Immune Response to Yersinia Outer Proteins and Other Yersinia pestis Antigens after Experimental Plague Infection in Mice

Abstract

There is limited information concerning the nature and extent of the immune response to the virulence determinants of Yersinia pestis during the course of plague infection. In this study, we evaluated the humoral immune response of mice that survived lethal Y. pestis aerosol challenge after antibiotic treatment. Such a model may replicate the clinical situation in humans and indicate which virulence determinants are expressed in vivo. Immunoglobulin G enzyme-linked immunosorbent assay and immunoblotting were performed by using purified, recombinant antigens including F1, V antigen, YpkA, YopH, YopM, YopB, YopD, YopN, YopE, YopK, plasminogen activator protease (Pla), and pH 6 antigen as well as purified lipopolysaccharide. The major antigens recognized by murine convalescent sera were F1, V antigen, YopH, YopM, YopD, and Pla. Early treatment with antibiotics tended to reduce the immune response and differences between antibiotic treatment regimens were noted. These results may indicate that only some virulence factors are expressed and/or immunogenic during infection. This information may prove useful for selecting potential vaccine candidates and for developing improved serologic diagnostic assays.

Establishing Efficacy of Human Products Using Animals

“…Current literature indicates that similarities exist between human and murine plague lesions 4 and that some critical elements of murine immunity are the same ones that are important in human immunity. 1 This knowledge could be the starting point to establish that the murine model could fulfill the requirements of the Animal Rule for plague.…”

Identificación de proteínas de secreción con capacidad inmunogénica de aislamientos de yersinia pseudotuberculosis provenientes de planteles cuyícolas del departamento de Nariño

“…Así mismo la función del SSTIII en la patogenicidad de Y. pseudotuberculosis también ha sido estudiada a través de ensayos in vitro con el objetivo de verificar sí el SSTIII puede modular la respuesta inmune de la célula del huésped (133) No obstante a nueve aislamientos no se les detectó genes de origen plasmídico (yadA y lcrF), pero sí amplificaron para el fragmento de 470pb del gen Inv de origen cromosomal. A pesar que estos aislamientos también causaron enfermedad en los planteles cuyiculas, es probable que la no detección de genes de origen plásmidico fue dada por la pérdida del pYV en los distintos pasajes por medios de cultivo en el proceso de aislamiento del microorganismo (113)(114)(115)(116)(117)(118)(119)(120)(121)(122)(123)(124)(125)(126)(127)(128)(129)(130)(131)(132).…”