Nitric oxide production by murine spleen cells stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans

Porphyromonas gingivalis, Gamma Interferon, and a Proapoptotic Fibronectin Matrix Form a Synergistic Trio That Induces c-Jun N-Terminal Kinase 1-Mediated Nitric Oxide Generation and Cell Death

“…However, the mechanisms by which these molecules mediate their pathogenic effects have not been fully delineated. Reports indicate that periodontopathic bacteria and bacterial components, including LPS, stimulate local gingival fibroblasts and inflammatory cells, including macrophages, to produce nitric oxide (2,7,12,17,41,46,61,66). In agreement with these findings, our data show for the first time that PDL cells also respond to an LPS challenge by producing increased levels of nitric oxide and iNOS.…”

Proinflammatory and Antimicrobial Nitric Oxide in Gingival Fluid of Diabetic Patients with Periodontal Disease

“…Recent data indicate that modulation of superoxide levels by NO influences phagocytic functions of neutrophils and macrophages and that NO is an important element of host defense against P. gingivalis (9). Since P. gingivalis LPS can also induce macrophages to produce NO in an L-arginine-and gamma interferon-dependent mechanism (27), this NO may potentially be an important mediator of bone resorption. In this regard, iNOS null mice demonstrate a significantly reduced osteoclast response (13).…”

Arginase activity in a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans

“…These previous results seem to indicate that this periodontopathogen is able to induce an immune response and concurrently stimulate both soft tissues and alveolar bone destruction. We and others have recently shown that lipopolysaccharide from periodontopathogens such as A. actinomycetemcomitans, Prevotella intermedia and Porphyromonas gingivalis induces nitric oxide production by murine macrophages and splenic macrophages (4, 14, 15, 27, 28, 30, 31). Of interest, nitric oxide production by these cells stimulated with A. actinomycetemcomitans ‐lipopolysaccharide was regulated by different cytokines; thus, interferon‐γ and IL‐12 up‐regulated but IL‐4 suppressed nitric oxide production (27, 31).…”

“…We and others have recently shown that lipopolysaccharide from periodontopathogens such as A. actinomycetemcomitans, Prevotella intermedia and Porphyromonas gingivalis induces nitric oxide production by murine macrophages and splenic macrophages (4, 14, 15, 27, 28, 30, 31). Of interest, nitric oxide production by these cells stimulated with A. actinomycetemcomitans ‐lipopolysaccharide was regulated by different cytokines; thus, interferon‐γ and IL‐12 up‐regulated but IL‐4 suppressed nitric oxide production (27, 31). We speculated that in A. actinomycetemcomitans ‐lipopolysaccharide‐activated murine macrophages, arginase activity may be increased by IL‐4 and depressed by interferon‐γ and IL‐12 (27, 31).…”

“…Of interest, nitric oxide production by these cells stimulated with A. actinomycetemcomitans ‐lipopolysaccharide was regulated by different cytokines; thus, interferon‐γ and IL‐12 up‐regulated but IL‐4 suppressed nitric oxide production (27, 31). We speculated that in A. actinomycetemcomitans ‐lipopolysaccharide‐activated murine macrophages, arginase activity may be increased by IL‐4 and depressed by interferon‐γ and IL‐12 (27, 31). However, arginase activity and its regulation in murine macrophages stimulated by A. actinomycetemcomitans‐ lipopolysaccharide is unknown.…”