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A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
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Neutrophil response of transgenic mice expressing human group IIA phospholipase A2 in bacterial infections
V J Laine1, A Rajamäki, D S Grass
1Department of Pathology, University of Turku, 20520 Turku, Finland.
Abstract:
Group IIA phospholipase A2 (PLA2) is a newly recognized acute phase protein with marked antibacterial properties. We have shown previously that transgenic C57BL/6 J mice expressing human group IIA PLA2 (PLA2+ mice) are more resistant to bacterial infections than nontransgenic C57BL/6 J mice that, among mice, are unusual in that they lack the mouse analogue of group IIA PLA2 (PLA2- mice). To elucidate the possible mechanisms involved in the host response of these mice in bacterial infection, peripheral inflammatory cell responses of PLA2+ and PLA2- mice were studied after i.p. administration of Escherichia coli, E. coli lipopolysaccharide or Staphylococcus aureus. Uninfected PLA2+ mice had higher numbers of lymphocytes and polymorphonuclear neutrophil leukocytes (PMNs) in their blood than PLA2- mice. In PLA2+ mice, the number of PMNs increased in peripheral blood in parallel with the concentration of group IIA PLA2 after the administration of bacteria, whereas these responses were not seen in PLA2- mice. High concentrations of group IIA PLA2 in PLA2+ mice may increase the synthesis of bioactive molecules, such as prostaglandins, which in turn may mobilize PMNs into circulation. Our results support the hypothesis that group IIA PLA2 is an important inflammatory mediator in bacterial infections.
Insights
Group IIA phospholipase A2 (PLA2) enhances resistance to bacterial infections by increasing circulating neutrophils. This suggests PLA2 is a key mediator in the host inflammatory response to bacteria.
Area of Science:
- Immunology
- Biochemistry
Background:
- Group IIA phospholipase A2 (PLA2) is an acute phase protein with demonstrated antibacterial properties.
- Transgenic mice expressing human group IIA PLA2 (PLA2+) exhibit increased resistance to bacterial infections compared to mice lacking this enzyme (PLA2-).
Purpose of the Study:
- To investigate the mechanisms underlying the host response in PLA2+ and PLA2- mice during bacterial infection.
- To elucidate the role of group IIA PLA2 in modulating peripheral inflammatory cell responses.
Main Methods:
- Comparative analysis of peripheral inflammatory cell counts in PLA2+ and PLA2- mice.
- Induction of bacterial infection using intraperitoneal administration of Escherichia coli, E. coli lipopolysaccharide, or Staphylococcus aureus.
- Monitoring of blood cell counts, specifically lymphocytes and polymorphonuclear neutrophil leukocytes (PMNs), and PLA2 concentrations.
Main Results:
- Uninfected PLA2+ mice showed higher baseline levels of lymphocytes and PMNs compared to PLA2- mice.
- Following bacterial challenge, PLA2+ mice exhibited a significant increase in circulating PMNs, correlating with elevated group IIA PLA2 concentrations.
- PLA2- mice did not display a similar increase in PMNs in response to bacterial administration.
Conclusions:
- Group IIA PLA2 appears to play a crucial role in the inflammatory response to bacterial infections.
- Elevated levels of group IIA PLA2 may stimulate the production of prostaglandins, leading to the mobilization of PMNs into circulation.
- These findings support the hypothesis that group IIA PLA2 is an important inflammatory mediator in combating bacterial infections.
