Related Experiment Videos
Phagocytosis and complement action
Abstract:
THe interaction of pathogenic mycoplasmas with two components of the "nonspecific" defence system is influenced by the lack of a cell wall and perhaps the tight attachment to host cells. On mycoplasmas, complement can act directly on the parasite membrane surface and cause damage comparable to the effects on animal cells, namely lysis and death. Results with Mycoplasma pneumoniae suggest a direct activation by this species of the complement sequence without participation of homologous antibody. Activation may occur via the alternate pathway and perhaps even by direct triggering of the classical pathway. The action results in rounding, opsonization and death of some or all of the cells. Since complement components have been found in bronchial washings, this direct activation may be of some importance in the first stages of infection. Furthermore, it sufficiently explains the fact that M. pneumoniae is found only on the surface but not in the deeper tissues of the respiratory tract even in severe infections. The interactions of mycoplasmas with phagocytes, one of the first lines of defence against infection, is of considerable interest. Mycoplasmas seem to be relatively resistant to phagocytosis as long as they are not opsonized. They have been observed attaching to macrophage surfaces without being ingested. Addition of homologous antibody triggered immediate engulfment and intracellular killing. The aspects of interaction of phagocytes with mycoplasmas are even more interesting because in most cases the mycoplasmas which have to be phagocytized are attached to the surface of other tissue cells. This raises the problem of secondary damage caused by the enzymes of the phagocytizing cell. Our knowledge about the mycoplasma-phagocyte-interaction is scarce and the experimental approaches are difficult.
Insights
Pathogenic mycoplasmas can directly activate the complement system, leading to cell damage and death. They also resist phagocytosis unless opsonized by antibodies, highlighting their unique immune evasion strategies.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Pathogenic mycoplasmas possess unique characteristics, including a lack of cell walls and tight adherence to host cells, influencing their interaction with the host immune system.
- Nonspecific defense mechanisms, such as complement and phagocytes, play crucial roles in combating microbial infections.
Purpose of the Study:
- To investigate the interaction of pathogenic mycoplasmas with key components of the host's innate immune system, specifically the complement system and phagocytes.
- To elucidate the mechanisms by which mycoplasmas evade or modulate these defense mechanisms.
Main Methods:
- In vitro studies examining the direct effects of complement on mycoplasma cell membranes.
- Analysis of Mycoplasma pneumoniae's ability to activate complement pathways (alternative and classical).
- Observation of mycoplasma-phagocyte interactions, including phagocytosis resistance and antibody-dependent engulfment.
Main Results:
- Mycoplasmas can directly activate the complement cascade, leading to cell lysis and death, potentially via both alternative and classical pathways without host antibodies.
- Mycoplasma pneumoniae activates complement, causing cell rounding, opsonization, and death, which may explain its superficial localization in respiratory tract infections.
- Mycoplasmas exhibit resistance to phagocytosis unless opsonized by antibodies, and their adherence to host cells complicates phagocytic clearance and raises concerns about secondary tissue damage.
Conclusions:
- The direct activation of complement by mycoplasmas is a significant innate immune evasion strategy, contributing to early infection stages and superficial colonization.
- Antibody-dependent opsonization is critical for effective phagocytosis of mycoplasmas, but interactions with host cells present challenges for phagocytic clearance and may lead to host tissue damage.