningitidis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-017-3616-7) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 94%

Transcriptomic buffering of cryptic genetic variation contributes to meningococcal virulence

et al. 2017

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“…8A), indicating that the growth of the cbp mutant was not defective in liquid medium. In previous experiments using meningococcal defined medium, Neisseria chemically defined medium (NCDM), developed by Catlin (30), was commonly used for N. meningitidis (31, 34).…”

Section: Resultsmentioning

confidence: 99%

“…Experimental data has indicated that many N. meningitidis strains are auxotrophs for at least 4 amino acids, namely, glutamate, cysteine, arginine, and glycine (30), and previous studies also demonstrated that glutamate uptake is required for bacterial intracellular growth/survival in human cells (31–33) as well as for survival and proliferation in mice (34, 35). Moreover, a reduced sulfur form of cysteine, cystine, was found to be necessary for meningococcal growth (36, 37), and many N.…”

Section: Introductionmentioning

confidence: 99%

The Meningococcal Cysteine Transport System Plays a Crucial Role in Neisseria meningitidis Survival in Human Brain Microvascular Endothelial Cells

Takahashi

Watanabe

Kim

et al. 2018

mBio

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Neisseria meningitidis colonizes at a nasopharynx of human as a unique host and has many strains that are auxotrophs for amino acids for their growth. To cause invasive meningococcal diseases (IMD) such as sepsis and meningitis, N. meningitidis passes through epithelial and endothelial barriers and infiltrates into blood and cerebrospinal fluid as well as epithelial and endothelial cells. However, meningococcal nutrients, including cysteine, become less abundant when it more deeply infiltrates the human body even during inflammation, such that N. meningitidis has to acquire nutrients in order to survive/persist, disseminate, and proliferate in humans. This was the first study to examine the relationship between meningococcal cysteine acquisition and the pathogenesis of meningococcal infections. The results of the present study provide insights into the mechanisms by which pathogens with auxotrophs acquire nutrients in hosts and may also contribute to the development of treatments and prevention strategies for IMD.

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“…When needed, rifampin (Sigma-Aldrich) was added to a final concentration of 36 g/ml. Meningococci were also cultured in the chemically defined medium MCDA (24,25) with different sodium ion concentrations [Na ϩ ]: 21.6 mM (MCDA-1), 41.6 mM, 61.6 mM (MCDA-2), 101.6 mM, and 121.6 mM (26). The pH of all media was adjusted to 7.4.…”

Section: Methodsmentioning

confidence: 99%

Fitness Cost of Rifampin Resistance in Neisseria meningitidis: In Vitro Study of Mechanisms Associated with rpoB H553Y Mutation

Colicchio

Pagliuca²,

Pastore

et al. 2015

Antimicrob Agents Chemother

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e Rifampin chemoprophylaxis against Neisseria meningitidis infections led to the onset of rifampin resistance in clinical isolates harboring point mutations in the rpoB gene, coding for the RNA polymerase ␤ chain. These resistant strains are rare in medical practice, suggesting their decreased fitness in the human host. In this study, we isolated rifampin-resistant rpoB mutants from hypervirulent serogroup C strain 93/4286 and analyzed their different properties, including the ability to grow/survive in different culture media and in differentiated THP-1 human monocytes and to compete with the wild-type strain in vitro. Our results demonstrate that different rpoB mutations (H553Y, H553R, and S549F) may have different effects, ranging from low-to high-cost effects, on bacterial fitness in vitro. Moreover, we found that the S549F mutation confers temperature sensitivity, possibly explaining why it is observed very rarely in clinical isolates. Comparative high-throughput RNA sequencing analysis of bacteria grown in chemically defined medium demonstrated that the low-cost H553Y substitution resulted in global transcriptional changes that functionally mimic the stringent response. Interestingly, many virulence-associated genes, including those coding for meningococcal type IV pili, porin A, adhesins/invasins, IgA protease, two-partner secretion system HrpA/HrpB, enzymes involved in resistance to oxidative injury, lipooligosaccharide sialylation, and capsular polysaccharide biosynthesis, were downregulated in the H553Y mutant compared to their level of expression in the wildtype strain. These data might account for the reduced capacity of this mutant to grow/survive in differentiated THP-1 cells and explain the rarity of H553Y mutants among clinical isolates.

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Nutritional Profiles of Neisseria gonorrhoeae, Neisseria meningitidis, and Neisseria lactamica in Chemically Defined Media and the Use of Growth Requirements for Gonococcal Typing

Cited by 298 publications

References 42 publications

Transcriptomic buffering of cryptic genetic variation contributes to meningococcal virulence

Transcriptomic buffering of cryptic genetic variation contributes to meningococcal virulence

The Meningococcal Cysteine Transport System Plays a Crucial Role in Neisseria meningitidis Survival in Human Brain Microvascular Endothelial Cells

Fitness Cost of Rifampin Resistance in Neisseria meningitidis: In Vitro Study of Mechanisms Associated with rpoB H553Y Mutation

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