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In vivo and in vitro studies on possible pathogenic mechanisms of Actinomyces viscosus
Abstract:
Actinomycotic infections are characterized by long-term inflammatory lesions containing large numbers of polymorphonuclear leukocytes (PMNs) and mononuclear cells. The pathogenic mechanisms involved in these lesions are not understood. Homogenates of Actinomyces viscosus (AVIS) induce an acute inflammatory response with a predominance of PMNs within 6 h after injection into the footpads of nonimmunized mice. These homogenates, when tested in vitro, contain potent chemotactic activity for human PMNs. In vitro chemotactic activity for human monocytes is weak but statistically significant (P less than 0.025). Doses of AVIS, which alone have little chemotactic activity, cause the generation of PMN chemotactic activity in fresh, but not complement-inactivated, serum. The injection of AVIS into the footpads of immunized mice induces an acute inflammatory response followed within 48 h by a mononuclear cell infiltrate, suggesting that factors affecting monocyte accumulation are generated by the immune host in response to challenge with the bacterial antigens. These findings indicate that the pathogenicity of the Actinomyces may result in part from (i) their direct chemotactic effect on PMNs, (ii) their cytotaxigenic effects on serum, and (iii) their ability to stimulate host immune cells to produce and release mediators of inflammation.
Insights
Actinomyces viscosus (AVIS) triggers inflammation by directly attracting polymorphonuclear leukocytes (PMNs) and stimulating the immune system to produce inflammatory mediators. This study elucidates key pathogenic mechanisms in actinomycotic infections.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Actinomycotic infections cause chronic inflammatory lesions with abundant polymorphonuclear leukocytes (PMNs) and mononuclear cells.
- The precise pathogenic mechanisms underlying these lesions remain poorly understood.
Purpose of the Study:
- To investigate the pathogenic mechanisms of Actinomyces viscosus (AVIS) in inducing inflammatory responses.
- To determine the chemotactic activities of AVIS on human leukocytes and its effects on serum.
Main Methods:
- Injection of AVIS homogenates into mouse footpads to assess inflammatory responses.
- In vitro testing of AVIS homogenates for chemotactic activity on human PMNs and monocytes.
- Evaluation of AVIS effects on fresh and complement-inactivated human serum to generate PMN chemotactic activity.
Main Results:
- AVIS homogenates induced acute PMN infiltration in non-immunized mice within 6 hours.
- AVIS demonstrated potent in vitro chemotactic activity for human PMNs and significant, though weaker, activity for monocytes.
- AVIS induced PMN chemotactic activity generation in fresh serum.
- Immunized mice showed an acute inflammatory response followed by a mononuclear cell infiltrate upon AVIS challenge.
Conclusions:
- Actinomyces pathogenicity may stem from direct PMN chemotaxis, serum cytotaxigenic effects, and stimulation of host immune cells to release inflammatory mediators.
- These findings offer insights into the inflammatory processes involved in actinomycotic infections.