Cell-mediated immunity to Bordetella pertussis: role of Th1 cells in bacterial clearance in a murine respiratory infection model

Mills, Kingston H.G.; Barnard, Amanda; Watkins, J.; Redhead, Keith

doi:10.1128/iai.61.2.399-410.1993

Cited by 288 publications

(194 citation statements)

References 56 publications

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“…In the mouse model natural infection or immunization with Pw induces Th1 cells and confers a high level of protection against infection with B. pertussis [12]. Although Pa also confer protection against infection in the murine respiratory challenge model, immunity induced by these vaccines appears to be PT-specific IgE was assessed in serum at 7 months (after three vaccinations with the five-component Pa), at 12 and 30 months of age and pre-and post-booster vaccination with Pa in five atopic (A1±A5) and 10 normal healthy children (N1±N5) at 4 years of age.…”

Section: Discussionmentioning

confidence: 99%

Booster immunization of children with an acellular pertussis vaccine enhances Th2 cytokine production and serum IgE responses against pertussis toxin but not against common allergens

Ryan

Nilsson²,

Kjellman³

et al. 2000

Clinical and Experimental Immunology

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SUMMARYAcellular pertussis vaccines (Pa) protect against severe pertussis in children. However, serum antibody responses decline quickly after immunization. Studies in animal models suggest that cell-mediated immunity also contributes to protection against Bordetella pertussis, and it has already been demonstrated that Pa induce T cells that secrete type-1 and type-2 cytokines in children. In this study we examined the persistence of the T cell response and the effect of booster immunization in 4±6-yearold children. Cell-mediated immunity to B. pertussis antigens was detected in a high proportion of children more than 42 months after their last immunization. Peripheral blood mononuclear cells (PBMC) from the majority of children secreted interferon-gamma (IFN-g) and a smaller proportion IL-5, in response to specific antigen stimulation in vitro. However, following booster immunization, significantly higher concentrations of IL-5, but not IFN-g , were produced by PBMC in response to B. pertussis antigens. Furthermore, plasma IL-4 and IL-5 concentrations were increased, whereas IFN-g concentrations were reduced following booster immunization. It has been suggested that childhood immunization with Th2-inducing vaccines may predispose some children to atopic disease. Although we found that pertussis toxin (PT)-specific IgE was significantly increased after booster immunization in both atopic and non-atopic children, the levels of IgE to common allergens and the prevalence of positive skin prick test were unaffected by the booster vaccination. Thus, despite the enhancement of type-2 responses to B. pertussis antigens, booster vaccination with Pa does not appear to be a risk factor for allergy.

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Section: Discussionmentioning

confidence: 99%

Booster immunization of children with an acellular pertussis vaccine enhances Th2 cytokine production and serum IgE responses against pertussis toxin but not against common allergens

Ryan

Nilsson²,

Kjellman³

et al. 2000

Clinical and Experimental Immunology

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“…Cellular immunity against B. pertussis is predominantly mediated by CD4 1 T lymphocytes, whereas CD8 1 T lymphocytes are mostly dispensable (Mills et al, 1993;Leef et al, 2000). Traditionally, CD4 1 cells have been subdivided as T helper type 1 (Th1) or Th2 cells, based on their cytokine expression profile (Mosmann & Coffman, 1989;Liew, 2002).…”

Section: T-cell Responses To B Pertussismentioning

confidence: 99%

Pertussis: a matter of immune modulation

et al. 2011

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Pertussis, or whooping cough, is a highly contagious, acute respiratory disease of humans that is caused by the Gram-negative bacterial pathogen Bordetella pertussis. In the face of extensive global vaccination, this extremely monomorphic pathogen has persisted and re-emerged, causing approximately 300,000 deaths each year. In this review, we discuss the interaction of B. pertussis with the host mucosal epithelium and immune system. Using a large number of virulence factors, B. pertussis is able to create a niche for colonization in the human respiratory tract. The successful persistence of this pathogen is mainly due to its ability to interfere with almost every aspect of the immune system, from the inhibition of complement- and phagocyte-mediated killing to the suppression of T- and B-cell responses. Based on these insights, we delineate ideas for the rational design of improved vaccines that can target the 'weak spots' in the pathogenesis of this highly successful pathogen.

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“…12,13 Consistent with these observations, we have demonstrated protection in a murine respiratory model in the absence of a detectable antibody response. 14 Athymic mice failed to clear the infection after respiratory challenge. However, adoptive transfer of immune spleen cells or purified CD4 + T cells from convalescent donors into nude or sublethally irradiated recipient mice conferred a high level of protection.…”

Section: Introductionmentioning

confidence: 99%

Th1/Th2 cell dichotomy in acquired immunity to Bordetella pertussis: variables in the in vivo priming and in vitro cytokine detection techniques affect the classification of T‐cell subsets as Th1, Th2 or Th0

et al. 1996

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SUMMARYIn studies of the mechanism of immunity to Bordetella pertussis in a murine respiratory infection model, we have previously demonstrated that natural infection of immunization with a whole cell vaccine induces a potent protective immune response, which is mediated by T-helper type-1 (Th1) cells. In contrast an acellular vaccine generates Th2 cells and is associated with delayed bacterial clearance following respiratory challenge. In the present study we have investigated the apparent Th1/Th2 cell dichotomy in acquired immunity and have examined the factors that affect their induction or detection. The cytokine profiles of B. pertussis-specific T cells in immune animals were determined using antigenstimulated ex vivo spleen cells or CD4T-cell lines and clones established in the presence of interleukin-2 (IL-2) or IL-4. Antigen-specific T cells derived from mice immunized with the acellular vaccine were almost exclusively of the Th2 cell type. In contrast, T-cell lines and clones established following respiratory infection or immunization with the whole cell vaccine were predominantly of the Th1 type. However, a proportion of T cells from convalescent mice, especially when cultured in the presence of IL-4, secreted IL-4 and IL-5 with or without detectable IL-2 and interferon-g (IFN-g), suggesting that Th0 or Th2 cells were also primed during natural infection in vivo. Furthermore, when mice were assessed 6 months after infection, spleen cells produced significant levels of IL-4 and IL-5, which were not evident at 6 weeks. The route of immunization and the genetic background of the mice were also found to influence the preferential priming of Th1 cells, and this was directly related to the level of protection against respiratory or intracerebral (i.c.) challenge. Our findings underline the critical role of CD4 Th1 cells in immunity to B. pertussis, but also demonstrate that a number of factors in the in vivo priming and in vitro restimulation can skew the apparent dominance of one Th cell type over another.

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Cell-mediated immunity to Bordetella pertussis: role of Th1 cells in bacterial clearance in a murine respiratory infection model

Cited by 288 publications

References 56 publications

Booster immunization of children with an acellular pertussis vaccine enhances Th2 cytokine production and serum IgE responses against pertussis toxin but not against common allergens

Booster immunization of children with an acellular pertussis vaccine enhances Th2 cytokine production and serum IgE responses against pertussis toxin but not against common allergens

Pertussis: a matter of immune modulation

Th1/Th2 cell dichotomy in acquired immunity to Bordetella pertussis: variables in the in vivo priming and in vitro cytokine detection techniques affect the classification of T‐cell subsets as Th1, Th2 or Th0

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