Proinflammatory IL-17 levels in serum/cerebrospinal fluid of patients with neurodegenerative diseases: a meta-analysis study

Gautam, Avtar Singh; Pulivarthi, Chinna Babu; Singh, Rakesh Kumar

doi:10.1007/s00210-022-02357-6

Cited by 8 publications

(8 citation statements)

References 43 publications

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“…In essence, systemic pro-inflammatory responses in MCI/AD may serve to propagate tissue injury and potentially drive the progression of neurodegeneration via their transport across the blood–brain barrier. The significantly elevated serum levels of IL-1β, IL-4, IL-5, IL-9, IL-13, IL-17a, eotaxin, MIP-1α, PDGF-bb, RANTES, and TNF-α detected herein corresponded with previous reports [ 35 , 43 , 44 , 51 , 58 , 64 , 92 , 119 , 120 , 121 , 122 ], linking the augmented expression of systemic inflammatory markers to early-stage neurodegeneration.…”

Section: Discussionsupporting

confidence: 92%

Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

de la Monte,

Tong,

Hapel

2023

Biomedicines

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Neuroinflammation may be a pathogenic mediator and biomarker of neurodegeneration at the boundary between mild cognitive impairment (MCI) and early-stage Alzheimer’s disease (AD). Whether neuroinflammatory processes are endogenous to the central nervous system (CNS) or originate from systemic (peripheral blood) sources could impact strategies for therapeutic intervention. To address this issue, we measured cytokine and chemokine immunoreactivities in simultaneously obtained lumbar puncture cerebrospinal fluid (CSF) and serum samples from 39 patients including 18 with MCI or early AD and 21 normal controls using a 27-plex XMAP bead-based enzyme-linked immunosorbent assay (ELISA). The MCI/AD combined group had significant (p < 0.05 or better) or statistically trend-wise (0.05 ≤ p ≤ 0.10) concordant increases in CSF and serum IL-4, IL-5, IL-9, IL-13, and TNF-α and reductions in GM-CSF, b-FGF, IL-6, IP-10, and MCP-1; CSF-only increases in IFN-y and IL-7 and reductions in VEGF and IL-12p70; serum-only increases in IL-1β, MIP-1α, and eotaxin and reductions in G-CSF, IL-2, IL-8 and IL-15; and discordant CSF–serum responses with reduced CSF and increased serum PDGF-bb, IL-17a, and RANTES. The results demonstrate simultaneously parallel mixed but modestly greater pro-inflammatory compared to anti-inflammatory or neuroprotective responses in CSF and serum. In addition, the findings show evidence that several cytokines and chemokines are selectively altered in MCI/AD CSF, likely corresponding to distinct neuroinflammatory responses unrelated to systemic pathologies. The aggregate results suggest that early management of MCI/AD neuroinflammation should include both anti-inflammatory and pro-neuroprotective strategies to help prevent disease progression.

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Section: Discussionsupporting

confidence: 92%

Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

de la Monte,

Tong,

Hapel

2023

Biomedicines

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“…The results of a META analysis suggested that patients with neurodegenerative diseases, including Alzheimer's disease and amyotrophic lateral sclerosis, had significantly increased serum IL‐17 levels. Furthermore, cerebrospinal fluid IL‐17 levels were found to be significantly higher in patients with amyotrophic lateral sclerosis compared to controls 83 . TNF‐α is associated with neurological inflammation and degenerative diseases.…”

Section: Nervous System Involved In Pathogenesis Of Psoriasismentioning

confidence: 89%

“…Furthermore, cerebrospinal fluid IL-17 levels were found to be significantly higher in patients with amyotrophic lateral sclerosis compared to controls. 83 TNFα is associated with neurological inflammation and degenerative diseases. Its receptors are notably expressed in higher concentrations in the limbic system of the cerebral cortex, participate in the control of mood states regulation and potentially influencing the development of depression.…”

Section: Nervous System Involvement In the Pathogenesis Of Psoriasismentioning

confidence: 99%

Effects on peripheral and central nervous system of key inflammatory intercellular signalling peptides and proteins in psoriasis

Tang,

Zhao,

Shi

et al. 2024

Experimental Dermatology

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Psoriasis is a chronic systemic inflammatory cutaneous disease. Where the immune system plays an important role in its pathogenesis, with key inflammatory intercellular signalling peptides and proteins including IL‐17 and IL‐23. The psychoneurological system also figures prominently in development of psoriasis. There is a high prevalence of comorbidity between psoriasis and mental health disorders such as depression, anxiety and mania. Patients with psoriasis often suffer from pathological pain in the lesions, and their neurological accidents could improve the lesions in innervated areas. The immune system and the psychoneurological system interact closely in the pathogenesis of psoriasis. Patients with psoriasis exhibit abnormal levels of neuropeptides both in circulating and localized lesion, acting as immunomodulators involved in the inflammatory response. Moreover, receptors for inflammatory factors are expressed in both peripheral and central nervous systems (CNSs), suggesting that nervous system can receive and be influenced by signals from immune system. Key inflammatory intercellular signalling peptides and proteins in psoriasis, such as IL‐17 and IL‐23, can be involved in sensory signalling and may affect synaptic plasticity and the blood–brain barrier of CNS through the circulation. This review provides an overview of the multiple effects on the peripheral and CNS under conditions of systemic inflammation in psoriasis, providing a framework and inspiration for in‐depth studies of neuroimmunomodulation in psoriasis.

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“…For example, it has been found that direct injection of glutamate into rat insula with no other intervention led to IENFD reductions, highlighting the possibility that imbalances in CNS excitatory neurotransmitters may play a role in IENFD [31]. Alternatively, a "top-around" effect in which signaling molecules or factors are released due to CNS injury could secondarily impact peripheral fibers through the bloodstream or other nonneural pathways [32][33][34][35][36].…”

Section: Discussionmentioning

confidence: 99%

Abnormal Intraepidermal Nerve Fiber Density in Disease: A Scoping Review

Thomas

Enders

Kaiser

et al. 2023

Preprint

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Background: Intraepidermal nerve fiber density (IENFD) has become an important biomarker for neuropathy diagnosis and research. The consequences of reduced IENFD can include sensory dysfunction, pain, and a significant decrease in quality of life. We examined the extent to which IENFD is being used as a tool in human and mouse models and compared the degree of fiber loss between diseases to gain a broader understanding of the existing data collected using this common technique. Methods: We conducted a scoping review of publications that used IENFD as a biomarker in human and non-human research. PubMed was used to identify 1,004 initial articles that were then screened to select articles that met the criteria for inclusion. Criteria were chosen to standardize publications so they could be compared rigorously and included having a control group, measuring IENFD in a distal limb, and using protein gene product 9.5 (PGP9.5). Results: We analyzed 397 articles and collected information related to publication year, the condition studied, and the percent IENFD loss. The analysis revealed that the use of IENFD as a tool has been increasing in both human and non-human research. We found that IENFD loss is prevalent in many diseases, and metabolic or diabetes-related diseases were the most studied conditions in humans and rodents. Our analysis identified 74 human diseases in which IENFD was affected, with 71 reporting IENFD loss and an overall average IENFD change of -47%. We identified 28 mouse and 21 rat conditions, with average IENFD changes of -31.6 % and -34.7% respectively. Additionally, we present data describing sub-analyses of IENFD loss according to disease characteristics in diabetes and chemotherapy treatments in humans and rodents. Interpretation: Reduced IENFD occurs in a surprising number of human disease conditions. Abnormal IENFD contributes to important complications, including poor cutaneous vascularization, sensory dysfunction, and pain. Our analysis informs future rodent studies so they may better mirror human diseases impacted by reduced IENFD, highlights the breadth of diseases impacted by IENFD loss, and urges exploration of common mechanisms that lead to substantial IENFD loss as a complication in disease.

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Proinflammatory IL-17 levels in serum/cerebrospinal fluid of patients with neurodegenerative diseases: a meta-analysis study

Cited by 8 publications

References 43 publications

Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

Effects on peripheral and central nervous system of key inflammatory intercellular signalling peptides and proteins in psoriasis

Abnormal Intraepidermal Nerve Fiber Density in Disease: A Scoping Review

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