Vaccination with Heat-Killed<i>Listeria</i>as Adjuvant Reverses Established Allergen-Induced Airway Hyperreactivity and Inflammation: Role of CD8+ T Cells and IL-18

Hansen, Gesine; Yeung, V. Peter; Berry, Gerald J.; Umetsu, Dale T.; DeKruyff, Rosemarie H.

doi:10.4049/jimmunol.164.1.223

Cited by 105 publications

(80 citation statements)

References 54 publications

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“…The administration of various bacteria that can induce Th1-type immune responses has also been reported to inhibit the development of allergic-induced AHR. 40,41 These mechanisms have indirect inhibitory effects on the development of allergic AHR, since sensitization of hosts to a few species of bacteria, such as mycobacteria species, which can induce immune responses results in the elicitation of bacteria-specific Th1-type immune responses.…”

Section: Il-4 Antagonistic Mutant Dna Inhibits Allergic Airway Inflammentioning

confidence: 99%

A single administration of interleukin-4 antagonistic mutant DNA inhibits allergic airway inflammation in a mouse model of asthma

et al. 2003

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Interleukin 4 (IL-4) is essential for the switching of B cells to IgE antibody production and for the maturation of T helper (Th) cells toward the Th2 phenotype. These mechanisms are thought to play a crucial role in the pathogenesis of the allergic airway inflammation observed in asthma. In the present study, we examined the anti-inflammatory effects of DNA administration of murine IL-4 mutant Q116D/Y119D (IL-4 double mutant, IL-4DM), which binds to the IL-4 receptor a and is an antagonist for IL-4. Immunization of BALB/c mice with alum-adsorbed ovalbumin (OVA) followed by aspiration with aerosolized OVA resulted in the development of allergic airway inflammation. A single administration of IL-4DM DNA before the aerosolized OVA challenge protected the mice from the subsequent induction of allergic airway inflammation. Serum IgE level and extent of eosinophil infiltration in bronchoalveolar lavage (BAL) from IL-4DM DNA-administered mice were significantly lower than those in BAL from control plasmid-immunized mice. In our study, IL-4 or IL-4 mutants were not detected in sera from mice that had received a single administration of IL-4DM DNA. The results of this study provide evidence for the potential utility of IL-4 mutant antagonist DNA inoculation as an approach to gene therapy for asthma.

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Section: Il-4 Antagonistic Mutant Dna Inhibits Allergic Airway Inflammentioning

confidence: 99%

A single administration of interleukin-4 antagonistic mutant DNA inhibits allergic airway inflammation in a mouse model of asthma

et al. 2003

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“…6 Many subsequent studies also showed supportive data for the importance of immune deviation in the prevention of allergy. 19,20,[24][25][26] Immune regulation Although the relationship between the Th1-promoting effects of infections and the consequent inhibition of allergy provides an explanation for the hygiene hypothesis, the mechanism has been challenged because some Th1-type autoimmune diseases have also increased over the past decades. Moreover, some pro-Th2 parasitic infections were found to also inhibit allergic diseases.…”

Section: Immune Deviationmentioning

confidence: 99%

“…19,20 Some studies showed that systemic or mucosal administration of killed bacteria, introduction of bacterial CpG, and intramuscular infection with adenovirus also inhibit allergic reactions. [21][22][23][24][25][26] We have shown that the Chlamydia trachomatis mouse pneumonitis strain, more recently called C. muridarum, and BCG infections have a significant imprinting effect on newborn or young adult C57BL/6 and Balb/c mice; the imprinting inhibited allergy/asthma induced by natural or model allergens later in life. [31][32][33][34][35][36][37][38] In particular, C. muridarum infection had a strong imprinting effect on the inhibition of allergy, even after the infection had long been cleared.…”

Section: Introductionmentioning

confidence: 99%

“…18 In addition to epidemiological observations, experimental studies have also provided support for the hygiene hypothesis. [19][20][21][22][23][24][25][26][27][28][29][30] For example, BCG infection prevented the development of asthma-like reactions in a murine asthma model. 19,20 Some studies showed that systemic or mucosal administration of killed bacteria, introduction of bacterial CpG, and intramuscular infection with adenovirus also inhibit allergic reactions.…”

Section: Introductionmentioning

confidence: 99%

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Role of dendritic cells: a step forward for the hygiene hypothesis

Yang

Gao

2010

Cell Mol Immunol

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The hygiene hypothesis was proposed more than two decades ago, but its mechanism remains unclear. This review focuses on recent advances in the field, especially on the role played by dendritic cells (DCs) and their modulating effects on various infections and allergic diseases, including allergic asthma. DCs isolated from mice long after the resolution of an infection were reported to have a significant modulating effect on allergen-specific Th2 responses in both in vitro and in vivo systems. These DCs showed DC1-like and/or tolerogenic DC capacity, which allowed for the inhibition of allergic responses by immune deviation (enhancing Th1 response) and immune regulation (through regulatory T-cell and Th2 hyporesponsiveness) mechanisms. These findings represented a significant advance in the elucidation of the mechanisms underlying the hygiene hypothesis. Further investigation on the mechanisms by which DCs are 'educated' by infectious agents and the influence of the type, time, and extent of infections on this 'education' process will help us understand immune regulation in disease settings and in the rational design of preventive/therapeutic approaches to allergy/asthma and infections.

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“…Mice were bled, and serum levels of OVA-specific IgG1, IgG2a, and IgE Abs were measured using modified OVA-specific ELISAs as previously described (17). Anti-OVA IgG1 and IgG2a mAbs 6C1 and 3A11, respectively, were used as standards for the quantification of each IgG subclass.…”

Section: Ova-specific Igs Assaymentioning

confidence: 99%

Critical Role for IL-13 in the Development of Allergen-Induced Airway Hyperreactivity

Walter¹,

McIntire²,

Berry

et al. 2001

The Journal of Immunology

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378

257

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Airway hyperresponsiveness to a variety of specific and nonspecific stimuli is a cardinal feature of asthma, which affects nearly 10% of the population in industrialized countries. Eosinophilic pulmonary inflammation, eosinophil-derived products, as well as Th2 cytokines IL-13, IL-4, and IL-5, have been associated with the development of airway hyperreactivity (AHR), but the specific immunological basis underlying the development of AHR remains controversial. Herein we show that mice with targeted deletion of IL-13 failed to develop allergen-induced AHR, despite the presence of vigorous Th2-biased, eosinophilic pulmonary inflammation. However, AHR was restored in IL-13−/− mice by the administration of recombinant IL-13. Moreover, adoptive transfer of OVA-specific Th2 cells generated from TCR-transgenic IL-13−/− mice failed to induce AHR in recipient SCID mice, although such IL-13−/− Th2 cells produced high levels of IL-4 and IL-5 and induced significant airway inflammation. These studies definitively demonstrate that IL-13 is necessary and sufficient for the induction of AHR and that eosinophilic airway inflammation in the absence of IL-13 is inadequate for the induction of AHR. Therefore, treatment of human asthma with antagonists of IL-13 may be very effective.

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Vaccination with Heat-KilledListeriaas Adjuvant Reverses Established Allergen-Induced Airway Hyperreactivity and Inflammation: Role of CD8+ T Cells and IL-18

Cited by 105 publications

References 54 publications

A single administration of interleukin-4 antagonistic mutant DNA inhibits allergic airway inflammation in a mouse model of asthma

A single administration of interleukin-4 antagonistic mutant DNA inhibits allergic airway inflammation in a mouse model of asthma

Role of dendritic cells: a step forward for the hygiene hypothesis

Critical Role for IL-13 in the Development of Allergen-Induced Airway Hyperreactivity

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