IL-17A synergistically stimulates TNF-α-induced IL-8 production in human airway epithelial cells: A potential role in amplifying airway inflammation

Honda, Kojiro; Wada, Hiroo; Nakamura, Masuo; Nakamoto, Keitaro; Inui, Toshiya; Sada, Mitsuru; Koide, Takao; Takata, Saori; Yokoyama, Takuma; Saraya, Takeshi; Kurai, Daisuke; Ishii, Haruyuki; Goto, Hajime; Takizawa, Hajime

doi:10.1080/01902148.2016.1190796

Cited by 40 publications

(25 citation statements)

References 41 publications

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“…6f). Given the well-described role of TNFα and IL-17A in driving neutrophil recruitment to sites of inflammation424344454647, we examined the numbers of neutrophils in the colons of the mice that received Ndfip1-deficient or –sufficient Th17 cells. We found that recipients of Ndfip1-deficient Th17 cells had significantly higher numbers of neutrophils (Fig.…”

Section: Resultsmentioning

confidence: 99%

Ndfip1 restricts Th17 cell potency by limiting lineage stability and proinflammatory cytokine production

Layman¹,

Sprout²,

Phillips³

et al. 2017

Sci Rep

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While Th17 cells can protect against colonization by pathogenic organisms, they also have the potential to become pathogenic and promote autoimmune and inflammatory diseases. Mechanisms that control their pathogenic potential remain poorly understood. Here we show that Ndfip1, a co-activator of the E3 ubiquitin ligase Itch, restricts the frequency and pathogenicity of Th17 cells. Mice lacking Ndfip1 have increased numbers of Th17 cells, and this increase is cell intrinsic. We found that Ndfip1 restricts production of the proinflammatory cytokines in Th17 cells. Increased cytokine production correlated with reduced degradation and accumulation of RORγT. When transferred in vivo, Th17 cells lacking Ndfip1 were more likely to maintain their ability to make IL-17, were more potent proinflammatory cytokine producers, and were powerful inducers of colitis. Together our data support an essential role for Ndfip1 in degrading RORγT and suppressing Th17 lineage stability, proinflammatory cytokine production, and pathogenicity.

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Section: Resultsmentioning

confidence: 99%

Ndfip1 restricts Th17 cell potency by limiting lineage stability and proinflammatory cytokine production

Layman¹,

Sprout²,

Phillips³

et al. 2017

Sci Rep

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“…This interleukin promotes chronic immune inflammation, contributing to occurrence and development of those lung diseases [5][6][7]. In airway, IL-17A could induce production of chemokine and cytokines from bronchial epithelial cells [8,9]. Interestingly, IL-17A not only promotes airway remodeling [10], but also directly induces EMT in alveolar epithelial cells [11].…”

Section: Introductionmentioning

confidence: 99%

Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling

Jiang

Zhao

et al. 2020

BMC Pulm Med

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Background: IL-17A directly induces epithelial-mesenchymal transition (EMT) in alveolar epithelial cells. It could coordinate with cigarette smoke extract (CSE) to promote proliferation of bronchial epithelial cells. In this study, we aim to explore the direct effect of IL-17A and CSE on EMT in bronchial epithelial cells. Methods: Bronchial epithelial cells were isolated from C57BL/6 mice, and cocultured with CSE or/and IL-17A. Ecadherin and Vimentin expressions in cells were detected using immunofluorescence staining. IL-17R expression was detected using immunohistochemistry staining. NF-κB expression was assessed using western blotting. When NF-κB was inhibited by BAY 11-7821, expressions of NF-κB, E-cadherin and Vimentin were measured. Results: The protein expression of E-cadherin in bronchial epithelial cells was lowest in CSE + IL-17A group, followed by CSE group. In contrast, the protein expression of Vimentin was highest in CSE + IL-17A group, followed by CSE group. Similarly, IL-17R and NF-κB expressions were highest in CSE + IL-17A group, followed by CSE group and IL-17A group. NF-κB inhibitor could inhibit the expressions of E-cadherin and Vimentin. Conclusions: Cigarette and IL-17A could synergistically induce EMT in bronchial epithelial cells through activating IL17R/NF-κB signaling. Our findings contribute to a better understanding in airway EMT and pathogenesis of respiratory diseases, which are involved IL-17A and cigarette smoking. Those will provide novel avenues in the immunotherapy of lung diseases.

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“…In our study, a higher level of IL-8 was detected in the BALF samples from the RMPP compared with the GMPP patients in contrast to the plasma IL-8 levels, which were similar. Moreover, recent research has determined that IL-17 synergistically stimulates TNF-α-induced IL-8 production in human airway epithelial cells (22). Considering the higher levels of IL-17 and TNF-α in the BALF samples from the RMPP patients, this phenomenon appears to play a potential role in amplifying airway inflammation in RMPP.…”

Section: Discussionmentioning

confidence: 94%

Distribution and Expression of IL-17 and Related Cytokines in Children with <i>Mycoplasma pneumoniae</i> Pneumonia

Fan

Yang

et al. 2019

Jpn J Infect Dis

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IL-17A synergistically stimulates TNF-α-induced IL-8 production in human airway epithelial cells: A potential role in amplifying airway inflammation

Abstract: IL-17A in the combination with TNF-α or IL-1β showed a synergistic augmenting effect on IL-8 and GM-CSF production in human airway epithelial cells.

Cited by 40 publications

References 41 publications

Ndfip1 restricts Th17 cell potency by limiting lineage stability and proinflammatory cytokine production

Ndfip1 restricts Th17 cell potency by limiting lineage stability and proinflammatory cytokine production

Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling

Distribution and Expression of IL-17 and Related Cytokines in Children with <i>Mycoplasma pneumoniae</i> Pneumonia

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