Involvement of Il-33 in the Pathogenesis and Prognosis of Major Respiratory Viral Infections: Future Perspectives for Personalized Therapy

Murdaca, Giuseppe; Paladin, Francesca; Tonacci, Alessandro; Borro, Matteo; Greco, Mónica; Gerosa, Alessandra; Isola, S.; Allegra, Alessandro; Gangemi, Sebastiano

doi:10.3390/biomedicines10030715

Cited by 17 publications

(12 citation statements)

References 86 publications

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“…RV is one of the most prevalent human pathogens that usually causes mild upper respiratory tract symptoms (33), while RSV is one of the main causes of bronchiolitis in infants and small children (34). Both RV and RSV infections seem to increase the production of IL-33 mediated by TLR2 and TLR3 signalling pathway (35). Recently, Zhang et al showed that infants with acute bronchiolitis caused by RSV, had significantly elevated levels of IL-33 and their Th1/Th2 ratio was imbalanced (36).…”

Section: Discussionmentioning

confidence: 99%

Association of Toll‐like receptor 2 rs111200466 polymorphism with low serum levels of IL‐33 in early childhood

Teräsjärvi¹,

Toivonen

Mertsola

et al. 2023

APMIS

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TLR2 is one of 10 human TLRs, which plays an important role in the recognition of pathogens and activation of the innate immunity via NF‐κB pathway. NF‐κB activation induces the expression of various pro‐inflammatory genes. This study examines the effect of TLR2 polymorphisms on the production of blood pro‐inflammatory cytokines in healthy Finnish children. One hundred forty‐six children who participated in a prospective observational birth cohort study in Turku, Finland, were included. DNA samples were analysed by PCR‐based sequencing for two common TLR2 polymorphisms (rs5743708 Arg753Gln; rs111200466–196 to –174del). Serum concentrations of IL‐33, IL‐31, IL‐17A and IL‐17F were measured by multiplex immunoassay and sST2 by ELISA in children at the age of 13 months. Children with variant type of TLR2 rs111200466 (ins/del or del/del) had significantly lower level of serum IL‐33 (median, 0.00 pg/mL; IQR 0.00–17.60) than those with ins/ins type of TLR2 (19.81 pg/mL; IQR 0.00–51.78) (p = 0.0001). Almost all study subjects had serum concentrations of IL‐17A, IL‐17F and IL‐31 below the detection limit and therefore not included in the final analyses. No differences in levels of above four cytokines and sST2 were found between TLR2 rs5743708 genotypes (GG and GA). Our results indicated that the TLR2 rs111200466 deletion was associated with a low level of serum IL‐33, suggesting that the polymorphism may impair the production of IL‐33.

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Section: Discussionmentioning

confidence: 99%

Association of Toll‐like receptor 2 rs111200466 polymorphism with low serum levels of IL‐33 in early childhood

Teräsjärvi¹,

Toivonen

Mertsola

et al. 2023

APMIS

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“…Increased mucosal node, which included CCL13, CCL17, IL-33, IL-5, IL-4 and CCL26, contributed to accelerated recovery and no primary outcome events. Previously these mediators have each been associated with viral infections in particular the alarmin, IL-33 (reviewed by Murdaca et al 23 ). In COVID-19 speci cally, IL-33 has been strongly associated with SARS-CoV-2 infection 24 and together with CCL26 has been found in plasma within 10 days of SARS-CoV-2 infection 25 .…”

Section: Discussionmentioning

confidence: 99%

Coordinated nasal mucosa-mediated immunity accelerates recovery from COVID-19

Cass

Nicolau

Baker

et al. 2023

Preprint

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Viral infection due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induce a dynamic immune environment. Using nasal mucosal samples in 139 participants from the STOIC study (community-based randomised clinical trial for the use of budesonide in early onset SARS-CoV-2, NCT04416399), we applied predefined immune mediator nodes in relation to clinical outcomes and viral burden. Interferon- and chemokine-dominant nodes increased expression as compared to health, validating our modular approach. Next, we demonstrated that an increase in mucosal immunity-like node consisting of CCL13, CCL17, IL-33, among others was associated with a mean 3.7-day quicker recovery with no primary outcome events, irrespective of treatment arm. By day 14 the mucosal node divided into two daughter nodes linked to interferon molecules and was transcriptionally detectable in nasal cavity basal, hillock and ciliated cells (as per public single cell dataset EGAD00001007718). Our data suggest mucosal-associated mediators are key for early symptom resolution of SARS-CoV-2.

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“…Allergens, viruses, and pollutants can directly elaborate TSLP, IL-25, and IL-33 from the lungs. 221 On the contrary, rhinoviruses probably act differently, inducing IL-33 release from nasal epithelium, 222,223 but they are not superantigens. IL-33 activates dendritic cells during antigen presentation, 221 and drives a T2 response.…”

Section: Rhinitis Alone and Rhinitis + Asthma Multimorbidity Represen...mentioning

confidence: 99%

Rhinitis associated with asthma is distinct from rhinitis alone: The ARIA‐MeDALL hypothesis

Bousquet

Melén

Haahtela

et al. 2023

Allergy

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Asthma, rhinitis, and atopic dermatitis (AD) are interrelated clinical phenotypes that partly overlap in the human interactome. The concept of "one-airway-one-disease," coined over 20 years ago, is a simplistic approach of the links between upper-and lower-airway allergic diseases. With new data, it is time to reassess the concept. This article reviews (i) the clinical observations that led to Allergic Rhinitis and its Impact on Asthma (ARIA), (ii) new insights into polysensitization and multimorbidity, (iii) advances in mHealth for novel phenotype definitions, (iv) confirmation in canonical epidemiologic studies, (v) genomic findings, (vi) treatment approaches, and (vii) novel concepts on the onset of rhinitis and multimorbidity. One recent concept, bringing together upper-and lower-airway allergic diseases with skin, gut, and neuropsychiatric multimorbidities, is the "Epithelial Barrier Hypothesis." This review determined that the "one-airway-one-disease" concept does not always hold true and that several phenotypes of disease can be defined. These phenotypes include an extreme "allergic" (asthma) phenotype combining asthma, rhinitis, and conjunctivitis.

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Involvement of Il-33 in the Pathogenesis and Prognosis of Major Respiratory Viral Infections: Future Perspectives for Personalized Therapy

Cited by 17 publications

References 86 publications

Association of Toll‐like receptor 2 rs111200466 polymorphism with low serum levels of IL‐33 in early childhood

Association of Toll‐like receptor 2 rs111200466 polymorphism with low serum levels of IL‐33 in early childhood

Coordinated nasal mucosa-mediated immunity accelerates recovery from COVID-19

Rhinitis associated with asthma is distinct from rhinitis alone: The ARIA‐MeDALL hypothesis

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