Glucocorticoids induce the production of the chemoattractant CCL20 in airway epithelium

Persson, C. G. A.; Uller, Lena

doi:10.1183/09031936.00179314

Cited by 2 publications

(2 citation statements)

References 10 publications

(21 reference statements)

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“…Similar to IL-8, IL-17A is capable of inducing airway neutrophilia [62,63], and this induced neutrophilic inflammation is independent of GC sensitivity. Moreover, IL-17A seems to induce GC insensitivity [64], and GCs can prolong the survival of neutrophils [65][66][67][68], which may be mediated, in part, by upregulation of neutrophil-active mediators in the asthmatic mucosa [69][70][71]. As noted, deregulation of constitutive neutrophil apoptosis has been demonstrated for airway neutrophils in sputum of severe neutrophilic asthma but independent of GCs [14].…”

Section: Severe Neutrophilic Asthmamentioning

confidence: 99%

“…Biol. 98: 549-556;2015. Abbreviations: AP = antigen presentation, BAL = bronchoalveolar lavage, BM = bone marrow, CD = cluster of differentiation, CRP = C-reactive protein, CXC = cysteine-X-cysteine, ENA-78 = epithelial-neutrophil activating peptide 78, FEV1 = forced expiratory volume in 1 s, FIF50% = forced inspiratory flow at the 50% point, GC = glucocorticoid, GERD = gastroesophageal reflux disease, G-MDSC = granulocytic myeloid-derived suppressor cells, (continued on next page) 0741-5400/15/0098-549…”

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confidence: 99%

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Targeting neutrophilic inflammation in severe neutrophilic asthma: can we target the disease-relevant neutrophil phenotype?

Bruijnzeel

Uddin

Koenderman

2015

Journal of Leukocyte Biology

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In severe, neutrophilic asthma, neutrophils are thought to have an important role in both the maintenance of the disease and during exacerbations. These patients often display excessive, mucosal airway inflammation with unresolving neutrophilia. Because this variant of asthma is poorly controlled by glucocorticoids, specific pharmacologic targeting of neutrophils seems a plausible therapeutic approach. However, most attempts with this approach have failed in the clinic. We propose that this could be attributed, in part, to an incomplete understanding of the emerging new insights underlying neutrophil homeostasis and life span, neutrophil reverse transmigration, neutrophil phenotypes, and neutrophil transdifferentiation in human health and disease. Of clinical relevance, recent translational studies have started to uncover distinct neutrophil subsets in humans, namely mature and hypersegmented phenotypes that have bimodal immunomodulatory functions during an acute inflammatory response. In this review, we will elaborate on some of the novel insights in neutrophil biology and attempt to translate them into potential consequences for pharmacologic intervention of severe neutrophilic asthma. We speculate that the disease-relevant neutrophil phenotype should be targeted selectively without compromising the immunomodulatory functions essential for homeostasis and pulmonary immunity. However, the identity and exact functional role of distinct neutrophil phenotypes in inflammatory diseases of the human airway remain elusive.

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