Differential display analysis of <i>Porphyromonas gingivalis</i> gene activation response to heat and oxidative stress

Shelburne, Charles E.; Gleason, Raymond M.; Coulter, Wilson A.; Lantz, Marilyn S.; Lopatin, Dennis E.

doi:10.1111/j.1399-302x.2005.00219.x

Cited by 9 publications

(9 citation statements)

References 48 publications

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“…P. gingivalis exhibits several unique stress responses, dependent upon the type of stressor. Heat stress, 57,58,59,60,61,62,63,64 O 2 oxidative stress, 57,59,65 H 2 O 2 oxidative stress, 57,65,66 pH stress, 59,60 heme limitation, 67 EtOH stress 60 and response to contact with epithelial cells 68 all induce extensive and unique responses in P. gingivalis with very little overlap (Supplementary Table 5). These well-documented stress responses have very little in common with the response induced by sapienic acid treatment.…”

Section: Discussionmentioning

confidence: 99%

Oral mucosal lipids are antibacterial against Porphyromonas gingivalis, induce ultrastructural damage, and alter bacterial lipid and protein compositions

et al. 2013

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Oral mucosal and salivary lipids exhibit potent antimicrobial activity for a variety of Gram-positive and Gram-negative bacteria; however, little is known about their spectrum of antimicrobial activity or mechanisms of action against oral bacteria. In this study, we examine the activity of two fatty acids and three sphingoid bases against Porphyromonas gingivalis, an important colonizer of the oral cavity implicated in periodontitis. Minimal inhibitory concentrations, minimal bactericidal concentrations, and kill kinetics revealed variable, but potent, activity of oral mucosal and salivary lipids against P. gingivalis, indicating that lipid structure may be an important determinant in lipid mechanisms of activity against bacteria, although specific components of bacterial membranes are also likely important. Electron micrographs showed ultrastructural damage induced by sapienic acid and phytosphingosine and confirmed disruption of the bacterial plasma membrane. This information, coupled with the association of treatment lipids with P. gingivalis lipids revealed via thin layer chromatography, suggests that the plasma membrane is a likely target of lipid antibacterial activity. Utilizing a combination of two-dimensional in-gel electrophoresis and Western blot followed by mass spectroscopy and N-terminus degradation sequencing we also show that treatment with sapienic acid induces upregulation of a set of proteins comprising a unique P. gingivalis stress response, including proteins important in fatty acid biosynthesis, metabolism and energy production, protein processing, cell adhesion and virulence. Prophylactic or therapeutic lipid treatments may be beneficial for intervention of infection by supplementing the natural immune function of endogenous lipids on mucosal surfaces.

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Section: Discussionmentioning

confidence: 99%

Oral mucosal lipids are antibacterial against Porphyromonas gingivalis, induce ultrastructural damage, and alter bacterial lipid and protein compositions

et al. 2013

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“…In the case of P. gingivalis, the degree of sensitivity to killing by LL-37 and human beta-defensins depends on the strain: W50, W83 and ATCC 49417 are less susceptible than ATCC 33277 (80,81,155). Interestingly, in the latter strain, as well as in other P. gingivalis strains, the high resistance to bactericidal activity of human betadefensins can be induced by pretreatment with sublethal levels of defensins and heat or peroxide stress (195). Taking into account that the latter treatments enhance expression of the rgpA and rgpB genes (194), and gingipains efficiently degrade defensins (18,51,106,147), it is likely that these proteases, at least partially, provide P. gingivalis with protection against cationic antimicrobial peptides.…”

Section: Degradation Of Antibacterial Peptidesmentioning

confidence: 99%

Dichotomy of gingipains action as virulence factors: from cleaving substrates with the precision of a surgeon’s knife to a meat chopper-like brutal degradation of proteins

Guo¹,

Nguyen²,

Potempa³

2010

Periodontology 2000

314

306

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“…Gingipain, a major virulence factor of this microorganism involved in colonization, impairs host defense systems and damages host tissue (34) . Rgp have been reported to be induced by environmental conditions such as oxygen stress (35) .…”

Section: It Is Possible That Noradrenaline Affects Acquisition Of Iromentioning

confidence: 99%

Exposure of P. gingivalis to noradrenaline reduces bacterial growth and elevates ArgX protease activity

Saito

Inagaki

Sakurai

et al. 2011

Archives of Oral Biology

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Objective: Periodontitis, an infectious disease caused by periodontopathic bacteria, including Porphyromonas gingivalis and spirochetes, is reported to be accelerated by stress, under which noradrenaline levels are increased in the bloodstream. The purpose of this study was to evaluate the effects of noradrenaline on P. gingivalis. Design: P. gingivalis was incubated in the presence of 25 µM, 50 µΜ, or 100 µM adrenaline or noradrenaline at 37°C for 12, 24 or 36 h and growth was evaluated by OD 660 .Auto-inducer-2 (AI-2) was measured by luminescence of Vibrio harveyi BB 170.Expression of P. gingivalis genes was evaluated using a microarray and RT-PCR. Rgp activity of arg-gingipainA and B (Rgp) was measured with a synthetic substrate.Results: Growth of P. gingivalis FDC381 was inhibited by noradrenaline at 24 and 36 h.Growth inhibition by noradrenaline increased dose-dependently. Inhibition of growth partially recovered with addition of propranolol. AI-2 production from P. gingivalis showed a marked decrease with addition of noradrenaline compared with peak production levels in the control group. Microarray analysis revealed an increase in expression in 18 genes and a decrease in expression in 2 genes. Among these genes, expression of the protease arg-gingipainB (RgpB) gene, a major virulence factor of P.gingivalis, was further analyzed. Expression of rgpB showed a significant increase with addition of noradrenaline, which was partially reduced by addition of propranolol.Cell-associated Rgp activity also increased with addition of noradrenaline.Conclusions: These results suggest that stressors influence the expression of the virulence factors of P. gingivalis via noradrenaline.3

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Differential display analysis of Porphyromonas gingivalis gene activation response to heat and oxidative stress

Abstract: These results emphasize the need for studies to measure the coordinated responses of bacteria like P. gingivalis which use a multitude of interrelated metabolic activities to survive the environmental hazards of the infection process.

Cited by 9 publications

References 48 publications

Oral mucosal lipids are antibacterial against Porphyromonas gingivalis, induce ultrastructural damage, and alter bacterial lipid and protein compositions

Oral mucosal lipids are antibacterial against Porphyromonas gingivalis, induce ultrastructural damage, and alter bacterial lipid and protein compositions

Dichotomy of gingipains action as virulence factors: from cleaving substrates with the precision of a surgeon’s knife to a meat chopper-like brutal degradation of proteins

Exposure of P. gingivalis to noradrenaline reduces bacterial growth and elevates ArgX protease activity

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