Macrophages in resistance to rickettsial infections: early host defense mechanisms in experimental scrub typhus
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Abstract:
Several early nonspecific host defense mechanisms were examined in resistant (BALB/c) and susceptible (C3H/He) mice after intraperitoneal inoculation with Rickettsia tsutsugamushi strain Gilliam. Inflammatory exudates were formed in both mouse strains in response to rickettsial inoculation, but the inflammatory response of C3H animals was delayed several days, and influx of peroxidase-positive macrophages occurred late in infection. Peritoneal cells of C3H mice became progressively infected, with 40% of both macrophages and lymphocytes containing intracellular rickettsiae by day 10. The early flammatory response of BALB/c mice was unexpectedly associated with a low percentage of infected peritoneal cells (1 to 2%). In vitro, no difference was detected in ability of resident macrophages of either strain to support the growth of R. tsutsugamushi or to become activated by treatment with lymphokines for rickettsiacidal activity. In vivo, however, macrophages from C3H mice inoculated with Gilliam were not activated on days 6 and 7 after infection, whereas BALB/c macrophages were continuously activated beginning on day 4. The lack of in vivo C3H macrophage activation was not secondary to deficient lymphokine production by infected lymphocytes, as levels of lymphokines produced by peritoneal lymphocytes of both strains were similar and peaked on day 7 after infection. Susceptibility to infection appears to be related to defective regulation of macrophage responses rather than to defects in macrophage function.
Insights
Susceptible mice show delayed inflammatory responses and progressive infection by Rickettsia tsutsugamushi. Resistant mice exhibit early macrophage activation, indicating defective regulation, not function, is key to host defense against this pathogen.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Nonspecific host defense mechanisms are crucial for controlling Rickettsia tsutsugamushi infections.
- Understanding differences in immune responses between resistant and susceptible mouse strains can elucidate mechanisms of pathogenesis.
Purpose of the Study:
- To investigate early host defense mechanisms in BALB/c (resistant) and C3H/He (susceptible) mice infected with Rickettsia tsutsugamushi.
- To compare inflammatory responses, peritoneal cell infection, and macrophage activation in vivo and in vitro.
Main Methods:
- Intraperitoneal inoculation of mice with Rickettsia tsutsugamushi strain Gilliam.
- Analysis of inflammatory exudates, peritoneal cell populations (macrophages, lymphocytes), and intracellular rickettsial load.
- In vitro assessment of macrophage growth support and lymphokine-activated killing.
- In vivo evaluation of macrophage activation following infection.
Main Results:
- C3H mice exhibited delayed inflammatory responses and progressive peritoneal cell infection compared to BALB/c mice.
- BALB/c mice showed early and sustained macrophage activation in vivo, while C3H mice did not.
- In vitro, macrophages from both strains supported rickettsial growth equally, and lymphokine production was similar.
Conclusions:
- Susceptibility to Rickettsia tsutsugamushi is linked to defective regulation of macrophage activation in vivo, not intrinsic macrophage dysfunction.
- Early and appropriate macrophage activation is critical for controlling Rickettsia tsutsugamushi infection in resistant hosts.
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