Related Experiment Video
Updated: Dec 22, 2025
Assessing Anti-fungal Activity of Isolated Alveolar Macrophages by Confocal Microscopy
Published on: July 9, 2014
Pneumocystis carinii Major Surface Glycoprotein Dampens Macrophage Inflammatory Responses to Fungal β-Glucan
Theodore J Kottom1, Deanne M Hebrink1, Eva M Carmona1
1Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Background:
Pneumocystis major surface glycoprotein (Msg) is a 120-kD surface protein complex on the organism with importance in adhesion and immune recognition. In this study, we show that Msg significantly impairs tumor necrosis factor (TNF)-α secretion by macrophages induced by Saccharomyces cerevisiae and Pneumocystis carinii (Pc) β-glucans.
Methods:
Major surface glycoprotein was shown to greatly reduce β-glucan-induced Dectin-1 immunoreceptor tyrosine-based activating motif (ITAM) phosphorylation. Major surface glycoprotein also down regulated Dectin-1 receptor messenger ribonucleic acid (mRNA) expression in the macrophages. It is interesting that Msg incubation with macrophages resulted in significant mRNA upregulation of both C-type lectin receptors (CLR) Mincle and MCL in Msg protein presence alone but to even greater amounts in the presence of Pc β-glucan.
Results:
The silencing of MCL and Mincle resulted in TNF-α secretions similar to that of macrophages treated with Pneumocystis β-glucan alone, which is suggestive of an inhibitory role for these 2 CLRs in Msg-suppressive effects on host cell immune response.
Conclusions:
Taken together, these data indicate that the Pneumocystis Msg surface protein complex can act to suppress host macrophage inflammatory responses to the proinflammatory β -glucan components of the organisms.
Insights
Pneumocystis major surface glycoprotein (Msg) suppresses macrophage inflammatory responses. Msg inhibits tumor necrosis factor-alpha secretion by impairing Dectin-1 signaling and upregulating other C-type lectin receptors.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Pneumocystis major surface glycoprotein (Msg) is a 120-kD complex crucial for Pneumocystis adhesion and immune recognition.
- Msg plays a role in modulating host immune responses to Pneumocystis infections.
Purpose of the Study:
- To investigate the effect of Pneumocystis major surface glycoprotein (Msg) on macrophage inflammatory responses.
- To elucidate the mechanisms by which Msg influences cytokine secretion and receptor expression.
Main Methods:
- Assessed tumor necrosis factor-alpha (TNF-α) secretion by macrophages stimulated with Saccharomyces cerevisiae and Pneumocystis carinii (Pc) β-glucans in the presence of Msg.
- Analyzed Dectin-1 immunoreceptor tyrosine-based activating motif (ITAM) phosphorylation and Dectin-1 receptor mRNA expression.
- Investigated the expression of C-type lectin receptors (CLRs) Mincle and MCL upon Msg incubation with macrophages.
Main Results:
- Msg significantly impaired TNF-α secretion induced by β-glucans.
- Msg reduced Dectin-1 ITAM phosphorylation and mRNA expression.
- Msg upregulated Mincle and MCL mRNA expression, particularly in the presence of Pc β-glucan.
Conclusions:
- Pneumocystis Msg suppresses host macrophage inflammatory responses to β-glucan components.
- Mincle and MCL appear to play an inhibitory role in Msg-mediated suppression of host immune responses.
Related Concept Videos
01:25Immune Surveillance by NK Cells and Phagocytes
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...
01:40Cell-mediated Immune Responses