Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Deng, Yi‐Ke; Ma, Jin; Wang, Zhichao; Xiang, Long; Chen, Cailing; Feng, Qiang; Zhang, Xin‐Hao; Zeng, Ming; Wang, Heng; Lu, Xiang; Liu, Zheng

doi:10.1002/alr.22430

Cited by 7 publications

(3 citation statements)

References 47 publications

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“…We found that 9 cytokines were significantly higher in the M2a hMdɸ-conditioned medium, while 15 cytokines were significantly higher in the M1 hMdɸ-conditioned medium (Table 2). Several of the 9 cytokines that were increased in the M2a hMdɸ-conditioned medium were previously reported to play a role in various inflammatory processes, including ocular inflammatory diseases and neurodegenerative diseases; these cytokines include CCL11 ( Deng et al, 2019 ; Mor et al, 2019 ; Segal-Salto et al, 2020 ; Shoji et al, 2017 ; Zeng et al, 2019 ), CCL13 ( El-asrar et al, 2019 ; Méndez-Enríquez et al, 2014 ; Mendez-Enriquez and García-Zepeda, 2013 ; Zeng et al, 2019 ), CCL17 ( Dai et al, 2015 ; Yu et al, 2011 ; Zeng et al, 2019 ), CCL23 ( Faura et al, 2020 ; Simats et al, 2018 ; Zeng et al, 2019 ), and CCL14 ( Liu et al, 2016 ).…”

Section: Resultsmentioning

confidence: 99%

CCR1 mediates Müller cell activation and photoreceptor cell death in macular and retinal degeneration

Elbaz-Hayoun,

Rinsky,

Hagbi-Levi

et al. 2023

eLife

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Mononuclear cells are involved in the pathogenesis of retinal diseases, including age-related macular degeneration (AMD). Here, we examined the mechanisms that underlie macrophage-driven retinal cell death. Monocytes were extracted from patients with AMD and differentiated into macrophages (hMdɸs), which were characterized based on proteomics, gene expression, and ex vivo and in vivo properties. Using bioinformatics, we identified the signaling pathway involved in macrophage-driven retinal cell death, and we assessed the therapeutic potential of targeting this pathway. We found that M2a hMdɸs were associated with retinal cell death in retinal explants and following adoptive transfer in a photic injury model. Moreover, M2a hMdɸs express several CCRI (C-C chemokine receptor type 1) ligands. Importantly, CCR1 was upregulated in Müller cells in models of retinal injury and aging, and CCR1 expression was correlated with retinal damage. Lastly, inhibiting CCR1 reduced photic-induced retinal damage, photoreceptor cell apoptosis, and retinal inflammation. These data suggest that hMdɸs, CCR1, and Müller cells work together to drive retinal and macular degeneration, suggesting that CCR1 may serve as a target for treating these sight-threatening conditions.

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Section: Resultsmentioning

confidence: 99%

CCR1 mediates Müller cell activation and photoreceptor cell death in macular and retinal degeneration

Elbaz-Hayoun,

Rinsky,

Hagbi-Levi

et al. 2023

eLife

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“…72 Moreover, hemokinin-1 and neurokinin 1 receptor mRNA and protein expression were upregulated in eosinophilic and non-eosinophilic nasal polyps compared with control tissues, with eosinophilic polyps demonstrating a higher upregulation compared with that of non-eosinophilic polyps. 73 This neurogenic inflammation may contribute to the pathophysiology of CRS; hence, any targeted intervention may provide alternative therapeutic options. The pathophysiological pathways involved in CRS neuroinflammation are depicted in Figure 1.…”

Section: Chronic Rhinosinusitis (Crs)mentioning

confidence: 99%

Further Understanding of Neuro-Immune Interactions in Allergy: Implications in Pathophysiology and Role in Disease Progression

Konstantinou¹,

Konstantinou²,

Koulias³

et al. 2022

JAA

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The complicated interaction between the central and the autonomic (sympathetic, parasympathetic, and enteric) nervous systems on the one hand and the immune system and its components, on the other hand, seems to substantially contribute to allergy pathophysiology, uncovering an under-recognized association that could have diagnostic and therapeutic potentials. Neurons connect directly with and regulate the function of many immune cells, including mast cells, the cells that have a leading role in allergic disorders. Proinflammatory mediators such as cytokines, neurotrophins, chemokines, and neuropeptides are released by immune cells, which stimulate sensory neurons. The release of neurotransmitters and neuropeptides caused by the activation of these neurons directly impacts the functional activity of immune cells and vice versa, playing a decisive role in this communication. Successful application of Pavlovian conditioning in allergic disorders supports the existence of a psychoneuroimmunological interplay in classical allergic hypersensitivity reactions. Activation of neuronal homeostatic reflexes, like sneezing in allergic rhinitis, coughing in allergic asthma, and vomiting in food allergy, offers additional evidence of a neuroimmunological interaction that aims to maintain homeostasis. Dysregulation of this interaction may cause overstimulation of the immune system that will produce profound symptoms and exaggerated hemodynamic responses that will lead to severe allergic pathophysiological events, including anaphylaxis. In this article, we have systematically reviewed and discussed the evidence regarding the role of the neuro-immune interactions in common allergic clinical modalities like allergic rhinitis, chronic rhinosinusitis, allergic asthma, food allergy, atopic dermatitis, and urticaria. It is essential to understand unknown – to most of the immunology and allergy experts – neurological networks that not only physiologically cooperate with the immune system to regulate homeostasis but also pathogenetically interact with more or less known immunological pathways, contribute to what is known as neuroimmunological inflammation, and shift homeostasis to instability and disease clinical expression. This understanding will provide recognition of new allergic phenotypes/endotypes and directions to focus on specialized treatments, as the era of personalized patient-centered medicine, is hastening apace.

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“…showed that γδT cells were more abundant in the nasal mucosa of AR patients and may regulate innate and adaptive immune responses and their interaction. Additionally, Deng et al . observed that hemokinin‐1 (HK‐1) and its high‐affinity tachykinin receptor neurokinin 1 receptor (NK1R) were upregulated in human nasal polyps, and correlated with tissue eosinophilia in eosinophilic nasal polyps.…”

mentioning

confidence: 99%

Evolving management of upper airway diseases: focus on Asia

Zhang¹

2019

Int Forum Allergy Rhinol

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Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Cited by 7 publications

References 47 publications

CCR1 mediates Müller cell activation and photoreceptor cell death in macular and retinal degeneration

CCR1 mediates Müller cell activation and photoreceptor cell death in macular and retinal degeneration

Further Understanding of Neuro-Immune Interactions in Allergy: Implications in Pathophysiology and Role in Disease Progression

Evolving management of upper airway diseases: focus on Asia

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