A tale of two cytokines: IL-17 and IL-22 in asthma and infection

Manni, Michelle L.; Robinson, Keven M.; Alcorn, John F.

doi:10.1586/17476348.2014.854167

Cited by 82 publications

(79 citation statements)

References 200 publications

(210 reference statements)

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“…This hypothesis is supported by in vitro data showing that the lung epithelial cells are capable of producing various chemokines including IL-8 and CXCL5 upon IL-17 stimulation (Manni et al, 2014). In situ hybridization staining on the lungs from K. pneumoniae infected mice also demonstrated that the mRNA expression of Cxcl1 and Cxcl2 are co-localized within the lung epithelium and administration of IL-17 augmented hybridization signals (Aujla et al, 2008).…”

Section: Discussionmentioning

confidence: 72%

IL-17 Receptor Signaling in the Lung Epithelium Is Required for Mucosal Chemokine Gradients and Pulmonary Host Defense against K. pneumoniae

Chen

Eddens

Trevejo-Nuñez

et al. 2016

Cell Host & Microbe

126

108

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Summary The cytokine IL17, and signaling via its heterodimeric IL-17RA/IL-17RC receptor, is critical for host defense against extracellular bacterial and fungal pathogens. Polarized lung epithelial cells express IL-17RA and IL-17RC basolaterally. However, their contribution to IL-17-dependent pulmonary defenses in vivo remains to be determined. To address this, we generated mice with conditional deletion of Il17ra or Il17rc in Scgb1a1-expressing club cells, a major component of the murine bronchiolar epithelium. These mice displayed an impaired ability to recruit neutrophils into the airway lumen in response to IL17, a defect in bacterial clearance upon mucosal challenge with the pulmonary pathogen Klebsiella pneumoniae, and substantially reduced epithelial expression of the chemokine Cxcl5. Neutrophil recruitment and bacterial clearance were restored by intranasal administration of recombinant CXCL5. Our data show that IL-17R signaling in the lung epithelium plays a critical role in establishing chemokine gradients that are essential for mucosal immunity against pulmonary bacterial pathogens.

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Section: Discussionmentioning

confidence: 72%

IL-17 Receptor Signaling in the Lung Epithelium Is Required for Mucosal Chemokine Gradients and Pulmonary Host Defense against K. pneumoniae

Chen

Eddens

Trevejo-Nuñez

et al. 2016

Cell Host & Microbe

126

108

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“…Furthermore, IL-17 levels are elevated during acute lung infection with Pseudomonas aeruginosa , which contributes to neutrophil recruitment and bacterial containment [108, 109]. Similarly, a deficiency in IL-17 or the IL-17-promoting cytokine IL-23 renders mice more susceptible to Citrobacter rodentium intestinal infection [23], as well as to a number of other bacterial pathogens (reviewed in [110, 111]).…”

Section: Il-17 Family Cytokines In Host Protection and Inflammationmentioning

confidence: 99%

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

Monin

Gaffen

2017

Cold Spring Harb Perspect Biol

263

235

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The cytokines of the IL-17 family play a central role in the control of infections, especially extracellular fungi. Conversely, if unrestrained, these inflammatory cytokines contribute to the pathology in numerous autoimmune and chronic inflammatory conditions. Recent advances have led to the approval of IL-17A-blocking biologics for the treatment of moderate to severe plaque psoriasis, but much remains to be understood about the biological functions, regulation and signaling pathways downstream of these factors. In this review, we outline the current knowledge on signal transduction and known physiological activities of IL-17 family cytokines. We will highlight in particular the current understanding of these cytokines in the context of skin manifestations of disease.

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“…Neutrophils have also been linked to IL-17-driven pathology in asthma 159 . For example, overexpression of IL-17 in mouse lung tissue can lead to neutrophil accumulation, and blockade of IL-17 receptor signalling with antibodies or genetic deficiency of IL-17 and IL-17 receptor A (IL-17RA) can decrease airway neutrophil accumulation in mouse models of allergic asthma 160,161 .…”

Section: Innate Immune Cellsmentioning

confidence: 99%

The role of airway epithelial cells and innate immune cells in chronic respiratory disease

et al. 2014

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An abnormal immune response to environmental agents is generally thought to be responsible for causing chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Based on studies of experimental models and human subjects, there is increasing evidence that the response of the innate immune system is crucial for the development of this type of airway disease. Airway epithelial cells and innate immune cells represent key components of the pathogenesis of chronic airway disease and are emerging targets for new therapies. In this Review, we summarize the innate immune mechanisms by which airway epithelial cells and innate immune cells regulate the development of chronic respiratory diseases. We also explain how these pathways are being targeted in the clinic to treat patients with these diseases.

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A tale of two cytokines: IL-17 and IL-22 in asthma and infection

Cited by 82 publications

References 200 publications

IL-17 Receptor Signaling in the Lung Epithelium Is Required for Mucosal Chemokine Gradients and Pulmonary Host Defense against K. pneumoniae

IL-17 Receptor Signaling in the Lung Epithelium Is Required for Mucosal Chemokine Gradients and Pulmonary Host Defense against K. pneumoniae

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

The role of airway epithelial cells and innate immune cells in chronic respiratory disease

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