Eosinophils and eosinophil-associated diseases: An update

O’Sullivan, Jeremy A.; Bochner, Bruce S.

doi:10.1016/j.jaci.2017.09.022

Cited by 93 publications

(72 citation statements)

References 90 publications

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“…53,54 The development of eosinophil-deficient mouse models (outlined in Table 2) has enabled researchers to better understand eosinophil function, particularly in inflammatory settings. As the focus of this review/ commentary is on homeostatic eosinophil function we refer readers to excellent reviews for more in-depth information on the role of eosinophils in the context of eosinophil-associated disorders 1,2,55,56 or anti-parasitic immunity. 57,58 These models have also opened new doors and avenues to explore the functional significance of eosinophil residency in tissues under homeostasis.…”

Section: Contributions Of Tissue-resident Eosinophils To Tissue Homeomentioning

confidence: 99%

The emerging roles of eosinophils in mucosal homeostasis

et al. 2020

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Eosinophils are granulocytes, typically implicated as end-stage effector cells in type-II immune responses. They are capable of producing a wide array of pre-formed molecules which render them with vast potential to influence a wide variety of processes. Nonetheless, eosinophil research has traditionally focused on their role in anti-helminthic responses and pathophysiological processes in type-II immune disorders, such as allergy and asthma, where eosinophilia is a hallmark phenotype. However, a number of key studies over the past decade have placed this restricted view of eosinophil function into question, presenting additional evidence for eosinophils as critical regulators of various homeostatic processes including immune maintenance, organ development, and tissue regeneration.

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Section: Contributions Of Tissue-resident Eosinophils To Tissue Homeomentioning

confidence: 99%

The emerging roles of eosinophils in mucosal homeostasis

et al. 2020

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“…Eosinophils accumulate at sites of allergic inflammation and play important roles in the pathogenesis of diseases, including EP, through the release of a variety of mediators, including specific granule proteins, such as major basic protein, cysteinyl leukotrienes (cysLTs), radical oxygen species, and cytokines [20]. Among them, IL-5 is a well-recognized cytokine associated with eosinophilic inflammation.…”

Section: Mechanisms For the Development Of Eosinophilic Airway Inflammentioning

confidence: 99%

Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia

Nakagome

Nagata

2020

Biomolecules

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Eosinophilic pneumonia (EP), including acute EP and chronic EP, is characterized by the massive pulmonary infiltration of eosinophils into the lung. However, the mechanisms underlying the selective accumulation of eosinophils in EP have not yet been fully elucidated. We reported that bronchoalveolar lavage fluid (BALF) from EP patients induced the transmigration of eosinophils across endothelial cells in vitro. The concentrations of eotaxin-2 (CCL24) and monocyte chemotactic protein (MCP)-4 (CCL13), which are CC chemokine receptor (CCR) 3 ligands, were elevated in the BALF of EP patients, and anti-CCR3 monoclonal antibody inhibited the eosinophil transmigration induced by the BALF of EP patients. The concentration of macrophage inflammatory protein 1β (CCL4), a CCR5 ligand that induces eosinophil migration, was increased in the BALF of EP patients. Furthermore, the concentration of interleukin (IL) 5 was increased in the BALF of EP patients, and it has been reported that anti-IL-5 antibody treatment resulted in remission and the reduction of glucocorticoid use in some cases of chronic EP. The concentrations of lipid mediators, such as leukotriene (LT) B 4 , damage-associated molecular pattern molecules (DAMPs), such as uric acid, or extracellular matrix proteins, such as periostin, were also increased in the BALF of EP patients. These findings suggest that chemokines, such as CCR3/CCR5 ligands, cytokines, such as IL-5, lipid mediators, such as LTB 4 , DAMPs, and extracellular matrix proteins may play roles in the accumulation or activation of eosinophils in EP.Biomolecules 2020, 10, 638 2 of 12 mechanisms of eosinophil accumulation in the airway of EP patients are discussed. The aim of this review is to better understand the mechanisms of eosinophil accumulation and activation in EP. AEP and CEPAEP is characterized by acute febrile illness with diffuse pulmonary infiltrates, severe hypoxemia, and increased eosinophils in bronchoalveolar lavage fluid (BALF) [3]. AEP is diagnosed based on the following: acute onset of respiratory failure, diffuse pulmonary infiltrates on chest roentgenogram, and increased numbers of eosinophils in BALF (more than 25% of total cells) [3]. Although the mechanisms of AEP have not yet been fully established, inhaled agents, such as cigarette smoke or chemical agents, are known causes of AEP [1,2,[5][6][7][8][9]. For example, a relationship was observed between the recent onset of cigarette smoking and the development of AEP [5][6][7]. Even short-term passive smoking can induce AEP [7]. The collapse of the World Trade Center towers [8] and the desert of the Middle East [9] have also been reported to induce AEP.

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“…Indeed, Muc5b KO mice show highly penetrant susceptibility to spontaneous middle ear infection. As it is becoming increasingly clear that the glycosylation pattern of mucins influences their immune function, it is noteworthy that glycans impact mucin differential targeting of immune effector cells and are key regulators in mucosal diseases [194]. Glycans are sugar molecules, such as sialic acids and fucose, that are attached to glycoproteins and are recognized by specific glycan-binding proteins leading to a variety of functions, such as proinflammatory and anti-inflammatory cellular responses [195].…”

Section: Host Inflammatory Responsementioning

confidence: 99%