Whole-cell pertussis vaccine protects against Bordetella pertussis exacerbation of allergic asthma

Ennis, Darren; Cassidy, Joseph P.; Mahon, Bernard P.

doi:10.1016/j.imlet.2004.10.011

Cited by 18 publications

(18 citation statements)

References 53 publications

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“…Circulating IgE antibodies against PT have also been found after primary immunization with Pa with or without a subsequent Pa or Pw booster (11,17,42). Furthermore, B. pertussis infection is known to modulate allergen priming and exacerbates the severity of allergen-driven pathology in a murine model (8); however, Th1-inducing vaccines (Pw) protect against this (7). In the present study we show that Pa immunization did not enhance the OVA-specific IgE response (Fig.…”

Section: Discussionmentioning

confidence: 49%

“…It has been proposed that prior Th1 responses to bacterial infections protect against allergic disease; however, Th1-inducing B. pertussis infection exacerbates airway hyperresponsiveness in OVA-sensitized mice (8). We have shown previously that prior immunization with a whole-cell pertussis vaccine, which induces a very similar immune response to B. pertussis, did not enhance but protected against the airway hyperresponsiveness exacerbated by B. pertussis (7). In the present study we examined the influence of Pa immunization on physiological lung function using whole-body plethysmography to measure enhanced pause, a surrogate marker associated with airway hyperreactivity.…”

Section: Resultsmentioning

confidence: 82%

“…Furthermore, we have demonstrated that Th1-inducing Pw protects against exacerbation of allergic asthma due to B. pertussis (7). In order to test whether immunization with Pa exacerbated asthma, we used a well-characterized murine model of acellular pertussis vaccination and B. pertussis infection in combination with the murine OVA model of airway hyperresponsiveness.…”

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confidence: 99%

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Acellular Pertussis Vaccine Protects against Exacerbation of Allergic Asthma Due toBordetella pertussisin a Murine Model

Ennis

Cassidy

Mahon

2005

Clin Vaccine Immunol

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The prevalence of asthma and allergic disease has increased in many countries, and there has been speculation that immunization promotes allergic sensitization. Bordetella pertussis infection exacerbates allergic asthmatic responses. We investigated whether acellular pertussis vaccine (Pa) enhanced or prevented B. pertussis-induced exacerbation of allergic asthma. Groups of mice were immunized with Pa, infected with B. pertussis, and/or sensitized to ovalbumin. Immunological, pathological, and physiological changes were measured to assess the impact of immunization on immune deviation and airway function. We demonstrate that immunization did not enhance ovalbumin-specific serum immunoglobulin E production. Histopathological examination revealed that immunization reduced the severity of airway pathology associated with sensitization in the context of infection and decreased bronchial hyperreactivity upon methacholine exposure of infected and sensitized mice. These data demonstrate unequivocally the benefit of Pa immunization to health and justify selection of Pa in mass vaccination protocols. In the absence of infection, the Pa used in this study enhanced the interleukin-10 (IL-10) and IL-13 responses and influenced airway hyperresponsiveness to sensitizing antigen; however, these data do not suggest that Pa contributes to childhood asthma overall. On the contrary, wild-type virulent B. pertussis is still circulating in most countries, and our data suggest that the major influence of Pa is to protect against the powerful exacerbation of asthma-like pathology induced by B. pertussis.

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Section: Discussionmentioning

confidence: 49%

Section: Resultsmentioning

confidence: 82%

mentioning

confidence: 99%

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Acellular Pertussis Vaccine Protects against Exacerbation of Allergic Asthma Due toBordetella pertussisin a Murine Model

Ennis

Cassidy

Mahon

2005

Clin Vaccine Immunol

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“…Current Pa vaccines have been shown to induce T H 2-type responses (14,15,30). T H 1-dominated immune responses have been linked with optimal immunity against B. pertussis (2,4,7,34).…”

Section: Discussionmentioning

confidence: 99%

A Live AttenuatedBordetella pertussisCandidate Vaccine Does Not Cause Disseminating Infection in Gamma Interferon Receptor Knockout Mice

Skerry

Cassidy

English

et al. 2009

Clin Vaccine Immunol

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Bordetella pertussis is the cause of whooping cough and responsible for 300,000 infant deaths per annum. Current vaccines require 6 months to confer optimal immunity on infants, the population at highest risk. Recently, an attenuated strain of B. pertussis (BPZE1) has been developed to be used as a low-cost, live, intranasal, single-dose vaccine for newborns. Preclinical proof of concept has been established; however, it is necessary to evaluate the safety of BPZE1, especially in immunodeficient models, prior to human clinical trials. Here, the preclinical safety of BPZE1 was examined in well-characterized murine models. Immunocompetent and gamma interferon (IFN-␥) receptor knockout mice were challenged by aerosol with either virulent B. pertussis or BPZE1. The two strains colonized the lung at equal levels, but inflammation was associated with carriage of only virulent bacteria. Virulent bacteria disseminated to the liver of IFN-␥ receptor-deficient mice, resulting in atypical pathology. In contrast, attenuated BPZE1 did not disseminate in either immunocompetent or immunodeficient mice and did not induce atypical pathology. In neonatal challenge models, virulent B. pertussis infection resulted in significant mortality of both immunodeficient and immunocompetent mice, whereas no mortality was observed for any neonatal mice challenged with BPZE1. BPZE1 was shown to elicit strong IFN-␥ responses in mice, equivalent to those elicited by the virulent streptomycin-resistant B. pertussis Tohama I derivative BPSM, also inducing immunoglobulin G2a, a process requiring T H 1 cytokines in mice. These data indicate that a live attenuated whooping cough vaccine candidate shows no signs of disseminating infection in preclinical models but rather evokes an immunological profile associated with optimal protection against disease.

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“…Animals (n between 5 and 8 per group per experiment) were sacrificed and lungs were removed, fixed in a paraformaldehyde/lysine/periodate fixative, paraffin embedded, sectioned and stained using haematoxylin and eosin, Discombes (identification of eosinophils), Alcian blue (identification of mucus), PAS (assessment of basement membrane thickness) and Van Gieson (identification of fibrosis) methods as previously described [8,20,21]. Histopathological changes evident were graded according to a semi-quantitative scoring system as mild, moderate or severe by two researchers without prior knowledge of the treatment group using a previously established scoring system.…”

Section: Respiratory Tract Histologymentioning

confidence: 99%

Inflammation of the respiratory tract is associated with CCL28 and CCR10 expression in a murine model of allergic asthma

et al. 2006

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Mouse models and in vitro cell culture were used to examine airway expression of the mucosal chemokine CCL28. Low levels of constitutively expressed mRNA were observed in transformed murine epithelial cells, but high levels could be induced by stimulation. Cytokines that signal through NF-B, including IL-1␤ and TNF-␣ or via JAK-STAT pathway including oncostatin M induced CCL28 in airway epithelial cells in vitro. Immunohistochemistry of murine airway tissue revealed that constitutive expression of CCL28 protein in vivo was low and not ubiquitous. However, abundant expression was detected in epithelia and lymphoid aggregates following allergic sensitization and challenge with ovalbumin. This was accompanied by increased detection of cells expressing CCR10 protein and mRNA in inflamed airways. Taken together, these data support a role for CCL28 in contributing to allergen driven airway pathologies, show that proinflammatory cytokines can induce this signal and suggest a role for CCR10 expressing cells in airway inflammation.

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Whole-cell pertussis vaccine protects against Bordetella pertussis exacerbation of allergic asthma

Cited by 18 publications

References 53 publications

Acellular Pertussis Vaccine Protects against Exacerbation of Allergic Asthma Due toBordetella pertussisin a Murine Model

Acellular Pertussis Vaccine Protects against Exacerbation of Allergic Asthma Due toBordetella pertussisin a Murine Model

A Live AttenuatedBordetella pertussisCandidate Vaccine Does Not Cause Disseminating Infection in Gamma Interferon Receptor Knockout Mice

Inflammation of the respiratory tract is associated with CCL28 and CCR10 expression in a murine model of allergic asthma

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