Eosinophil Accumulation and Activation in Antigen-Induced Late Asthmatic Response in Guinea Pigs

Sugiyama, Haruhito; Eda, Ryosuke; Okada, Chiharu; Hopp, Russell J.; Bewtra, Againdra K.; Townley, Robert G.

doi:10.3109/02770909509089498

Cited by 8 publications

(3 citation statements)

References 22 publications

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“…However, it can not be excluded that NO is involved in adhesion and chemotaxis of eosinophils because it has been reported that eosinophils have iNOS (Pozo et al , 1997) and NO inhibits apoptosis of eosinophils (Beauvais et al , 1995). Moreover, eosinophils are reported to produce a large amount of superoxide in LAR (Sugiyama et al , 1995) and it is possible that eosinophils produce peroxynitrite and worsen airway inflammation. Consequently, the mechanisms by which NOS inhibitors suppress eosinophilic inflammation appear to be complicated.…”

Section: Discussionmentioning

confidence: 99%

Role of endogenous nitric oxide in allergen‐induced airway responses in guinea‐pigs

Iijima

Uchida

Endo

et al. 1998

British J Pharmacology

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1 Endogenous nitric oxide (NO) can be detected in exhaled air and accumulates in in¯amed airways. However its physiological role has not been fully elucidated. In this study, we investigated a role for endogenous NO in allergen-induced airway responses. Sensitised guinea-pigs were treated with N G -nitro-L-arginine methyl ester L-NAME (2.0 mM) or aminoguanidine (AG) (2.0 mM) 30 min before the allergen challenge, and 3 and 4 h after the challenge. Alternatively, L-arginine (2.4 mM) treatment was performed 30 min before, and 2 and 3 h after the challenge. In all groups, ovalbumin (OVA) challenge (2 mg ml 71 for 2 min) was performed, and airway responses, NO production, in®ltration of in¯ammatory cells, plasma exudation and histological details were examined. 2 Allergen-challenged animals showed an immediate airway response (IAR) and a late airway response (LAR), which synchronised with an increase in exhaled NO. Treatment with L-NAME and AG did not aect IAR while they signi®cantly blocked LAR (72% and 80% inhibition compared to vehicle) and production of NO (35% and 40% inhibition). On the other hand, treatment with L-arginine did not aect IAR but potentiated LAR (74% augmentation). 3 In bronchoalveolar lavage (BAL)¯uid, allergen-induced increases in eosinophils were reduced by 48% for L-NAME treatment compared to vehicle, and increased by 56% for L-arginine treatment. 4 Treatment with L-NAME signi®cantly decreased airway microvascular permeability to both Monastral blue (MB) and Evans blue (EB) dye (50.6% and 44% inhibition). 5 We conclude that allergen-induced LAR is closely associated with NO production, and that NO plays a critical role in in¯ammatory cell in®ltration and plasma exudation in the allergic condition.

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Section: Discussionmentioning

confidence: 99%

Role of endogenous nitric oxide in allergen‐induced airway responses in guinea‐pigs

Iijima

Uchida

Endo

et al. 1998

British J Pharmacology

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“…Previous reports have shown that the number of eosinophils recovered in BALF was correlated with AHR in asthmatic subjects (6,(25)(26)(27)(28)(29), sensitized guinea pigs (7,23,30), sensitized primates (31), sensitized dogs (32) exposed to allergen, as well as in rats after repeted injections of Sephadex beads (19). However, in asthmatic subjects (33,34), sensitized guinea pigs (10,(35)(36)(37)(38), sensitized primates (39) and sensitized rats (40) exposed to allergen, and in ozone-induced AHR in dogs (41) BALF eosinophilia failed to be correlated to the development of AHR.…”

Section: Discussionmentioning

confidence: 99%

Kinetics of eosinophilia and eosinophil activation in the development of non-allergic bronchial hyperresponsiveness in guinea pigs injected with Sephadex beads

et al. 1996

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Eosinophils are believed to play a crucial role in the pathogenesis of airway hyperresponsiveness (AHR). In the present study, the involvement of blood and pulmonary eosinophilia as well as the eosinophil activation in the onset of non-allergic AHR caused by the injection of G-50 Sephadex beads in guinea pigs was investigated. Reactivity of the isolated lower bronchus to histamine was measured ex vivo in a bioassay system. The increase of reactivity of the isolated lower bronchus of Sephadex-injected animals to histamine was observed as early as 3 h after the Sephadex injection and was maximal between 6-24 h. Sephadex-induced blood eosinophilia was characterized by two successive increases of blood eosinophil counts peaking at 3 and 12 h respectively. The recruitment of inflammatory cells into the lungs as measured in bronchoalveolar lavage fluid (BALF) have shown that the neutrophils were initially increased at 3 h whereas the number of eosinophils increased only 6 h after the bead injection; both cell populations were maximal 24 h later. Eosinophil peroxidase (EPO) activity was used as a marker for the apparent number of eosinophils in airways and the degree of activation of eosinophils recovered in BALF. Results have shown that EPO activity in the lower bronchus of Sephadex-injected animals increased at 6 h, decreased at 12 h and was maximal 24 h later. The EPO activity recovered in BALF was maximal between 6 to 24 h after the bead injection in guinea pigs. Correlation between the number of eosinophils and the EPO activity in BALF suggests that BALF eosinophils have been activated and have degranulated in airways. Correlation studies also indicated that both Sephadex induced blood eosinophilia and eosinophil activation were associated to the development of AHR. In contrast, the increase of EPO activity in the lower bronchus and BALF eosinophilia were not correlated to the development of AHR in our model. In conclusion, our results suggest that Sephadex induced non-allergic AHR in guinea pigs could be related, at least in part, to blood eosinophilia and eosinophil activation. Whether blood, airway and BALF eosinophilia as well as eosinophil activation are relevant factors to determine the potential role of eosinophils in the pathogenesis of AHR is discussed.

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“…In this allergic murine model of asthma, we have examined many of the important features of asthma, including airway hyperresponsiveness to methacholine, which has long been used to characterize asthma 21 . Tissue and blood eosinophilia are also hallmarks of asthma 22,23 24 was also examined in this allergic murine model of asthma.…”

Section: Mycobacterial Vaccines In a Mouse Model Of Asthmamentioning

confidence: 99%

Immunomodulation in the treatment and/or prevention of bronchial asthma

Townley

Hopp

Agrawal

et al. 2002

Allergology International

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The immunologic hallmark of atopic allergy and asthma is an increased production of IgE and T helper (h) type 2 cell cytokines (interleukin (IL)-4, IL-5, IL-9 and IL-13) by Th cells reacting to common environmental allergens. All of us inhale allergens and healthy non-atopics produce allergen-specific IgG1, IgG4 and the Th1 cytokine interferon-α, as well as IL-12 from macrophages. We now have many modalities of immunomodulation to decrease the effect of IL-4 or IL-5 or production and level of IgE or agents to shift the immune response from a Th2 to a Th1 response, thereby decreasing the allergic inflammatory response in the airways. In the present review we focus on conventional immunotherapy, mycobacterial vaccines, DNA vaccines using cytosine guanosine, inhibitors of IL-4 and IL-5 and anti-IgE: Omalizumab.

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Eosinophil Accumulation and Activation in Antigen-Induced Late Asthmatic Response in Guinea Pigs

Cited by 8 publications

References 22 publications

Role of endogenous nitric oxide in allergen‐induced airway responses in guinea‐pigs

Role of endogenous nitric oxide in allergen‐induced airway responses in guinea‐pigs

Kinetics of eosinophilia and eosinophil activation in the development of non-allergic bronchial hyperresponsiveness in guinea pigs injected with Sephadex beads

Immunomodulation in the treatment and/or prevention of bronchial asthma

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