The eosinophilic leukocyte and the pathology of fatal bronchial asthma: Evidence for pathologic heterogeneity

Gleich, Gerald J.; Motojima, Seiji; Frigas, Evangelo; Kephart, Gail M.; Fujisawa, Takao; Kravis, Lillian P.

doi:10.1016/0091-6749(87)90063-7

Cited by 57 publications

(22 citation statements)

References 14 publications

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“…Eosinophilic inflammation has been correlated with the severity of asthma (1), and fatal asthma is associated with accumulation of eosinophils in airway mucosa and submucosa (2,3). A recent study conducted in transgenic mice lacking eosinophils demonstrated the unequivocal importance of eosinophils in allergic inflammation and experimental asthma (4).…”

Section: Introductionmentioning

confidence: 99%

ROS generated by pollen NADPH oxidase provide a signal that augments antigen-induced allergic airway inflammation

Boldogh¹

2005

Journal of Clinical Investigation

326

366

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Pollen exposure induces allergic airway inflammation in sensitized subjects. The role of antigenic pollen proteins in the induction of allergic airway inflammation is well characterized, but the contribution of other constituents in pollen grains to this process is unknown. Here we show that pollen grains and their extracts contain intrinsic NADPH oxidases. The pollen NADPH oxidases rapidly increased the levels of ROS in lung epithelium as well as the amount of oxidized glutathione (GSSG) and 4-hydroxynonenal (4-HNE) in airwaylining fluid. These oxidases, as well as products of oxidative stress (such as GSSG and 4-HNE) generated by these enzymes, induced neutrophil recruitment to the airways independent of the adaptive immune response. Removal of pollen NADPH oxidase activity from the challenge material reduced antigen-induced allergic airway inflammation, the number of mucin-containing cells in airway epithelium, and antigen-specific IgE levels in sensitized mice. Furthermore, challenge with Amb a 1, the major antigen in ragweed pollen extract that does not possess NADPH oxidase activity, induced low-grade allergic airway inflammation. Addition of GSSG or 4-HNE to Amb a 1 challenge material boosted allergic airway inflammation. We propose that oxidative stress generated by pollen NADPH oxidases (signal 1) augments allergic airway inflammation induced by pollen antigen (signal 2).

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Section: Introductionmentioning

confidence: 99%

ROS generated by pollen NADPH oxidase provide a signal that augments antigen-induced allergic airway inflammation

Boldogh¹

2005

Journal of Clinical Investigation

326

366

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“…Studies have demonstrated that MBP is toxic to human tracheal epithelium [5,20]. Gleich et al [21] have reported that eosinophil products contribute to the latephase asthmatic reaction and pathogenesis of asthma.…”

Section: Discussionmentioning

confidence: 99%

Major Basic Protein and Topical Administration of Ketotifen in Pollinosis under Natural Allergen Provocation

Kato

Hattori²,

Kitamura³

et al. 1995

ORL

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In this study we investigated the potential relation among subjective symptoms, blood eosinophil counts and the levels of major basic protein (MBP) in serum throughout the pre- to postpollen season. In addition, we compared the effects of topical administration of ketotifen on these parameters between the prophylactic treatment group (n = 10) and the postsymptomatic treatment group (n = 10). We found that (1) the levels of MBP in serum during the season were significantly higher than those before the season and (2) the levels of the above three parameters in the prophylactic treatment group were significantly lower than those in the postsymptomatic treatment group during the season. It was concluded from these results that the action of MBP may be involved in the pathogenesis of allergic rhinitis. Furthermore, for the first time we provided evidence that topical ketotifen administration could suppress the systemic upregulation of the blood eosinophil count and MBP level in subjects with pollinosis.

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“…Either intact eosinophils or deposits of eosinophil major basic protein are especially abundant near areas of epithelial damage, but neutrophils are conspicuously absent. Bronchial mucous glands are enlarged, and bronchial smooth muscle is hypertrophied [14, 15]. Although the bulk of this information comes from autopsies, both biopsies and studies of bronchial secretions have confirmed that similar inflammatory changes are present in the airways even when the disease is mild [16, 17].…”

Section: Histopathology Of Bronchial Asthma [13]mentioning

confidence: 99%

Simple Understanding and Optimistic Strategy for Coping with Atopic Diseases

Okudaira

Mori²

1998

Int Arch Allergy Immunol

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In this article, accumulated investigations were reviewed to present an 'IL–5 central hypothesis' for eosinophilic inflammation. In this simple working hypothesis, mechanisms of clinical amelioration of atopic diseases manifested by glucocorticoids or immunosuppressants such as cyclosporin A or FK506 were easily understood to stem from the inhibition of IL–5 production and gene transcription. Screening of macrolide molecules resulted in the detection of nonactin (code name: OM–01), which inhibits production and gene transcription of IL–5 but not of IL–2 or IL–4. It was suggested that this kind of approach may open a new era of 'specific gene transcription control' for the management of allergic and other human disorders.

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The eosinophilic leukocyte and the pathology of fatal bronchial asthma: Evidence for pathologic heterogeneity

Cited by 57 publications

References 14 publications

ROS generated by pollen NADPH oxidase provide a signal that augments antigen-induced allergic airway inflammation

ROS generated by pollen NADPH oxidase provide a signal that augments antigen-induced allergic airway inflammation

Major Basic Protein and Topical Administration of Ketotifen in Pollinosis under Natural Allergen Provocation

Simple Understanding and Optimistic Strategy for Coping with Atopic Diseases

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