The relationship between inflammation and remodeling in childhood asthma: A systematic review

Castro-Rodriguez, José A.; Saglani, Sejal; Rodríguez‐Martínez, Carlos E.; Oyarzún, María Angélica; Fleming, Louise; Bush, Andrew

doi:10.1002/ppul.23968

Cited by 59 publications

(48 citation statements)

References 62 publications

(511 reference statements)

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“…In children with severe asthma, airway wall remodeling correlated with eosinophilia, but not with type-2 cytokines [24]. The link between inflammation and airway wall remodeling in childhood asthma was analyzed by Castro-Rodriguez et al [17], performing a meta-analysis over 39 studies including 2390 children under the age of 18 years. This study suggested that airway inflammation and remodeling was not present in children under 12 months of age, but occurred in older children.…”

Section: Asthmamentioning

confidence: 99%

“…The only new aspect that seems to show up in many studies was the important role of the interaction between the environment and the lung, based on epigenetic gene regulation. Many of the "-omic" studies indicated that tissue remodeling is a major pathology and against previous assumption occurs independent from inflammation [15][16][17]. Furthermore, many studies reported that the different asthma phenotypes, which were described based on patient symptoms, could not be well separated by specific cellular pathologies [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

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Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Fang

Sun

Roth

2020

IJMS

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Asthma increases worldwide without any definite reason and patient numbers double every 10 years. Drugs used for asthma therapy relax the muscles and reduce inflammation, but none of them inhibited airway wall remodeling in clinical studies. Airway wall remodeling can either be induced through pro-inflammatory cytokines released by immune cells, or direct binding of IgE to smooth muscle cells, or non-immunological stimuli. Increasing evidence suggests that airway wall remodeling is initiated early in life by epigenetic events that lead to cell type specific pathologies, and modulate the interaction between epithelial and sub-epithelial cells. Animal models are only available for remodeling in allergic asthma, but none for non-allergic asthma. In human asthma, the mechanisms leading to airway wall remodeling are not well understood. In order to improve the understanding of this asthma pathology, the definition of “remodeling” needs to be better specified as it summarizes a wide range of tissue structural changes. Second, it needs to be assessed if specific remodeling patterns occur in specific asthma pheno- or endo-types. Third, the interaction of the immune cells with tissue forming cells needs to be assessed in both directions; e.g., do immune cells always stimulate tissue cells or are inflamed tissue cells calling immune cells to the rescue? This review aims to provide an overview on immunologic and non-immunologic mechanisms controlling airway wall remodeling in asthma.

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Section: Asthmamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Fang

Sun

Roth

2020

IJMS

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“…The relationship between inflammation and remodeling is controversial. It is unknown in children if repeated airway inflammation precedes remodeling changes 2 …”

Section: Introductionmentioning

confidence: 99%

Airway hyperresponsiveness, remodeling and inflammation in infants with wheeze

Malmström

Malmberg

Kotaniemi‐Syrjänen

et al. 2020

Clin Experimental Allergy

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Background:The relationship of airway hyperresponsiveness to airway remodeling and inflammation in infants with wheeze is unclear.Objective: To investigate airway hyperresponsiveness, remodeling and inflammation in infants with wheeze and troublesome breathing.Methods: Inclusion criteria were as follows: full-term, 3-23 months of age; doctor -diagnosed wheeze and persistent recurrent troublesome breathing; without obvious structural defect, suspicion of ciliary dyskinesia, cystic fibrosis, immune deficiency or specified use of corticosteroids. Airway hyperresponsiveness (AHR) was evaluated by performing a methacholine bronchial challenge test combined with whole body plethysmography and rapid thoracoabdominal compression. Endobronchial biopsies were analysed for remodeling (thickness of reticular basement membrane and amount of airway smooth muscle) and for inflammation (numbers of inflammatory cells). Correlation analyses were performed.Results: Forty-nine infants fulfilled the inclusion criteria for the present study.Median age was 1.06 years (IQR 0.6; 1.5). Lung function was impaired in 39/49 (80%) children, at the median age of 1.1 years. Methacholine challenge was successfully performed in 38/49 children. Impaired baseline lung function was correlated with AHR (P = .047, Spearman). In children with the most sensitive quartile of AHR, the percentage of median bronchial airway smooth muscle % and the number of bronchial mast cells in airway smooth muscle were not significantly higher compared to others (P = .057 and 0.056, respectively). No association was found between AHR and thickness of reticular basement membrane or inflammatory cells.Only a small group of children with both atopy and AHR (the most reactive quartile) had thicker airway smooth muscle area than non-atopics with AHR (P = .031). Conclusions and Clinical Relevance:These findings do not support the concept that AHR in very young children with wheeze is determined by eosinophilic inflammation or clear-cut remodeling although it is associated with impaired baseline lung function. The possible association of increased airway smooth muscle area among atopic children with AHR remains to be confirmed. K E Y W O R D S asthma, eosinophils, paediatrics, remodeling | 559 MALMSTRÖM eT AL. Oxygen saturation, pre provocation (%) 97 (96; 99) Oxygen saturation, post provocation (%) 94 (93; 95) B-eosinophils (10E9/L) 0.29 (0.16; 0.41) B-eosinophils (%) 3.0 (2.0; 4.0) S-IgE (kU/L) 20.5 (7.8; 52.3)Note: Data presented as median (interquartile range) or n (n%).Abberivations: FRC, functional residual capacity; PD, provocative dose; sGaw, specific airway conductance; V'maxFRC, maximal airflow at FRC.

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“…AI can be assessed directly by bronchial biopsy or BAL. However, Castro‐Rodriguez et al found only seven studies in which AI was analyzed in both BAL and biopsy . The extent to which the inflammatory cell counts in BAL correlate with those in the bronchial mucosa is unclear.…”

mentioning

confidence: 99%

“…Although very informative, these studies were designed to analyze a small number of easily measured parameters, mainly LF and atopy. The paucity of data on AI and AR underscored by Castro‐Rodriguez et al supports the need for interventional studies, with endoscopy and bronchial biopsy, to describe asthma endotypes in children. Performing endoscopy with biopsy does not carry a higher risk of complications than performing endoscopy with BAL .…”

mentioning

confidence: 99%

Assessment of airway inflammation and remodeling in children with severe asthma: The next challenge

Lezmi

Blic

2018

Pediatric Pulmonology

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The relationship between inflammation and remodeling in childhood asthma: A systematic review

Cited by 59 publications

References 62 publications

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Airway hyperresponsiveness, remodeling and inflammation in infants with wheeze

Assessment of airway inflammation and remodeling in children with severe asthma: The next challenge

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