Analysis of the local and systemic inflammatory response in hospitalized infants with respiratory syncitial virus bronchiolitis

Moreno‐Solís, Gloria; Torres-Borrego, J.; Torre-Aguilar, María José de la; Fernández‐Gutiérrez, Fernando; Llorente-Cantarero, Francisco J.; Pérez-Navero, Juan Luís

doi:10.1016/j.aller.2014.02.002

Cited by 18 publications

(17 citation statements)

References 42 publications

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“…In a previous study by our research group interleukin levels were used to analyse the inflammatory response in hospitalised infants with respiratory syncytial virus bronchiolitis. In the current study, we detected a significant negative correlation between the GSH/GSSG ratio and the levels of IL‐6 ( P : 0.014), IL‐8 ( P : 0.014) and IL‐10 ( P : 0.033).…”

Section: Resultsmentioning

confidence: 99%

“…The plasma levels of interleukins have also been studied in RSV‐induced respiratory infections . Clinical manifestations of AB are mainly respiratory, although some studies have detected interleukin activity in the peripheral blood and that an elevation in the serum levels of some interleukins is associated with the severity of AB . To our knowledge, there are no current investigations of the association between OS biomarkers and the inflammatory response induced by RSV‐AB, which is measured through interleukin levels.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress and inflamatory plasma biomarkers in respiratory syncytial virus bronchiolitis

Moreno‐Solís

Torre-Aguilar

Torres-Borrego

et al. 2016

Clinical Respiratory J

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Oxidative stress and inflamatory plasma biomarkers in respiratory syncytial virus bronchiolitis

Moreno‐Solís

Torre-Aguilar

Torres-Borrego

et al. 2016

Clinical Respiratory J

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“…Th1 lymphocytes produce tumor necrosis factor-alpha (TNFα) and interferon-gamma (IFNγ) which enhance the in ammatory response, whereas Th2 lymphocytes produce interleukins 4 (IL-4), 5 (IL-5), 13 (IL-13), which are associated with the promotion of IgE and IL-10 showing an anti-in ammatory response. A prevalence of either Th1 or Th2 cytokines or even a mixed Th1-Th2 in ammatory response has been reported in different studies, with contradictory results that point out the complexity of the regulatory mechanisms that modulate the in ammatory/anti-in ammatory response in bronchiolitis [13][14][15][16][17] .…”

Section: What This Study Addsmentioning

confidence: 99%

Randomized trial: inflammatory response to corticoids versus placebo in moderate and severe bronchiolitis. COTHEBstudy.

Felipe¹,

Balaguer²,

Alejandre³

et al. 2020

Preprint

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Background: The use of corticosteroids has been shown not to improve the prognosis of patients with bronchiolitis, but it could be assumed that steroids will reduce inflammation. This study aimed to assess whether corticoid therapy influenced the inflammatory and clinical response of critically ill infants. Methods: Prospective, randomized, double blind placebo-controlled trial of glucocorticoids (GCT) in infants of less than 12 monthswith severe or moderate bronchiolitis. Patients were randomized to receive systemic corticoid therapy or placebo. The main outcomes were: a) levels of lymphocyte subsets; b) levels of IL-2, IL-12, and IFNγ as pro-inflammatory factors,and c) levels of IL-4 and IL-10 as anti-inflammatory response. Secondary outcomes related with the clinical response were also analyzed. Results: 97 patients were randomized. Evolution of lymphocyte subsets was similar in both groups. Pro-inflammatory interleukins and interferon decreased, but without differences. Anti-inflammatory interleukins showed a significant decrease from baseline to the end of the study, and IL-10 values were significantly lower (p = 0.046) in the GCT group [1.82 pg/ml (1.2-3.5)] vs non-GCT [4 pg/ml (1.5-6.3)]. GCT group showed a lower time of mechanical ventilation and of hospitalization, but without statistically significant differences. No cases of severe adverse reaction to steroids were detected. Conclusions: administration of systemic GCT did not modify the inflammatory nor the clinical response of patients with severe bronchiolitis, except for IL-10 levels that were significantly lower in the GCT group. This can open a line of investigation about the relation of IL-10 and response to bronchiolitis.Trial registration: Glucocorticoid Therapy Impact on the Inflammatory Response and Clinical Evolution in Patients With Severe Bronchiolitis, Clinical Trials.gov registration number: NCT02571517.Study start date: Nov 2011.

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“…1 RSV infection also induces a wide spectrum of pro-inflammatory cytokines such as IL-6, 5,6 which have been suggested to contribute to the pathogenesis of RSV-induced bronchiolitis. 7,8 In murine models, early-life RSV infection leads to sensitization against multiple allergens and development of type 2 immune responses, including acute eosinophilia in the lungs. [9][10][11] Th2 cytokines, such as IL-5 and IL-13, are elevated in the bronchoalveolar lavage fluid (BALF) of RSV-infected children, 12,13 suggesting a role for these cytokines in RSV pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary IL‐33 orchestrates innate immune cells to mediate respiratory syncytial virus‐evoked airway hyperreactivity and eosinophilia

Lai

Chi

et al. 2019

Allergy

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Background: Respiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL-33 is elevated and promotes immune cell activation, leading to the development of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL-33-activated innate immune cells, including ILC2s and ST2 + myeloid cells, in RSV infection-triggered pathophysiology. Methods:The role of IL-33/ILC2 axis in RSV-induced AHR inflammation and eosinophilia were evaluated in the IL-33-deficient and YetCre-13 Rosa-DTA mice. Myeloidspecific, IL-33-deficient or ST2-deficient mice were employed to examine the role of IL-33 and ST2 signaling in myeloid cells. Results:We found that IL-33-activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2-derived IL-13 was sufficient for RSV-driven AHR, since reconstitution of wild-type ILC2 rescued RSV-driven AHR in IL-13-deficient mice. Meanwhile, myeloid cell-derived IL-33 was required for airway inflammation, ST2 + myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL-33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL-33 signaling. Conclusions:This study highlights the importance of IL-33-activated ILC2s in mediating RSV-triggered AHR and eosinophilia. In addition, IL-33 signaling in myeloid cells is crucial for airway inflammation. K E Y W O R D S asthma, eosinophilia, IL-33, ILC2, respiratory syncytial virus | 819 WU et al.

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Analysis of the local and systemic inflammatory response in hospitalized infants with respiratory syncitial virus bronchiolitis

Cited by 18 publications

References 42 publications

Oxidative stress and inflamatory plasma biomarkers in respiratory syncytial virus bronchiolitis

Oxidative stress and inflamatory plasma biomarkers in respiratory syncytial virus bronchiolitis

Randomized trial: inflammatory response to corticoids versus placebo in moderate and severe bronchiolitis. COTHEBstudy.

Pulmonary IL‐33 orchestrates innate immune cells to mediate respiratory syncytial virus‐evoked airway hyperreactivity and eosinophilia

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