Cross-reactive lymphocyte responses and protective immunity against other spotted fever group rickettsiae in mice immunized with Rickettsia conorii

Abstract

Lymphocyte proliferation in response to antigens on spotted fever group rickettsiae was used as a method to investigate the group-specific protective immunity to rechallenge characteristic of this group of rickettsiae at the T-cell receptor level. Spleen cells from Rickettsia conorii-immune C3H/HeJ mice proliferated in response to R. rickettsii Sheila Smith, R. sibirica 246, R. australis, and all tested strains of R. conorii (Casablanca, Moroccan, and Malish). Spleen cells from these mice, however, responded poorly or not at all to antigens prepared from the Kaplan or Hartford strain ofR. akari. Proliferation of immune T cells maintained as in vitro cell lines showed a similar pattern of reactivity to these antigens; however, response to R. akari was consistently demonstrable. Spleen cells from C3H/HeJ mice immunized with R. akari responded to R. akari and R. conorii antigens as well as antigens from the other spotted fever group rickettsiae. Lymphocytes obtained from lymph nodes draining foot pads infected with R. conorii or R. akari demonstrated cross-reactivity similar to that found with immune spleen cells. If immunization was accomplished with R. conorii antigen emulsified in Freund complete adjuvant, the resulting lymph node cells were able to respond to R. akari antigens. These data suggest that infection with R. conorii induces a population of T lymphocytes that recognize an antigen(s) that also is found on other spotted fever rickettsiae and that may be responsible for cross-protective immunity. This antigen probably is not a major antigen on R. akari.

Species-specific BALB/c mouse antibodies to rickettsiae studied by Western blotting

“…The accepted method for differentiating SFG rickettsiae is serotyping by comparative microimmunofluorescence (MIF) [5]. Although some cross-reactivity occurs between mouse antisera [6,7], the antibody response in Swiss Webster mice is considered to be directed towards species-specific rather than group-specific antigens. Yu et al [8] have shown that antisera to Rickettsia sibirica obtained following i.v.…”

Alcohol-mediated polarization of type 1 and type 2 immune responses

“…anti-DNS responses of these sera show similarly shaped binding curves on DNS 62 -, DNS 38 -, and DNS 10 -BSA coated plates. The lowest hapten conjugation ratio (DNS 10 -BSA) revealed a difference in the anti-DNS response between the dietary groups, similar to DNS 29 -BSA responses seen in Figure 2.…”

“…Relative affinities were calculated for all the ELISA data (from Figure 2) and are illustrated graphically in Figure 5 for SD (open bars), LCD (hatched bars), and LED30 (gray bars). Only those LED30 groups indicated by black bars (DNS 10 -BSA for IgG 2a , IgG 2b for DNS 62 -, DNS 38 -, and DNS 10 -BSA) have LogED 50 values are significantly lower ( p < 0.001), than SD sera assayed on the same ELISA plate. Therefore, ethanol-consumption down-regulates haptenspecific responses by Th1-regulated antibodies (67).…”

“…Alcohol-consuming mice tend to limit their caloric In contrast, binding of these same sera shows both a >10-fold decrease in antibody titer and that the anti-DNS content of the LED30 sera is less than that of the SD or LCD sera. On dietary day 14, the sera from these mice were assayed on FγG, DNS 62 -, DNS 38 -and DNS 10 -BSA coated (protein concentration held constant at 10 µg/ml) ELISA plates and developed with biotin-labeled, goat anti-mouse total (IgM + IgG) or isotype (IgG 1 , IgG 2a or IgG 2b ) specific antibodies, followed by reaction with horseradish conjugated streptavidin, and colorimetric detection of acidified TMB substrate. Data are represented as absorbencies at 450 nm versus the reciprocal sera dilution for SD (n), LCD (s), LED30 (m) and NMS (u).…”

“…Dietary ethanol decreases overall splenic cellularity in experimental animals by as much as 50% with greatest losses occurring in B and T lymphocyte populations (28,31,37,38). Previous studies from our laboratory and others have shown that ethanol impairs CD4 T-cell dependent, cell-mediated immunity, whereas antibody responses are largely unaffected (22,34,39,40).…”