Targeting IL-33 in Autoimmunity and Inflammation

Theoharides, Theoharis C.; Petra, Anastasia I.; Taracanova, Alexandra; Panagiotidou, Smaro; Conti, Pio

doi:10.1124/jpet.114.222505

Cited by 81 publications

(62 citation statements)

References 160 publications

(154 reference statements)

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“…Moreover, MCs can secrete IL-17 themselves (Kenna and Brown, 2013), as shown both in arthritic joints (Hueber et al, 2010) and in psoriatic lesions (Lin et al, 2011). We also measured IL-31 because it has been involved in allergies (Rabenhorst and Hartmann, 2014) and IL-33 because it is involved in autoimmunity and inflammation (Theoharides et al, 2015a). The serum levels of IL-31 and IL-33 were significantly lower in the FMS group compared with healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells

Tsilioni

Russell

Stewart

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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Fibromyalgia syndrome (FMS) is a chronic, idiopathic condition of widespread musculoskeletal pain affecting more women than men. Even though clinical studies have provided evidence of altered central pain pathways, the lack of definitive pathogenesis or reliable objective markers has hampered development of effective treatments. Here we report that the neuropeptides corticotropin-releasing hormone (CRH), substance P (SP), and SP-structurally-related hemokinin-1 (HK-1) were significantly (P 5 0.026, P , 0.0001, and P 5 0.002, respectively) elevated (0.82 6 0.57 ng/ml, 0.39 6 0.18 ng/ml, and 7.98 6 3.12 ng/ml, respectively) in the serum of patients with FMS compared with healthy controls (0.49 6 0.26 ng/ml, 0.12 6 0.1 ng/ml, and 5.71 6 1.08 ng/ml, respectively). Moreover, SP and HK-1 levels were positively correlated (Pearson r 5 0.45, P 5 0.002) in FMS. The serum concentrations of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF) were also significantly (P 5 0.029 and P 5 0.006, respectively) higher (2.97 6 2.35 pg/ml and 0.92 6 0.31 pg/ml, respectively) in the FMS group compared with healthy subjects (1.79 6 0.62 pg/ml and 0.69 6 0.16 pg/ml, respectively). In contrast, serum IL-31 and IL-33 levels were significantly lower (P 5 0.0001 and P 5 0.044, respectively) in the FMS patients (849.5 6 1005 pg/ml and 923.2 6 1284 pg/ml, respectively) in comparison with healthy controls (1281 6 806.4 pg/ml and 3149 6 4073 pg/ml, respectively). FMS serum levels of neurotensin were not different from controls. We had previously shown that CRH and SP stimulate IL-6 and TNF release from mast cells (MCs). Our current results indicate that neuropeptides could stimulate MCs to secrete inflammatory cytokines that contribute importantly to the symptoms of FMS. Treatment directed at preventing the secretion or antagonizing these elevated neuroimmune markers, both centrally and peripherally, may prove to be useful in the management of FMS.

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Section: Discussionmentioning

confidence: 99%

Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells

Tsilioni

Russell

Stewart

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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“…Scientific attention has recently been directed toward the evaluation of IL-33 in the brain and immune-related diseases (63). There is enough evidence to show upregulated IL-33 expression by astrocytes and peripheral leukocytes in MS patients (64).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

Alsahebfosoul

Rahimmanesh

Shajarian

et al. 2017

Biomolecular Concepts

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Cytokines are implicated in the immunopathogenesis of multiple sclerosis (MS). Interleukin (IL)-33, one of the recently discovered members of the IL-1 superfamily, is a dual functional cytokine involved in various autoimmune disorders. In a case-control study, venous blood was collected from healthy subjects categorized as control group (n = 44) and MS patients (n = 44). All recruited patients were clinically diagnosed with relapsing-remitting MS (RRMS), including patients without treatment (new identified cases, n = 16) and those treated with interferon beta (IFN-β) (n = 28). The plasma levels of IL-33 in subjects were measured with ELISA. Significantly elevated IL-33 plasma levels were observed in RRMS patients (p = 0.005). Furthermore, IFN-β-treated MS patients had lower levels of IL-33 compared to the untreated patients (p < 0.001). Increased IL-33 plasma levels in the patient group might be associated with development of MS. These results could contribute to our better understanding about the role of IL-33 in the immunopathogenesis of MS.

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“…ИЛ33 является членом семейства цитокинов ИЛ1, индуцирует продукцию Th2-цитокинов и эозинофилов, принимает участие в развитии бронхиальной астмы, аллер-гических реакций и, как полагают, участвует в патогенезе РА [62][63][64][65]. ИЛ33 стимулирует остеокластогенез, а также продукцию синовиальными фибробластами ФНОα [66][67][68]; у пациентов с РА продемонстрирована корреля-ция уровня ИЛ33 с активностью заболевания [69].…”

Section: молекулярные биомаркеры эффективности терапии ритуксимабом пunclassified

The Role of Laboratory Biomarkers in Predicting the Efficiency of Rituximab Therapy for Rheumatoid Arthritis: New Evidence

Авдеева¹,

Kusevich²

2017

rsp

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Targeting IL-33 in Autoimmunity and Inflammation

Abstract: Interleukin-33 (IL-33) belongs to the IL-1 family of cytokines.

Cited by 81 publications

References 160 publications

Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells

Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells

Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

The Role of Laboratory Biomarkers in Predicting the Efficiency of Rituximab Therapy for Rheumatoid Arthritis: New Evidence

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