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Published on: June 8, 2012
Priming of rabbit alveolar macrophages for enhanced oxidative responses by herpes simplex virus type 2 infection
G Giridhar1, H Hayakawa, L S Kucera
1Department of Microbiology and Immunology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27103.
Abstract:
The effect of herpes simplex virus type 2 (HSV-2) infection on the oxidative response in infant and adult rabbit alveolar macrophages (AM) was studied using either phorbol myristate acetate (0.5 microgram PMA/ml) or latex (250 micrograms/ml) as eliciting agents in a chemiluminescence (CL) assay. Results indicated that uninfected infant AM responded to a latex-elicited but not PMA-elicited CL response. HSV-2 infection (moi = 1.0) of infant AM for 2 hr at 37 degrees C did not alter the PMA or latex-elicited CL responses. In contrast, uninfected adult AM exhibited a markedly increased CL response when elicited with either PMA or latex. HSV-2 infection (moi = 1) of adult AM for 2 hr further increased both PMA- and latex-elicited CL responses. Increasing the moi to 10 inhibited both PMA- and latex-elicited CL responses. Incubation of uninfected control and HSV-2 infected adult AM for 18 hr at 37 degrees C resulted in spontaneous priming of the cells for increased CL responses. In the absence of PMA HSV-2 alone failed to elicit a CL response in adult AM. Infection with heat-inactivated HSV-2 (moi = 1.0 before heat inactivation) did not prime adult AM for enhanced CL responses. AM from BCG immunized adult rabbit produced a considerably higher level CL response that nonimmunized AM; however, HSV-2 infection of these cells did not further enhance the response. In summary, these data indicate that adult AM but not infant AM can be primed by active HSV-2 infection for an increased CL response elicited by either PMA or latex.
Insights
Herpes simplex virus type 2 (HSV-2) infection primes adult rabbit alveolar macrophages (AM) for an enhanced oxidative response. Infant AM, however, showed no significant change in response after HSV-2 infection.
Area of Science:
- Immunology
- Virology
- Cellular Biology
Background:
- Alveolar macrophages (AM) play a crucial role in lung immunity.
- Herpes simplex virus type 2 (HSV-2) is a common viral pathogen with immunomodulatory effects.
- Age-related differences in immune cell function are well-documented.
Purpose of the Study:
- To investigate the impact of HSV-2 infection on the oxidative burst response of infant and adult rabbit alveolar macrophages.
- To determine if HSV-2 infection primes macrophages for an enhanced response to stimuli.
- To compare the effects of HSV-2 on macrophages from different age groups.
Main Methods:
- Alveolar macrophages (AM) were isolated from infant and adult rabbits.
- Cells were infected with HSV-2 at various multiplicities of infection (MOI).
- Oxidative response was measured using a chemiluminescence (CL) assay with phorbol myristate acetate (PMA) or latex as eliciting agents.
Main Results:
- Uninfected infant AM showed a latex-elicited CL response, but not PMA-elicited.
- HSV-2 infection did not alter infant AM responses.
- Uninfected adult AM exhibited a higher CL response than infant AM.
- HSV-2 infection (MOI=1) enhanced PMA- and latex-elicited CL responses in adult AM.
- Higher MOI (10) of HSV-2 inhibited adult AM responses.
- Heat-inactivated HSV-2 did not enhance adult AM responses.
- BCG immunization increased CL response, but HSV-2 did not further enhance it in these cells.
Conclusions:
- Active HSV-2 infection primes adult rabbit alveolar macrophages for an enhanced oxidative burst response.
- Infant rabbit alveolar macrophages do not exhibit priming by HSV-2 infection.
- The observed enhancement is dependent on active viral replication and MOI.
- These findings highlight age-dependent differences in macrophage response to viral infection.
