Thymic stromal lymphopoietin, IL-33, and periostin in hospitalized infants with viral bronchiolitis

Abstract

Much attention has recently been focused on thymic stromal lymphopoietin (TSLP), IL-33, and periostin in allergic disease, but less is known about their role in viral bronchiolitis.The aim of the study was to investigate whether infants exhibit enhanced nasal airway secretion of TSLP, IL-33, and periostin during natural respiratory viral bronchiolitis compared to healthy controls.In total, 213 infants < 2 years of age, hospitalized with bronchiolitis from October/2013 to April/2016 were enrolled alongside 45 healthy infants. Nasopharyngeal aspirates (NPA) were screened for respiratory viruses by the polymerase chain reaction. TSLP, IL-33, and periostin were measured in NPAs. Clinical data were recorded.At least 1 virus was detected in 186 (87.3%) hospitalized infants: 149 (70%) respiratory syncytial virus (RSV); 42 (19.7%) rhinovirus (HRV); 16 (7.5%) parainfluenza virus (PIV); 9 (4.2%) adenovirus; 10 (4.7%) bocavirus; and 7 (3.3%) metapneumovirus (hMPV). Infants with bronchiolitis had higher levels of TSLP (P = .02), IL-33 (P<.001), and periostin (P = .003) than healthy controls.Detectable levels of TSLP and periostin were more frequent in virus-positive than in virus-negative patients (P = .05). TSLP and IL-33 were also more common in coinfections, mainly RSV and HRV, than in single-infections (P < .05). No patient with bronchiolitis but with negative viral detection had detectable levels of nasal TSLP or IL-33. Infants with hospital stay ≥5 days were more likely to have detectable levels of nasal TSLP and periostin after adjusting by age (P = .01).Bronchiolitis by common respiratory viruses is associated with elevated nasal levels of TSLP, IL-33, and periostin, factors known to be important in the development of Th2-response. Respiratory viruses in early life might shift immune responses toward Th2, involving asthma, and allergic diseases.

IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection

“…ST2 axis in viral respiratory diseases in children, with conflicting results. Similar to our findings, García-García et al [13] reported higher detectable IL-33 NPA levels in infants infected by RSV and rhinovirus on hospital admission when comparing to healthy controls, although no associations between higher IL-33 detections and ICU admissions or longer hospital lengths of stay were found. Saravia et al [16] described higher IL-33 NPA concentrations in 19 infants with RSV acute viral bronchiolitis on hospital admission when compared to IL-33 NPA concentrations 28 days later, after hospital discharge.…”

“…While young age, prematurity and co-morbidities have been identified as predictors of poor outcomes [6][7][8][9], the role of virus types and host inflammatory responses in disease severity is not well defined, as published results are inconsistent [10,11]. Lately, a model of immune inflammatory response in which an imbalance between T helper (Th)1, Th2 and regulatory T cells could be responsible for severe cases of ALRI in infants and young children has been suggested [10,12,13]. In addition, Interleukin (IL)-33, a member of the interleukin-1 family expressed in epithelium surfaces, along with its receptor, suppression of tumorigenicity (ST)2, may play an important role in the immune response associated with asthma, autoimmune disorders and infections [14,15].…”

<p>Confounding Patient Factors Affecting the Proper Interpretation of the Periostin Level as a Biomarker in Asthma Development</p>

“…Another suspected factor is human rhinovirus infection (HRV), which is known to cause loss of control in asthmatic symptoms thus leading to emergency room visits and augmentation in asthma management. 31 Such common respiratory viruses are known to induce local POSTN levels to shift immune responses toward Th2 in children 32 especially during a rhinovirus-induced asthma exacerbation. 33 In our analysis using adult bronchial epithelium, there was no effect of HRV on POSTN expression.…”

Interleukin‐33 in the developing lung—Roles in asthma and infection

“…Attention has therefore focused on the role of RSV in early life and its potential to lead to asthma through induction of type 2 immune responses. Increased IL‐33 is seen in nasopharyngeal aspirates of infants with RSV bronchiolitis, while single nucleotide polymorphisms (SNPs) in Il1rl1 are implicated in susceptibility to both RSV bronchiolitis and asthma . In mouse models of infection, RSV causes release of IL‐33 and expansion of ILC2s .…”