Inhibition of airway eosinophilia and pulmonary pathology in a mouse model of allergic asthma by the live vaccine strain of <i>Francisella tularensis</i>

KuoLee, Rhonda; Zhou, Hongyan; Harris, Greg; Zhao, Xigeng; Qiu, Hongyu; Patel, G. B.; Chen, W.

doi:10.1111/j.1365-2222.2008.02956.x

Cited by 10 publications

(13 citation statements)

References 48 publications

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“…This idea is supported by many experimental and clinical studies with several microbes and their products [8]–[17].…”

Section: Introductionmentioning

confidence: 86%

“…Airway eosinophilia in the mouse model was induced as described before [17] and is illustrated in Figure 1. Briefly, mice were sensitized by intraperitoneal (i.p) injection of 2 µg OVA (Sigma Chemical Co., St Louis, MO, USA) admixed in 100 µl alum (Pierce Laboratories, Rockford, IL, USA) at day 0 and 14.…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted using TRIzol (Invitrogen Canada, Burlington). Relative abundance of cytokine mRNA in lungs were evaluated using a real-time RT-PCR-based method, as described elsewhere [17]. Briefly, single stranded cDNA was prepared through reverse transcription, cytokine genes were amplified and quantified using primers and probes designed with the Primer3 program [22].…”

Section: Methodsmentioning

confidence: 99%

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Acinetobacter baumannii Infection Inhibits Airway Eosinophilia and Lung Pathology in a Mouse Model of Allergic Asthma

et al. 2011

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Allergic asthma is a dysregulation of the immune system which leads to the development of Th2 responses to innocuous antigens (allergens). Some infections and microbial components can re-direct the immune response toward the Th1 response, or induce regulatory T cells to suppress the Th2 response, thereby inhibiting the development of allergic asthma. Since Acinetobacter baumannii infection can modulate lung cellular and cytokine responses, we studied the effect of A. baumannii in modulating airway eosinophilia in a mouse model of allergic asthma. Ovalbumin (OVA)-sensitized mice were treated with live A. baumannii or phosphate buffered saline (PBS), then intranasally challenged with OVA. Compared to PBS, A. baumannii treatment significantly reduced pulmonary Th2 cytokine and chemokine responses to OVA challenge. More importantly, the airway inflammation in A. baumannii-treated mice was strongly suppressed, as seen by the significant reduction of the proportion and the total number of eosinophils in the bronchoalveolar lavage fluid. In addition, A. baumannii-treated mice diminished lung mucus overproduction and pathology. However, A. baumannii treatment did not significantly alter systemic immune responses to OVA. Serum OVA-specific IgE, IgG1 and IgG2a levels were comparable between A. baumannii- and PBS-treated mice, and tracheobronchial lymph node cells from both treatment groups produced similar levels of Th1 and Th2 cytokines in response to in vitro OVA stimulation. Moreover, it appears that TLR-4 and IFN-γ were not directly involved in the A. baumannii-induced suppression of airway eosinophilia. Our results suggest that A. baumannii inhibits allergic airway inflammation by direct suppression of local pulmonary Th2 cytokine responses to the allergen.

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“…This idea is supported by many experimental and clinical studies with several microbes and their products [8]–[17].…”

Section: Introductionmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Acinetobacter baumannii Infection Inhibits Airway Eosinophilia and Lung Pathology in a Mouse Model of Allergic Asthma

et al. 2011

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“…Similarly, it has been suggested that induction of IL-4 following LVS infection of macrophages exacerbates disease [24]. In contrast, other laboratories have shown that production of IL-4 aids in clearance of LVS infection and that LVS can inhibit inflammation mediated, in part, by IL-4 [25], [26]. Furthermore, the ability of attenuated strains to provoke cytokine production and activate the inflammasome among infected host cells has also been a point of controversy [27]–[30].…”

Section: Introductionmentioning

confidence: 99%

Generation of a Convalescent Model of Virulent Francisella tularensis Infection for Assessment of Host Requirements for Survival of Tularemia

2012

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Francisella tularensis is a facultative intracellular bacterium and the causative agent of tularemia. Development of novel vaccines and therapeutics for tularemia has been hampered by the lack of understanding of which immune components are required to survive infection. Defining these requirements for protection against virulent F. tularensis , such as strain SchuS4, has been difficult since experimentally infected animals typically die within 5 days after exposure to as few as 10 bacteria. Such a short mean time to death typically precludes development, and therefore assessment, of immune responses directed against virulent F. tularensis . To enable identification of the components of the immune system that are required for survival of virulent F. tularensis , we developed a convalescent model of tularemia in C57Bl/6 mice using low dose antibiotic therapy in which the host immune response is ultimately responsible for clearance of the bacterium. Using this model we demonstrate αβTCR + cells, γδTCR + cells, and B cells are necessary to survive primary SchuS4 infection. Analysis of mice deficient in specific soluble mediators shows that IL-12p40 and IL-12p35 are essential for survival of SchuS4 infection. We also show that IFN-γ is required for survival of SchuS4 infection since mice lacking IFN-γR succumb to disease during the course of antibiotic therapy. Finally, we found that both CD4 + and CD8 + cells are the primary producers of IFN-γand that γδTCR + cells and NK cells make a minimal contribution toward production of this cytokine throughout infection. Together these data provide a novel model that identifies key cells and cytokines required for survival or exacerbation of infection with virulent F. tularensis and provides evidence that this model will be a useful tool for better understanding the dynamics of tularemia infection.

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“…There is a consensus that airway eosinophilia plays a key role in allergic occupational and nonoccupational rhinitis and asthma. Interestingly, a recent animal study demonstrated the capability of a live vaccine strain to suppress airway eosinophilia and lung pathology using a murine model of allergic disease [34]. This constitutes a potential novel treatment avenue that should be explored further.…”

Section: Diagnostic Means and Treatmentmentioning

confidence: 98%

Occupational Rhinitis and Asthma: Where Do We Stand, Where Do We Go?

Castaño

Malo

2010

Curr Allergy Asthma Rep

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This review provides an overview of current and emerging issues regarding occupational rhinitis (OR) and occupational asthma (OA), focusing on studies discussing concepts and results that are relevant to both diseases. OA and OR are conditions that affect the upper and lower airways, are characterized by reduced airway caliber and hyperresponsiveness and by inflammation, and are caused by agents present in the workplace. To explain disease expression, research is moving from the T-helper type 1/type 2 cells paradigm to consider the contribution of diverse alternative pathways such as neural inflammation, a dysfunctional epithelial barrier, and autoimmune mechanisms, among others. Objective assessment of OR and OA has been improved and tested for research and, currently, clinical application. Further developments in the field of OR are expected to lead to more generalized clinical applications, following the example of what has been achieved for OA.

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Inhibition of airway eosinophilia and pulmonary pathology in a mouse model of allergic asthma by the live vaccine strain of Francisella tularensis

Abstract: F. tularensis LVS is capable of suppressing allergic airway inflammation probably through a Th1-mediated suppression of an ongoing Th2 response mechanism, and raises the possibility of exploring LVS and its components as potential therapeutic modalities for human allergic asthma.

Cited by 10 publications

References 48 publications

Acinetobacter baumannii Infection Inhibits Airway Eosinophilia and Lung Pathology in a Mouse Model of Allergic Asthma

Acinetobacter baumannii Infection Inhibits Airway Eosinophilia and Lung Pathology in a Mouse Model of Allergic Asthma

Generation of a Convalescent Model of Virulent Francisella tularensis Infection for Assessment of Host Requirements for Survival of Tularemia

Occupational Rhinitis and Asthma: Where Do We Stand, Where Do We Go?

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