Antiallergic Effects of Anti-Interleukin-33 are Associated with Suppression of Immunoglobulin Light Chain and Inducible Nitric Oxide Synthase

Park, Chang‐Shin; Jang, Tae Young; Jung, Ah-Yeoun; Kim, Young Hyo

doi:10.2500/ajra.2015.29.4251

Cited by 4 publications

(3 citation statements)

References 40 publications

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“…Apart from the small molecules with specific target in the IL-33/ST2 axis as mentioned above, blocking IL-33 and its receptor by monoclonal antibodies is the major therapeutic approach in targeting IL-33/ST2 axis of allergic inflammatory diseases, and serval clinical trials are in progress (105, 107–111). The main side effect of monoclonal antibody administration is the risk of immune reactions such as serum sickness and acute anaphylaxis which may be fatal (112, 113).…”

Section: Il-33 As the New Therapeutic Target For Allergic Diseasesmentioning

confidence: 99%

IL33: Roles in Allergic Inflammation and Therapeutic Perspectives

et al. 2019

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Interleukin (IL)-33 belongs to IL-1 cytokine family which is constitutively produced from the structural and lining cells including fibroblasts, endothelial cells, and epithelial cells of skin, gastrointestinal tract, and lungs that are exposed to the environment. Different from most cytokines that are actively secreted from cells, nuclear cytokine IL-33 is passively released during cell necrosis or when tissues are damaged, suggesting that it may function as an alarmin that alerts the immune system after endothelial or epithelial cell damage during infection, physical stress, or trauma. IL-33 plays important roles in type-2 innate immunity via activation of allergic inflammation-related eosinophils, basophils, mast cells, macrophages, and group 2 innate lymphoid cells (ILC2s) through its receptor ST2. In this review, we focus on the recent advances of the underlying intercellular and intracellular mechanisms by which IL-33 can regulate the allergic inflammation in various allergic diseases including allergic asthma and atopic dermatitis. The future pharmacological strategy and application of traditional Chinese medicines targeting the IL-33/ST2 axis for anti-inflammatory therapy of allergic diseases were also discussed.

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Section: Il-33 As the New Therapeutic Target For Allergic Diseasesmentioning

confidence: 99%

IL33: Roles in Allergic Inflammation and Therapeutic Perspectives

et al. 2019

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“…COX-2 inhibition has an antiallergic effect via the downregulation of prostaglandin D2 [ 24 ], and thus, the antiallergic effect of anti-IL-33 might also be related to COX-2 inhibition. On the other hand, iNOS protein levels were not significantly different between the four groups, although it tended to be lower in group D. In our previous study on mice with allergic asthma, iNOS protein expression was significantly higher in mice with allergic asthma and this increase was effectively suppressed by treating lung tissues with anti-IL-33 [ 25 ]. However, the role of iNOS and nitric oxide in the glomerulus have been extensively debated.…”

Section: Discussionmentioning

confidence: 99%

Anti-interleukin-33 Reduces Ovalbumin-Induced Nephrotoxicity and Expression of Kidney Injury Molecule-1

Park¹,

Shinn²,

Kang³

et al. 2016

Int Neurourol J

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Purpose:To evaluate the effect of anti-interleukin-33 (anti-IL-33) on a mouse model of ovalbumin (OVA)-induced acute kidney injury (AKI).Methods:Twenty-four female BALB/c mice were assigned to 4 groups: group A (control, n=6) was administered sterile saline intraperitoneally (i.p.) and intranasally (i.n.); group B (allergic, n=6) was administered i.p./i.n. OVA challenge; group C (null treatment, n=6) was administered control IgG i.p. before OVA challenge; and group D (anti-IL-33, n=6) was pretreated with 3.6 µg of anti-IL-33 i.p. before every OVA challenge. The following were evaluated after sacrifice: serum blood urea nitrogen and creatinine levels, Kidney injury molecule-1 gene (Kim-1) and protein (KIM-1) expression in renal parenchyma, and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), phosphorylated endothelial NOS (p-eNOS), and phosphorylated AMP kinase (p-AMPK) proteins in renal parenchyma.Results:After OVA injection and intranasal challenge, mice in groups B and C showed significant increases in the expression of Kim-1 at both the mRNA and protein levels. After anti-IL-33 treatment, mice in group D showed significant Kim-1 down-regulation at the mRNA and protein levels. Group D also showed significantly lower COX-2 protein expression, marginally lesser iNOS expression than groups B and C, and p-eNOS and p-AMPK expression at baseline levels.Conclusions:Kim-1 could be a useful marker for detecting early-stage renal injury in mouse models of OVA-induced AKI. Further, anti-IL-33 might have beneficial effects on these mouse models.

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“…Other work published in this issue of the American Journal of Rhinology & Allergy includes a murine model of allergic rhinitis by Park et al 3 In this study, the mice were sensitized and then treated with anti-IL 33. By blocking this cytokine, the authors found that immunoglobulin free light chain expression was decreased and that nitric oxide synthase 2 was also decreased.…”

mentioning

confidence: 99%

Electrocauterization and No Packing may be Comparable with Nasal Packing for Postoperative Hemorrhage after Endoscopic Sinus Surgery

Kim

Rhee²,

Kim³

2016

Am J Rhinol�Allergy

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Antiallergic Effects of Anti-Interleukin-33 are Associated with Suppression of Immunoglobulin Light Chain and Inducible Nitric Oxide Synthase

Abstract: The antiallergic effect of anti-IL-33 can be explained by suppression of IgFLC and NOS2 in a murine model of allergic rhinitis.

Cited by 4 publications

References 40 publications

IL33: Roles in Allergic Inflammation and Therapeutic Perspectives

IL33: Roles in Allergic Inflammation and Therapeutic Perspectives

Anti-interleukin-33 Reduces Ovalbumin-Induced Nephrotoxicity and Expression of Kidney Injury Molecule-1

Electrocauterization and No Packing may be Comparable with Nasal Packing for Postoperative Hemorrhage after Endoscopic Sinus Surgery

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