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Septicaemia models using Streptococcus pneumoniae and Listeria monocytogenes: understanding the role of complement
Aline Dupont1, Fatima Mohamed, Nur'Ain Salehen
1Department of Infection, Immunity and Inflammation, Maurice Shock Medical Sciences Building, University of Leicester, University Road, Leicester, LE1 9HN, UK.
Abstract:
Streptococcus pneumoniae and Listeria monocytogenes, pathogens which can cause severe infectious disease in human, were used to infect properdin-deficient and wildtype mice. The aim was to deduce a role for properdin, positive regulator of the alternative pathway of complement activation, by comparing and contrasting the immune response of the two genotypes in vivo. We show that properdin-deficient and wildtype mice mounted antipneumococcal serotype-specific IgM antibodies, which were protective. Properdin-deficient mice, however, had increased survival in the model of streptococcal pneumonia and sepsis. Low activity of the classical pathway of complement and modulation of FcγR2b expression appear to be pathogenically involved. In listeriosis, however, properdin-deficient mice had reduced survival and a dendritic cell population that was impaired in maturation and activity. In vitro analyses of splenocytes and bone marrow-derived myeloid cells support the view that the opposing outcomes of properdin-deficient and wildtype mice in these two infection models is likely to be due to a skewing of macrophage activity to an M2 phenotype in the properdin-deficient mice. The phenotypes observed thus appear to reflect the extent to which M2- or M1-polarised macrophages are involved in the immune responses to S. pneumoniae and L. monocytogenes. We conclude that properdin controls the strength of immune responses by affecting humoral as well as cellular phenotypes during acute bacterial infection and ensuing inflammation.
Insights
Properdin deficiency enhances survival in pneumococcal infections but impairs defense against listeriosis. This highlights properdin's crucial role in regulating immune responses to bacterial pathogens.
Area of Science:
- Immunology
- Microbiology
- Complement System
Background:
- Properdin is a key regulator of the alternative pathway of complement activation.
- The role of properdin in vivo during bacterial infections is not fully understood.
- Understanding properdin's function is critical for developing new therapeutic strategies against infectious diseases.
Purpose of the Study:
- To investigate the in vivo role of properdin in host defense against Streptococcus pneumoniae and Listeria monocytogenes.
- To compare the immune responses of properdin-deficient and wildtype mice during infection.
- To elucidate the mechanisms underlying properdin's influence on cellular and humoral immunity.
Main Methods:
- Infection of properdin-deficient and wildtype mice with S. pneumoniae and L. monocytogenes.
- Assessment of survival rates and immune cell populations.
- Analysis of complement pathway activity and FcγR2b expression.
- In vitro studies using splenocytes and bone marrow-derived myeloid cells.
Main Results:
- Properdin-deficient mice showed increased survival in a model of pneumococcal pneumonia and sepsis.
- Properdin-deficient mice exhibited reduced survival and impaired dendritic cell function in listeriosis.
- Opposing outcomes were linked to a skewing of macrophage activity towards an M2 phenotype in properdin-deficient mice.
- Humoral (IgM antibodies) and cellular immune responses were modulated by properdin deficiency.
Conclusions:
- Properdin plays a differential role in host defense against S. pneumoniae and L. monocytogenes.
- Properdin influences both humoral and cellular immune responses, affecting macrophage polarization.
- The findings underscore properdin's importance in controlling the strength and type of immune response during acute bacterial infections.
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