Emerging roles of innate lymphoid cells in inflammatory diseases: Clinical implications

Background Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in association with virus infection, pollution, and excess of nutrient, but it is not known whether chronic chlorine exposure can activate innate immune cells. The aim of this study was to evaluate the impact of chlorine inhalation on the innate immunity such as ILCs and macrophages in relation with the development of asthma by using murine ovalbumin (OVA) sensitization/challenge model. Methods Six‐week‐old female BALB/c mice were sensitized and challenged with OVA in the presence and absence of chronic low‐dose chlorine exposure by inhalation of naturally vaporized gas of 5% sodium hypochlorite solution. AHR, airway inflammatory cells, from BALF and the population of ILCs and macrophages in the lung were evaluated. Results The mice exposed to chlorine with OVA (Cl + OVA group) showed enhanced AHR and eosinophilic inflammation compared to OVA‐treated mice (OVA group). The population of TH2 cells, ILC2s, and ILC3s increased in Cl + OVA group compared with OVA group. CD11cint macrophages also remarkably increased in Cl + OVA group compared with OVA group. The deletion of macrophages by clodronate resulted in reduction of ILC2s and ILC3s population which was restored by adoptive transfer of CD11cint macrophages. Conclusions Chronic chlorine inhalation contributes to the exacerbation of airway inflammation in asthmatic airway by mobilizing pro‐inflammatory macrophage into the lung as well as stimulating group 2 and 3 ILCs.

Section: Discussionmentioning

confidence: 99%

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Shim

Lee

Park

et al. 2019

“…Mast cell activation appears to play a key role in CysLTs formation when COX‐1 is inhibited, although other cells could participate, as in other related diseases including tissue eosinophils and platelets . PGD2 is the main product of COX‐1, and higher urinary basal levels of the stable metabolite PGD2‐M were reported in NERD, which further increased after ASA‐DPT .…”

Section: Underlying Mechanisms and Endotypesmentioning

confidence: 99%

Progress in understanding hypersensitivity reactions to nonsteroidal anti‐inflammatory drugs

Doña

Pérez‐Sánchez

Eguiluz‐Gracia

et al. 2019

Nonsteroidal anti‐inflammatory drugs (NSAIDs), the medications most commonly used for treating pain and inflammation, are the main triggers of drug hypersensitivity reactions. The latest classification of NSAIDs hypersensitivity by the European Academy of Allergy and Clinical Immunology (EAACI) differentiates between cross‐hypersensitivity reactions (CRs), associated with COX‐1 inhibition, and selective reactions, associated with immunological mechanisms. Three phenotypes fill into the first group: NSAIDs‐exacerbated respiratory disease, NSAIDs‐exacerbated cutaneous disease and NSAIDs‐induced urticaria/angioedema. Two phenotypes fill into the second one: single‐NSAID‐induced urticaria/angioedema/anaphylaxis and single‐NSAID‐induced delayed reactions. Diagnosis of NSAIDs hypersensitivity is hampered by different factors, including the lack of validated in vitro biomarkers and the uselessness of skin tests. The advances achieved over recent years recommend a re‐evaluation of the EAACI classification, as it does not consider other phenotypes such as blended reactions (coexistence of cutaneous and respiratory symptoms) or food‐dependent NSAID‐induced anaphylaxis. In addition, it does not regard the natural evolution of phenotypes and their potential interconversion, the development of tolerance over time or the role of atopy. Here, we address these topics. A state of the art on the underlying mechanisms and on the approaches for biomarkers discovery is also provided, including genetic studies and available information on transcriptomics and metabolomics.

“…The etiology of allergic disease is poorly understood, and its potential biologic mechanisms are still unclear . As other allergic inflammatory diseases, AR is considered to have complex associations with genetic and environment factors in etiology.…”

Section: Risk Factorsmentioning

confidence: 99%

Recent developments and highlights in allergic rhinitis

Meng

Wang

Zhang

2019

135

105

Allergic rhinitis (AR) is a disease with high prevalence all over the world and therefore needs to be thoroughly investigated and treated accordingly. The mechanisms underlying the pathology and treatment of AR have been widely studied, but many aspects remain unclear and warrant further investigations. This review presents an overview of recently published papers highlighting the risk factors, mechanisms, and treatment of AR. Additionally, recent studies discussing the role of single nucleotide polymorphism, DNA methylation, regulatory B cells, group 2 innate lymphoid cells, immunotherapy, and biologics in AR are also covered. K E Y W O R D Sallergic rhinitis, biologics, epigenetics, risk factors, treatment | 2321 MENG Et al.