TNF-Alpha Inhibitors and Rhinosinusitis—A Systematic Review and Meta-Analysis

Piski, Zalán; Gerlinger, Imre; Nepp, Nelli; Farkas, Nelli; Weber, Rainer

doi:10.1177/1945892419898988

Cited by 3 publications

(3 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[33][34][35] This uncertainty is further compounded by ongoing debate regarding whether the TNFA inhibitor class of medications predispose patients to sinusitis. 36 To further define the role of CCL19/CCR7-mediated inflammatory consequences in CRSwNP and potential association with TNA-α, additional mechanistic studies are warranted.…”

Section: Discussionmentioning

confidence: 99%

Chemokine CCL19 and Its Receptors CCR7 and CCRL1 in Chronic Rhinosinusitis

Mahomva,

Smith,

Minkah

et al. 2024

JIR

View full text Add to dashboard Cite

Background CCL19 has been shown to predict disease severity in COVID-19 and treatment response in rheumatoid arthritis. CCL19 can exert both pro- and anti-inflammatory effects and is elevated in chronic rhinosinusitis (CRS). However, its role in CRS remains unknown. This study sought to determine the transcriptional changes in CCL19, its receptors, and associated cytokines and their association with disease severity in CRS. Methods A clinical database of control subjects and patients with CRS was examined. Lund-Kennedy, Lund-Mackay, Sinonasal Outcomes Test 22 (SNOT-22), and rhinosinusitis disability index (RSDI) scores were collected at enrollment. mRNA was extracted from sinonasal tissues and subjected to multiplex gene expression analysis. Gene transcript differences between patients with CRS and controls were compared and correlated with disease severity metrics. Immunohistochemical analyses of CCL19, CCR7, and CCRL1 were conducted to compare differences in protein expression between cohorts. A subgroup analysis was performed to compare transcriptional and protein expression difference between patients with (CRSwNP) and without (CRSsNP) nasal polyps and controls. Results Thirty-eight subjects (control group, n=7; CRS group, n=31) were included in this study. CCRL1 ( p =0.0093) and CCR7 ( p =0.017) levels were significantly elevated in CRS compared to those in controls. CCL19 ( p =0.038) and CCR7 ( p =0.0097) levels were elevated in CRSwNP and CCRL1 was elevated in CRSsNP ( p =0.0004). CCR7 expression was significantly elevated in sinonasal epithelial cells in CRSwNP ( p =0.04). CCL19 expression was positively correlated with TNFA expression ( p <0.0002). CCL19 and CCR7 expression was positively correlated with SNOT-22 and RSDI scores ( p <0.05). Conclusion CCL19 and CCR7 may modulate TNF-α-driven pro-inflammatory signaling and contribute to increased disease severity in CRS. Mechanistic studies are required to further elucidate the role of CCRL1 in CRS.

show abstract

Section: Discussionmentioning

confidence: 99%

Chemokine CCL19 and Its Receptors CCR7 and CCRL1 in Chronic Rhinosinusitis

Mahomva,

Smith,

Minkah

et al. 2024

JIR

View full text Add to dashboard Cite

show abstract

“…This process may lead to the aggregation of neutrophils and eosinophils, and enable inflammatory cells to secrete inflammatory mediators such as leukotrienes and chemokines and injure nasal mucosa. 21 In addition, some studies have pointed out that TNF-α could activate the NF-kappaB and stimulate the expression of mRNA, and therefore likely to prompt the amplification effect between cells and factors, and aggravate the inflammatory response. 22 IL-1, mainly produced by macrophages, plays an essential role in transmitting information, activating and regulating immune cells, proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Correlation analysis of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α in refractory chronic rhinosinusitis: A retrospective study

Wen

Zhu

Ruixia

et al. 2022

Allergol Immunopathol

View full text Add to dashboard Cite

Objective: To investigate the potential correlation of transforming growth factor-β (TGF-β), matrix metalloprotein 9 (MMP-9), tissue inhibitor of metalloproteinases 1 (TIMP-1), Interleukin 1 (IL-1), IL-4, IL-6, IL-17, and tumor necrosis factor alpha (TNF-α) in refractory chronic rhinosinusitis. Methods: A total of 150 participants were retrospectively included in this study from August 2018 to February 2020. The people enrolled were equally allocated into refractory group (patients with refractory chronic rhinosinusitis), chronic group (patients with chronic rhinosinusitis), and control group (normal people). The level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α were recorded. The unconditional multivariate binary logistic regression was used to analyze the factors affecting refractory chronic rhinosinusitis. Results: The Davos score, T&T olfactometer threshold test, and Lund-Mackay CT scores in refractory group were significantly higher than the chronic group (P<0.05). The level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α in the refractory group were significantly higher than the chronic group and the control group (all P<0.05). Similarly, the level of the above mentioned indexes in the chronic group were significantly higher than the control group (P<0.05). The Davos score, T&T olfactometer threshold test score, Lund-Mackay CT score, and the level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α positively correlated with refractory chronic rhinosinusitis. Moreover, the unconditional multivariate binary logistic regression showed that the influencing factors of refractory chronic rhinosinusitis included TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α. Conclusion: The findings of the present study provide evidence for TGF-β1, MMP-9, TIMP-1, IL-4, IL-6, IL-17, and TNF-α as the influencing factors of refractory chronic rhinosinusitis.

show abstract

“…Consistently, clinical data show that anti-TNF agents are effective for treating osteoarthritis pain, 302 lower back pain, 303 and rheumatoid arthritis. 304 Systematic review and meta-analysis indicate the agents have many side effects, including infection 305 , 306 and psoriasis. 307 To date, no agent for normalization of neuroinflammation is available in clinic.…”

Section: A New Strategy For Treatment Of Chronic Painmentioning

confidence: 99%

Normalization of Neuroinflammation: A New Strategy for Treatment of Persistent Pain and Memory/Emotional Deficits in Chronic Pain

Liu¹

2022

JIR

View full text Add to dashboard Cite

Chronic pain, which affects around 1/3 of the world population and is often comorbid with memory deficit and mood depression, is a leading source of suffering and disability. Studies in past decades have shown that hyperexcitability of primary sensory neurons resulting from abnormal expression of ion channels and central sensitization mediated pathological synaptic plasticity, such as long-term potentiation in spinal dorsal horn, underlie the persistent pain. The memory/emotional deficits are associated with impaired synaptic connectivity in hippocampus. Dysregulation of numerous endogenous proteins including receptors and intracellular signaling molecules is involved in the pathological processes. However, increasing knowledge contributes little to clinical treatment. Emerging evidence has demonstrated that the neuroinflammation, characterized by overproduction of pro-inflammatory cytokines and glial activation, is reliably detected in humans and animals with chronic pain, and is sufficient to induce persistent pain and memory/emotional deficits. The abnormal expression of ion channels and pathological synaptic plasticity in spinal dorsal horn and in hippocampus are resulting from neuroinflammation. The neuroinflammation is initiated and maintained by the interactions of circulating monocytes, glial cells and neurons. Obviously, unlike infectious diseases and cancer, which are caused by pathogens or malignant cells, chronic pain is resulting from alterations of cells and molecules which have numerous physiological functions. Therefore, normalization (counterbalance) but not simple inhibition of the neuroinflammation is the right strategy for treating neuronal disorders. Currently, no such agent is available in clinic. While experimental studies have demonstrated that intracellular Mg 2+ deficiency is a common feature of chronic pain in animal models and supplement Mg 2+ are capable of normalizing the neuroinflammation, activation of upregulated proteins that promote recovery, such as translocator protein (18k Da) or liver X receptors, has a similar effect. In this article, relevant experimental and clinical evidence is reviewed and discussed.

show abstract

TNF-Alpha Inhibitors and Rhinosinusitis—A Systematic Review and Meta-Analysis

Cited by 3 publications

References 18 publications

Chemokine CCL19 and Its Receptors CCR7 and CCRL1 in Chronic Rhinosinusitis

Chemokine CCL19 and Its Receptors CCR7 and CCRL1 in Chronic Rhinosinusitis

Correlation analysis of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α in refractory chronic rhinosinusitis: A retrospective study

Normalization of Neuroinflammation: A New Strategy for Treatment of Persistent Pain and Memory/Emotional Deficits in Chronic Pain

Contact Info

Product

Resources

About