The role of the cell‐mediated immune response to <i>Actinobacillus actinomycetemcomitans</i> and <i>Porphyromonas gingivalis</i> in periodontitis

Zadeh, Homayoun H.; Nichols, Frank C.; Miyasaki, Kenneth T.

doi:10.1111/j.1600-0757.1999.tb00163.x

Cited by 63 publications

(70 citation statements)

References 249 publications

(184 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Th1 cells secrete interleukin-2 and interferon-c (IFN-c), whereas Th2 cells produce IL-5, IL-6, IL-4, IL-10 and IL-13. Both cell types produce IL-3, TNFa and granulocyte-macrophage colony-stimulating factor (GM-CSF) (Kelso 1995, Zadeh et al 1999. The major role of the Th1 cytokines IL-2 and IFN-c is to enhance cell-mediated responses, whereas the Th2 signature cytokine IL-4 suppresses cell-mediated responses (Modlin & Nutman 1993).…”

Section: Adaptive Immunitymentioning

confidence: 99%

See 1 more Smart Citation

Infection and inflammatory mechanisms

Dyke

Winkelhoff

2013

Journal of Periodontology

146

123

View full text Add to dashboard Cite

This introductory article examines the potential mechanisms that may play a role in the associations between periodontitis and the systemic conditions being considered in the EFP/AAP Workshop in Segovia, Spain. Three basic mechanisms have been postulated to play a role in these interactions; metastatic infections, inflammation and inflammatory injury, and adaptive immunity. The potential role of each alone and together is considered in in vitro and animal studies and in human studies when available. This is not a systematic or critical review, but rather an overview of the field to set the stage for the critical reviews in each of the working groups.

show abstract

Section: Adaptive Immunitymentioning

confidence: 99%

“…For example, Th1 cells direct B cell secretion of immunoglobulin G2 (IgG2), whereas Th2 cells up-regulate IgG1 secretion. CD8 T cells (cytotoxic T-cells) are immune effector cells that also secrete cytokines that are characteristic of either Th1 or Th2 cells (Zadeh et al 1999).…”

Section: Adaptive Immunitymentioning

confidence: 99%

Infection and inflammatory mechanisms

Dyke

Winkelhoff

2013

Journal of Periodontology

146

123

View full text Add to dashboard Cite

show abstract

“…Periodontal diseases are chronic inflammatory diseases that are mediated in part by virulence factors that are capable of direct tissue damage (Fives-Taylor et al, 1999). In addition, the host also mediates much of the pathogenic effects of the bacteria through a multitude of immune mediators including neutralization of the bacteria by oxidative mechanisms (Zadeh et al, 1999). Therefore, it was of interest to determine if msrA is present in the A. actinomycetemcomitans genome and if this enzyme contributes to the virulence of this pathogen.…”

mentioning

confidence: 99%

Peptide methionine sulfoxide reductase (MsrA) is not a major virulence determinant for the oral pathogen Actinobacillus actinomycetemcomitans a aThe GenBank accession number for the msrA sequence reported in this paper is AY026361.

Mintz

Moskovitz

et al. 2002

Microbiology

View full text Add to dashboard Cite

Actinobacillus actinomycetemcomitans is an oral pathogen that is a causative agent for periodontal disease as well as other non-oral infections. The chronic inflammation associated with periodontal diseases suggests that the bacterium must be able to neutralize oxygen intermediates to survive in the host tissues. Methionine sulfoxide reductase (MsrA) is an enzyme that has been demonstrated to have a role in protection against oxidative damage and has also been identified to be required for the proper expression or maintenance of functional adhesins on the surface of several pathogenic bacteria. The A. actinomycetemcomitans homologue of msrA has been isolated and a chromosomal insertion mutant constructed by allele replacement mutagenesis. Inactivation of the gene led to a complete loss of enzymic activity toward a synthetic substrate. However, the isogenic mutant was not more sensitive to oxidative stress or less adherent to epithelial cells as compared with the parent strain. These data suggest that this strain of A. actinomycetemcomitans has redundant systems that compensate for the MsrA activities ascribed for other organisms.Keywords : adhesion, oxidative stress, periodontal disease INTRODUCTIONExposure to reactive oxygen intermediates such as superoxide anions, hydrogen peroxide and hydroxyl radicals, which are by-products of aerobic metabolism, can damage proteins, nucleic acids and cell membranes (Storz & Imlay, 1999). These intermediates can oxidize methionine residues in proteins to methionine sulfoxide, which may result in the loss of the biological function of the protein (reviewed by Brot & Weissbach, 1991). In vitro, the function can be restored by incubation of the oxidized protein with the enzyme methionine sulfoxide reductase, MsrA, in a thioredoxin-dependent reaction (Moskovitz et al., 2000). MsrA is a ubiquitous enzyme that is found in a variety of animal tissues and organisms (Brot et al., 1981 ; Kuschel et al., 1999 ; Moskovitz et al., 1996a The GenBank accession number for the msrA sequence reported in this paper is AY026361.with a defence against oxidative stress. A role of MsrA in protecting cells against oxidative damage is supported by the decrease in viability of null mutants during oxidative stress (Dhandayuthapani et al., 2001 ; Hassouni et al., 1999 ; Moskovitz et al., 1995 Moskovitz et al., , 1998Moskovitz et al., , 2001Vriesema et al., 2000). Furthermore, the overexpression of MsrA in Escherichia coli, yeast and stable transfected human T cells provides higher resistance to hydrogen peroxide treatment (Moskovitz et al., 1995(Moskovitz et al., , 1998. In addition to a role in protection to oxidative damage, MsrA has been proposed to be a virulence factor for numerous micro-organisms. Inactivation of msrA reduces bacterial adhesion of Streptococcus pneumoniae to human cells and reduces type I fimbriaemediated haemagglutination of red blood cells by enteropathogenic E. coli (Wizemann et al., 1996). This enzyme has also been shown to be a virulence determinant in Erwinia chrysanth...

show abstract

“…Severe periodontitis afects approximately 10% of the global population [39]. Periodontal disease is the consequence of a shift in oral microbiota population from a symbiotic to a dysbiotic microbial community in the mouth.…”

Section: Periodontitismentioning

confidence: 99%

Neutrophil Role in Periodontal Disease

Rosales¹,

Uribe‐Querol²

2017

Role of Neutrophils in Disease Pathogenesis

View full text Add to dashboard Cite

Oral tissues are constantly exposed to damage from the mechanical efort of eating and from the invasion of foreign microorganisms such as bacteria, fungi, and virus. In healthy oral tissues, there is a balance between symbiotic bacteria and cells from the innate immune system, mainly neutrophils. When this balance is broken, inlammation appears and more immune cells are recruited to the gingiva. Neutrophils form a barrier against dysbiotic bacteria. However, when neutrophils are insuicient, bacteria thrive causing periodontitis, a chronic inlammatory disease that destroys the tooth-supporting tissues or periodontium. Damage of periodontal tissues leads to tooth loss, and in severe cases, it can also afect systemic health by increasing a person's risk for atherosclerosis, rheumatoid arthritis, diabetes, and even cancer. The mechanisms neutrophil employ to keep a balance with bacteria in order to maintain healthy oral tissues is the focus of this chapter. We discuss how neutrophil antimicrobial functions keep bacteria at check and how some dysbiotic bacteria block neutrophils to promote an inlammatory state. Also, novel therapeutic approaches for periodontitis are discussed.

show abstract

The role of the cell‐mediated immune response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontitis

Cited by 63 publications

References 249 publications

Infection and inflammatory mechanisms

Infection and inflammatory mechanisms

Peptide methionine sulfoxide reductase (MsrA) is not a major virulence determinant for the oral pathogen Actinobacillus actinomycetemcomitans a aThe GenBank accession number for the msrA sequence reported in this paper is AY026361.

Neutrophil Role in Periodontal Disease

Contact Info

Product

Resources

About