Literature DB >> 12221019

Enhanced neutrophil emigration and Porphyromonas gingivalis reduction following PGG-glucan treatment of mice.

Richard Niederman1, Hans Kelderman, Sigmund Socransky, Gary Ostroff, Caroline Genco, Ralph Kent, Philip Stashenko.   

Abstract

Periodontal disease is the consequence of a mixed Gram-negative infection in the gingival sulcus and has been associated with deficits in the neutrophil response. A novel, and heretofore untested, alternative approach to therapy is the use of biological-response modulators that enhance the neutrophil response. Poly-beta1-6-glucotriosyl-beta1-3-glucopyranose glucan (PGG-glucan) is an immunomodulator, derived from yeast, which specifically enhances neutrophil priming, phagocytosis and bacterial killing while failing to induce inflammatory cytokine expression. The hypothesis tested was that PGG-glucan could enhance host resistance to a Gram-negative periodontal pathogen, Porphyromonas gingivalis. Chambers were implanted subcutaneously in the dorsolumbar region of C57BL/6J mice and allowed to heal for 14 days. PGG-glucan was administered subcutaneously to one-half of the animals and saline to the other half. In the first set of experiments the chambers were inoculated with P. gingivalis (A7436) at 4 x 10 (6), 4 x 10 (7), and 4 x 10 (8) colony-forming units (CFU). In the second set of experiments the chambers were inoculated with 5 x 10 (8) CFU of either P. gingivalis or Streptococcus sanguis, a Gram-positive oral microbe that is not periodontopathic. Chambers were sampled over the following 2 weeks. The results demonstrated that: (1). bacterial CFU and neutrophils increased with increasing bacterial inoculum (P<0.02); (2). bacterial CFU were lower in the PGG-glucan-treated animals than in the saline controls (P<0.02); and (3). neutrophil counts were higher in the PGG-glucan-treated animals than in the saline controls (P<0.01). These results indicate that PGG-glucan significantly enhances neutrophil emigration and bacterial killing, thus decreasing the bacterial infection in this model system.

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Year:  2002        PMID: 12221019     DOI: 10.1016/s0003-9969(02)00042-0

Source DB:  PubMed          Journal:  Arch Oral Biol        ISSN: 0003-9969            Impact factor:   2.633


  4 in total

1.  Pathogenic bacterial species associated with endodontic infection evade innate immune control by disabling neutrophils.

Authors:  Aritsune Matsui; Jun-O Jin; Christopher D Johnston; Hajime Yamazaki; Yael Houri-Haddad; Susan R Rittling
Journal:  Infect Immun       Date:  2014-07-14       Impact factor: 3.441

Review 2.  Aggregatibacter actinomycetemcomitans leukotoxin: from threat to therapy.

Authors:  S C Kachlany
Journal:  J Dent Res       Date:  2010-03-03       Impact factor: 6.116

3.  Protective role of osteopontin in endodontic infection.

Authors:  Susan R Rittling; Craig Zetterberg; Kader Yagiz; Stephen Skinner; Noriyuki Suzuki; Akira Fujimura; Hajime Sasaki
Journal:  Immunology       Date:  2009-09-11       Impact factor: 7.397

4.  Effect of BETA 1, 3/1, 6 GLUCAN on Upper Respiratory Tract Infection Symptoms and Mood State in Marathon Athletes.

Authors:  Shawn Talbott; Julie Talbott
Journal:  J Sports Sci Med       Date:  2009-12-01       Impact factor: 2.988

  4 in total

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