Does airway colonization cause systemic inflammation in bronchiectasis?

B, Ergan Arsava; Çöplü, Lütfi

doi:10.5578/tt.2934

Cited by 19 publications

(15 citation statements)

References 29 publications

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“…There were isolated exceptions but overall, clinical markers of systemic inflammation including CRP, white cell count, neutrophils and platelets were within normal ranges. In contrast, adult based bronchiectasis studies have described systemic inflammation, although this may be transient and associated with bacterial infection [11,25]. We found no significant association between plasma and BAL IL-1β or IL-6 and no significant association between markers of systemic inflammation and the capacity for NTHi-specific IFN-γ production by blood mononuclear cells.…”

Section: Discussioncontrasting

confidence: 83%

High Pulmonary Levels of IL-6 and IL-1β in Children with Chronic Suppurative Lung Disease Are Associated with Low Systemic IFN-γ Production in Response to Non-Typeable Haemophilus influenzae

et al. 2015

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Non-typeable Haemophilus influenzae (NTHi) is commonly associated with chronic suppurative lung disease in children. We have previously shown that children with chronic suppurative lung disease have a reduced capacity to produce IFN-γ in response to NTHi compared with healthy control children. The aim of this study was to determine if deficient NTHi-specific IFN-γ production is associated with heightened systemic or airway inflammation. We measured a panel of cytokines (IFN-γ, IL-1β, IL-6, IL-8, IL-12 p70), antimicrobial proteins (LL-37, IP-10) as well as cellular and clinical factors associated with airway and systemic inflammation in 70 children with chronic suppurative lung disease. IFN-γ was measured in peripheral blood mononuclear cells challenged in vitro with live NTHi. Regression analysis was used to assess the association between the systemic and airway inflammation and the capacity to produce IFN-γ. On multivariate regression, NTHi-specific IFN-γ production was significantly negatively associated with the BAL concentrations of the inflammatory cytokines IL-6 (β=-0.316; 95%CI -0.49, -0.14; p=0.001) and IL-1β (β=-0.023; 95%CI -0.04, -0.01; p=0.001). This association was independent of bacterial or viral infection, BAL cellularity and the severity of bronchiectasis (using modified Bhalla score on chest CT scans). We found limited evidence of systemic inflammation in children with chronic suppurative lung disease. In summary, increased local airway inflammation is associated with a poorer systemic cell-mediated immune response to NTHi in children with chronic suppurative lung disease. These data support the emerging body of evidence that impaired cell-mediated immune responses and dysregulated airway inflammation may be linked and contribute to the pathobiology of chronic suppurative lung disease.

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Section: Discussioncontrasting

confidence: 83%

High Pulmonary Levels of IL-6 and IL-1β in Children with Chronic Suppurative Lung Disease Are Associated with Low Systemic IFN-γ Production in Response to Non-Typeable Haemophilus influenzae

et al. 2015

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“…Systemic inflammation is relatively common in adults with bronchiectasis. Elevated levels of circulating inflammatory cells (neutrophils and total white cell count) as well as soluble serum mediators [including transforming growth factor (TGF)-β, CRP, fibrinogen, and soluble adhesion molecules] have been described in adults with long-standing disease (17,(24)(25)(26)(27). A high level of systemic inflammation is associated with an accelerated decline in lung function (28).…”

Section: Systemic Inflammationmentioning

confidence: 99%

Bronchiectasis in Children: Current Concepts in Immunology and Microbiology

2017

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Bronchiectasis is a complex chronic respiratory condition traditionally characterized by chronic infection, airway inflammation, and progressive decline in lung function. Early diagnosis and intensive treatment protocols can stabilize or even improve the clinical prognosis of children with bronchiectasis. However, understanding the host immunologic mechanisms that contribute to recurrent infection and prolonged inflammation has been identified as an important area of research that would contribute substantially to effective prevention strategies for children at risk of bronchiectasis. This review will focus on the current understanding of the role of the host immune response and important pathogens in the pathogenesis of bronchiectasis (not associated with cystic fibrosis) in children.

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“…Emerging evidence indicates that altered microbial colonization patterns are involved in the physiologic, immunologic, and metabolic deregulation seen in asthma and other chronic inflammatory diseases . Most studies have focused on the role of the gut microbiome in subjects with ongoing chronic inflammatory diseases, whereas few studies have investigated the airway microbiome and systemic inflammation in chronic inflammatory diseases, and no studies have investigated the relationship between the early‐life airway microbiome and systemic inflammation before disease development.…”

Section: Discussionmentioning

confidence: 99%

Neonates colonized with pathogenic bacteria in the airways have a low‐grade systemic inflammation

Fink

Chawes

Thorsen

et al. 2018

Allergy

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Does airway colonization cause systemic inflammation in bronchiectasis?

Abstract: ÖZET Bronşektazide hava yolu kolonizasyonu sistemik inflamasyona neden olur mu? 0.42 (0.30-0.77) mg/dL, 433.5 (390.3-490.3) ve 392.0 (327.0-416.0)

Cited by 19 publications

References 29 publications

High Pulmonary Levels of IL-6 and IL-1β in Children with Chronic Suppurative Lung Disease Are Associated with Low Systemic IFN-γ Production in Response to Non-Typeable Haemophilus influenzae

High Pulmonary Levels of IL-6 and IL-1β in Children with Chronic Suppurative Lung Disease Are Associated with Low Systemic IFN-γ Production in Response to Non-Typeable Haemophilus influenzae

Bronchiectasis in Children: Current Concepts in Immunology and Microbiology

Neonates colonized with pathogenic bacteria in the airways have a low‐grade systemic inflammation

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