Class-specific immune response to Yersinia enterocolitica serotype O9 antigens as determined by enzyme-linked immunosorbent assay

Fernández-Lago, Luis; Santoyo, F J; Vizcaı́no, Nieves; Chordi, A

doi:10.1128/jcm.29.6.1243-1248.1991

Cited by 6 publications

(2 citation statements)

References 36 publications

(41 reference statements)

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“…Thus, the cytokine products of antigen-stimulated Th1 and Th2 cells have been shown to exert distinct regulatory and counterregulatory effects on the target B cells with which they react. While this work has provided an excellent foundation for our understanding of the molecular mechanisms of class switching, results presented here and elsewhere in the context of infectious-disease model systems (17,31,32,35,(56)(57)(58)61) have modified earlier hypotheses based on classical approaches. Considering the complexities of antigens presented by pathogens and the intricate immunoregulatory events triggered by certain infections, it is not surprising that observations concerning Ig class switching are different from those derived from earlier, better-defined in vitro systems.…”

Section: Discussionmentioning

confidence: 92%

Interleukin-4-Dependent Immunoglobulin G1 Isotype Switch in the Presence of a Polarized Antigen-Specific Th1-Cell Response to the Trypanosome Variant Surface Glycoprotein

Schopf

Filutowicz

et al. 1998

Infect Immun

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This study examines B-cell immunoglobulin (Ig) class-switching events in the context of parasite antigen-specific Th-cell responses in experimental African trypanosomiasis. Inbred mice were infected withTrypanosoma brucei rhodesiense, and the coordinate stimulation of Th-cell cytokine responses and B-cell responses to the trypanosome variant surface glycoprotein (VSG) was measured. The cytokines produced by T cells in response to VSG, at both the transcript and protein levels, were gamma interferon and interleukin-2 (IL-2) but not IL-4 or IL-5. Isotype profiles of antibodies specific for VSG showed that IgG1, IgG2a, and IgG3 switch responses predominated; no VSG-specific IgE responses were detected. To determine whether cryptic IL-4 responses played a role in promoting the unexpected IgG1 switch response, IL-4 knockout mice were infected; the cytokine responses and Ig isotype profiles of IL-4 knockout mice were identical to those of the wild-type control mice except for dramatically reduced IgG1 levels in response to VSG. Thus, these results revealed an IL-4-dependent component of the VSG-driven B-cell Cμ-to-Cγ1 switch. We speculate that an IL-4 response is mediated primarily by cells other than T lymphocytes since IL-4-secreting but parasite antigen-unresponsive, “background” cells were detected in all infected mice and since infected nude mice also displayed a detectable IgG1 switch response. Overall, our results suggest that B-cell clonal stimulation, maturation, and Ig class switching in African trypanosomiasis may be partially regulated by unusual mechanisms that do not include antigen-specific Th1 or Th2 cells.

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Section: Discussionmentioning

confidence: 92%

Interleukin-4-Dependent Immunoglobulin G1 Isotype Switch in the Presence of a Polarized Antigen-Specific Th1-Cell Response to the Trypanosome Variant Surface Glycoprotein

Schopf

Filutowicz

et al. 1998

Infect Immun

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“…have not been reported, except for iron-overloaded mice [31]. Fernandez-Lago et al [32] have used a rabbit experimental model to study the antibody response to serotype 09 antigens, and their results suggest that the virulence plasmid plays its role in the establishment of infection when rabbits were infected by the orogastric route but not by the intravenous route. Thus, the plasmid-mediated determinants of virulence play their role in the infection by the oral route, but in at least some extraintestinal infections they may be unnecessary, or even disadvan-tegous as suggested by Kapperud et al [33] for the specific case of YadA expression.…”

Section: Discussionmentioning

confidence: 99%

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Ruiz‐Bravo

1994

FEMS Immunology and Medical Microbiology

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The survival of Yersinia enterocolitica serotype O9 within mouse peritoneal macrophages was investigated. To evaluate the role of the virulence plasmid in the resistance to intracellular killing, an isogenic pair of virulent (plasmid-bearing) and avirulent (plasmid-less) O9 strains was used. The virulent strain was able to express plasmid-encoded outer membrane proteins and to colonize the Peyer's patches of orally infected mice. When mice were infected intraperitoneally, both strains were recovered at similar rates and over the same time from the peritoneal cavity. When in vitro assays were performed, both strains showed similar resistance to intracellular killing by monolayers of resident and inflammatory peritoneal macrophages. Previous opsonization of bacteria did not modify their survival within macrophage monolayers. We concluded that serotype O9 strains display a chromosome-mediated resistance to intracellular killing by mouse peritoneal macrophages. Moreover, macrophage resistance does not seem to be of importance for virulence of serotype O9 strains in mice.

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Experimental Infection of Mice with Yersinia enterocolitica Serotype O9 by Oral and Parenteral Routes: Spreading and Enterotropism of Virulent Yersiniae

et al. 1999

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An isogenic pair of Yersinia enterocolitica serotype O9 strains, with and without virulence plasmid, was used to study the plasmid role in the infection of BALB/c mice by oral, intraperitoneal, and intravenous routes. The plasmid-bearing strain, but not its plasmid-less derivative, caused enteric infection after challenge by all three routes. The virulence plasmid did not influence the peritoneal clearance of yersiniae, but only the plasmid-bearing yersiniae were able to move from the peritoneal cavity to the bloodstream, and thus they spread to spleen and liver. Moreover, plasmid-bearing yersiniae were able to move from the liver to the gallbladder, and they shed in bile into the intestine. Western blot analysis of antibody responses to chromosomally encoded outer membrane proteins revealed similar patterns with sera from mice challenged with each one of two strains by intraperitoneal route. In contrast, only the plasmid-bearing strain elicited an antibody response to these antigens in mice challenged by oral route. Although mice experimentally infected with plasmid-bearing O9 yersiniae developed an enteric infection, irrespective of the inoculation route, differences between the first steps in infection by oral and parenteral routes may be important, especially when the infection model is used as an approach to study the yersinia-host interactions.

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Class-specific immune response to Yersinia enterocolitica serotype O9 antigens as determined by enzyme-linked immunosorbent assay

Cited by 6 publications

References 36 publications

Interleukin-4-Dependent Immunoglobulin G1 Isotype Switch in the Presence of a Polarized Antigen-Specific Th1-Cell Response to the Trypanosome Variant Surface Glycoprotein

Interleukin-4-Dependent Immunoglobulin G1 Isotype Switch in the Presence of a Polarized Antigen-Specific Th1-Cell Response to the Trypanosome Variant Surface Glycoprotein

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Experimental Infection of Mice with Yersinia enterocolitica Serotype O9 by Oral and Parenteral Routes: Spreading and Enterotropism of Virulent Yersiniae

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