Susceptibility of various oral bacteria to antimicrobial peptides and to phagocytosis by neutrophils

Ji, Sang-Hoon; Hyun, Jae‐Eun; Park, E.; Lee, B.-L.; Kim, K.-K.; Choi, Youngnim

doi:10.1111/j.1600-0765.2006.00962.x

Cited by 114 publications

(111 citation statements)

References 37 publications

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“…In addition, P. gingivalis has been reported to resist killing by the cathelicidin, LL-37, as well as β-defensin 3 which constitute important mechanisms of leukocyte and epithelial cellmediated antimicrobial host (Bals, 2000;Yang et al, 2004;Ji et al, 2007;Reddy et al, 2009). Interestingly, the ability of P. gingivalis to evade LL-37-dependent killing closely parallels its ability to resist neutrophil phagocytosis (Ji et al, 2007). Future experiments will be aimed at determining the role of PGN_0524 in evading endogenous host cationic antimicrobial peptide activity.…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Resistance to Polymyxin B Is Determined by the Lipid A 4′‐Phosphatase, PGN_0524

Coats

Jain

et al. 2009

Int J Oral Sci

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). Approximately 2,700 independent Tn4400'-derived mutants of P. gingivalis were examined for increased sensitivity to PMB killing at a relatively low dose (50 µg⋅mL -1 ). A single PMB-sensitive mutant was obtained in this phenotypic screen. We determined that the Tn4400' transposon was integrated into the gene encoding the lipid A 4'-phosphatase, PGN_0524, demonstrating that this insertion event was responsible for its increased susceptibility of this clone to PMB-dependent killing. The resulting mutant strain, designated 0524-Tn4400', was highly sensitive to PMB killing relative to wild-type P.gingivalis, and exhibited the same sensitivity as the previously characterized strain, 0524KO, which bears a genetically engineered deletion in the PGN_0524 locus. Positive ion mass spectrometric structural (MALDI-TOF MS) analyses revealed that lipid A isolates from 0524-Tn4400' and 0524KO strains displayed strikingly similar MALDI-TOF MS spectra that were substantially different from the wildtype P. gingivalis lipid A spectrum. Finally, intact 0524-Tn4400' and 0524KO mutant bacteria, as well as their corresponding LPS isolates, were significantly more potent in stimulating Toll-like receptor 4 (TLR4)-dependent E-selectin expression in human endothelial cells relative to intact wild-type P. gingivalis or its corresponding LPS isolate. Conclusion The combined molecular evidence provided in this report suggests that PGN_0524, a lipid A 4'-phosphatase, is the sole genetic element conferring the ability of the periodontopathogen, P. gingivalis, to evade the killing activity of cationic antimicrobial peptides, such as PMB. These data strongly implicate PGN_0524 as a critical virulence factor for the ability of P. gingivalis to evade front-line host innate defenses that are dependent upon cationic antimicrobial peptide activity and TLR4 sensing.

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Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Resistance to Polymyxin B Is Determined by the Lipid A 4′‐Phosphatase, PGN_0524

Coats

Jain

et al. 2009

Int J Oral Sci

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“…The membrane was allowed to react with the anti-Td92 Ab, and the reaction was detected as described above. An irrelevant histidine-tagged recombinant protein, MspTL (30), and E. coli lysates were used as negative controls.…”

Section: Bacteria and Cellsmentioning

confidence: 99%

Highly Conserved Surface Proteins of Oral Spirochetes as Adhesins and Potent Inducers of Proinflammatory and Osteoclastogenic Factors

Jun¹,

Kang²,

Lee³

et al. 2008

Infect Immun

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Oral spirochetes include enormously heterogeneous Treponema species, and some have been implicated in the etiology of periodontitis. In this study, we characterized highly conserved surface proteins in four representative oral spirochetes (Treponema denticola, T. lecithinolyticum, T. maltophilum, and T. socranskii subsp. socranskii) that are homologs of T. pallidum Tp92, with opsonophagocytic potential and protective capacity against syphilis. Tp92 homologs of oral spirochetes had predicted signal peptides (20 to 31 amino acids) and molecular masses of 88 to 92 kDa for mature proteins. They showed amino acid sequence identities of 37.9 to 49.3% and similarities of 54.5 to 66.9% to Tp92. The sequence identities and similarities of Tp92 homologs of oral treponemes to one another were 41.6 to 71.6% and 59.9 to 85.6%, respectively. The tp92 gene homologs were successfully expressed in Escherichia coli, and the recombinant proteins were capable of binding to KB cells, an epithelial cell line, and inhibited the binding of the whole bacteria to the cells. Antiserum (the immunoglobulin G fraction) raised against a recombinant form of the T. denticola Tp92 homolog cross-reacted with homologs from three other species of treponemes. The Tp92 homologs stimulated various factors involved in inflammation and osteoclastogenesis, like interleukin-1␤ (IL-1␤), tumor necrosis factor alpha, IL-6, prostaglandin E 2 , and matrix metalloproteinase 9, in host cells like monocytes and fibroblasts. Our results demonstrate that Tp92 homologs of oral spirochetes are highly conserved and may play an important role in cell attachment, inflammation, and tissue destruction. The coexistence of various Treponema species in a single periodontal pocket and, therefore, the accumulation of multiple Tp92 homologs may amplify the pathological effect in periodontitis.Numerous studies examining epidemiology and virulence factors have revealed strong evidence for the implication of oral spirochetes in the etiology of periodontitis, and the presence of spirochetes in the subgingival plaque is associated with an increased severity of periodontitis (16,38,48). Oral spirochetes include at least 50 phylotypes (12) and account for 20 to

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“…Moreover, we demonstrated that all the C. albieans, C. tropiealis, C. parapsilosis and C. glabrata induced a significant up-regulation in the oral cell line of IL-l a and IL-8 expression as early as 6 h of contact. However, an increase in IL-6 and TNF-a expression were evident at 24 h. In addition to the secretion of cytokines, other local defence mechanisms against mucosal infection include the salivary proteins, such as b-defensins, and immunoglobulin A, which are activated in the immune response against Candida infection (28). These salivary proteins can impair adhesion and growth of Candida in the oropharyngeal cavity.…”

Section: Discussionmentioning

confidence: 99%

Assessment of Host Defence Mechanisms Induced by Candida Species

Paoletti

Fusco

Grimaldi

et al. 2013

Int J Immunopathol Pharmacol

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Some species of Candida are opportunistic pathogens that can cause disease in a host immunocompromised by underlying local or systemic pathological processes. C. albicans is the species most often associated with oral lesions, but other species of Candida, including C. glabrata, C. tropicalis and C. parapsilosis, have also been isolated in the saliva of subjects with and without candidiasis. In the present study we evaluated the host defence mechanisms induced by Candida albicans and other Candida species in monocytes and oral epithelial cells in order to establish the existence of a species-specific cellular response. Our results indicated that, during Candida species infection, the epithelial cells actively participate in the host defence by producing antimicrobial peptides and proinflammatory cytokines. Moreover, in infections caused by Candida tropicalis and Candida glabrata, the host defence may be strengthened by the release of perforin and granzyme by polymorphonuclear leukocytes recruited at the site of infection.

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Susceptibility of various oral bacteria to antimicrobial peptides and to phagocytosis by neutrophils

Abstract: Our results indicate that immune evasion may contribute to the pathogenicity of some periodontopathic bacteria.

Cited by 114 publications

References 37 publications

Porphyromonas gingivalis Resistance to Polymyxin B Is Determined by the Lipid A 4′‐Phosphatase, PGN_0524

Porphyromonas gingivalis Resistance to Polymyxin B Is Determined by the Lipid A 4′‐Phosphatase, PGN_0524

Highly Conserved Surface Proteins of Oral Spirochetes as Adhesins and Potent Inducers of Proinflammatory and Osteoclastogenic Factors

Assessment of Host Defence Mechanisms Induced by Candida Species

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