Identification of basophils by immunohistochemistry in the airways of post‐mortem cases of fatal asthma

Koshino, Takeshi; Teshima, Shin‐ichi; Fukushima, Naoya; Takaishi, Toshiaki; Hirai, Koichi; Miyamoto, Yukio; Arai, Yasuo; Sano, Yamato; Itō, Kōji; Morita, Yutaka

doi:10.1111/j.1365-2222.1993.tb00276.x

Cited by 93 publications

(59 citation statements)

References 31 publications

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“…In asthma and, according to some reports, in nonasthmatic subjects, the ASM bundle is infiltrated by mast cells, predominately of the chymase-positive phenotype [11][12][13][14][15][16][17][18]. Mast cell-ASM interactions in asthma are summarised in figure 1.…”

Section: Inflammatory Cell Localisation To Asm Bundlementioning

confidence: 99%

“…To date, little attention has been paid to the localisation of inflammatory cells within structural compartments of the airway wall. Recently, enthusiasm for the view that microlocalisation is important in obstructive airway diseases has been fuelled by studies showing inflammatory cells within the ASM in asthma [11][12][13][14][15][16][17][18] and COPD [19], but not in normal controls. Most notably, in asthma the ASM is infiltrated by mast cells and the number of mast cells within the ASM bundle was associated with the degree of AHR [11].…”

mentioning

confidence: 99%

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Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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Airway inflammation is a critical feature of the airway diseases asthma and chronic obstructive pulmonary disease (COPD). There is emerging evidence that structural cells play a key role in the development and perpetuation of the inflammatory response and are pivotal in the development of the changes in the airway structures that lead to airway remodelling.To date, little attention has been given to the localisation of inflammatory cells to airway structures or the potential interactions between these intimately located cells. However, it is likely that interactions between inflammatory and structural cells in the airway contribute enormously to the pathophysiology of asthma and COPD.Indeed, recent evidence suggests that mast cells localised to the airway smooth muscle bundle may be important in the development of airway hyperresponsiveness in asthma.In the present article, the authors aim to summarise: 1) the current understanding of which inflammatory cells locate to airway structures; 2) the proposed mechanisms that may be involved in mediating this microlocalisation; 3) the possible consequences of interactions between inflammatory and structural cells; and 4) the pressing need to investigate whether modulating these interactions is beneficial in asthma and chronic obstructive pulmonary disease.

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Section: Inflammatory Cell Localisation To Asm Bundlementioning

confidence: 99%

mentioning

confidence: 99%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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“…5 Basophils are found in the lungs of patients with allergic asthma, and probably contribute to pathogenesis during fatal asthma. 6,7 On the other hand, they might contribute to protective immunity against helminths since basophils are an important source for IL-4 and IL-13. 8 Recently, basophils have been shown to be implicated in polarization of T-helper 2 (Th2) cells by allergens with protease activity 9 and IgG1-mediated anaphylaxis, 10 which further demonstrates their important functions during type 2 immune responses.…”

Section: Introductionmentioning

confidence: 99%

Basophil effector function and homeostasis during helminth infection

Ohnmacht¹,

Voehringer²

2009

Blood

179

161

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IntroductionBasophil development and function is poorly understood, although this rare cell type was identified by Paul Ehrlich in 1879. 1 Basophils constitute less than 0.3% of leukocytes in the peripheral blood. They are functionally closely related to mast cells, since both cell types express the high-affinity receptor for IgE and produce similar effector molecules, including histamine, lipid mediators (eg, leukotrienes and prostaglandins), serine proteases, and interleukins (eg, IL-4, IL-13, and IL-6). 2 However, the developmental and functional relationship of basophils to other cell types is not clearly established. Helminth infections of mice cause a dramatic increase in basophil numbers, which is thought to be mediated by However, naive IL-3-deficient mice have normal levels of basophils, indicating that IL-3 promotes basophil development and/or survival but is not essential for the basophil lineage. 3 Increased numbers of basophils are found in the skin during the late-phase response of contact dermatitis 4 or atopic dermatitis. 5 Basophils are found in the lungs of patients with allergic asthma, and probably contribute to pathogenesis during fatal asthma. 6,7 On the other hand, they might contribute to protective immunity against helminths since basophils are an important source for IL-4 and IL-13. 8 Recently, basophils have been shown to be implicated in polarization of T-helper 2 (Th2) cells by allergens with protease activity 9 and IgG1-mediated anaphylaxis, 10 which further demonstrates their important functions during type 2 immune responses.The turnover of basophils has not yet been described, and their localization in tissues is essentially unknown. Basophils could enhance Th2-associated immune responses since they release IL-4 within minutes of activation. 11,12 Activation can occur by crosslinking of surface-bound IgE molecules or by a large variety of substances in an antigen-unspecific manner (reviewed in Falcone et al 2 ). Mast cells and basophils express constitutively low levels of IL-4, which can be visualized by using sensitive IL-4 reporter mice expressing enhanced green fluorescent protein (eGFP) under control of regulatory elements of IL-4 (4get mice 13 ). Infection of 4get mice with the helminth Nippostrongylus brasiliensis causes massive type 2 immune responses in the lung and small intestine, providing a valuable model to study basophil function during parasitic infections in vivo.Here, we analyzed basophil development and turnover by flow cytometry, BrdU incorporation, and adoptive transfer. We determined the localization of basophils in the spleen, lung, and small intestine of N brasiliensis-infected mice by immunofluorescence staining of tissue sections. Basophils were found to promote differentiation of alternatively activated macrophages in the lung, induce systemic eosinophilia, and contribute to worm expulsion in N brasiliensis-infected mice, demonstrating their central role during the effector phase of a type 2 immune response against helminths. MethodsMice IL-4 reporter ...

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“…Twenty-four hours after ICHT-F in Group A, the level of IL-18 correlated with the proportion of basophils at the 4 h time-point. These cells are major inducers of allergic infl ammation [18][19][20]. Yoshimoto et al [31] has demonstrated that IL-18 has a potential to stimulate basophils to release large amounts of IL-4 and IL-13 in vitro in the presence of IL-3.…”

Section: Discussionmentioning

confidence: 99%

“…Twenty-four hours after the provocation with fl our allergens, basophil proportion was also signifi cantly higher in Group A than in Group C. Basophils play a signifi cant role in allergic response [17]. They have been reported in the respiratory tract of patients dying of asthma, during the exacerbations of this disease and during the late asthmatic response to the allergen [18][19][20]. It is estimated that in the late asthmatic reaction, more than 95% of all metachromatic cells in the bronchoalveolar lavage fl uid are basophils [20,21].…”

Section: Il-18 Levels In Nlf After Icht-fmentioning

confidence: 99%

IL-18 Levels in Nasal Lavage After Inhalatory Challenge Test with Flour in Bakers Diagnosed with Occupational Asthma

Krakowiak

Walusiak²,

Wiszniewska³

et al. 2008

International Journal of Occupational Medicine and Environmental Health

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Objectives: The authors discuss the outcomes of a study on IL-18 concentration in nasal washings after the inhalatory challenge test with fl our allergens (ICHT-F) in bakers with fl our-induced occupational airway allergy (OAA) Methods: We measured IL-18 concentration using ELISA kit and assessed morphological changes in nasal lavage fl uid (NLF) before, and 4 h and 24 h after ICHT-F in three groups of subjects: Group A -9 patients with diagnosed OAA (occupational asthma and rhinitis), Group B -10 patients with atopic asthma and rhinitis, and Group C -9 healthy volunteers. Results: In Group A, signifi cant differences in the basophil proportion in NLF were noted only 24 h after ICHT-F. Both the basophil proportion and total eosinophil count were higher in Group A than in Group C at this time-point. Group A also showed a statistically signifi cant increase in IL-18 levels 4 h after the challenge. A signifi cant relationship was noted between the proportion of basophils 4 h after ICHT-F and IL-18 level at 24 h after the test. Conclusions: This is the fi rst study demonstrating an increased expression of IL-18 in nasal washings of subjects diagnosed with OAA to fl our allergens. The observed higher concentrations of IL-18 in nasal washings after ICHT as well as the increase in the proportion of basophils provide evidence for the important role of IL-18 in persistent allergic infl ammation.

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Identification of basophils by immunohistochemistry in the airways of post‐mortem cases of fatal asthma

Cited by 93 publications

References 31 publications

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Basophil effector function and homeostasis during helminth infection

IL-18 Levels in Nasal Lavage After Inhalatory Challenge Test with Flour in Bakers Diagnosed with Occupational Asthma

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