Contribution of monocyte and macrophage extracellular traps to neutrophilic airway inflammation in severe asthma

Quoc, Quang Luu; Cao, Thi Bich Tra; Moon, Ji‐Young; Jang, Jae-Hyuk; Shin, Yoo Seob; Choi, Youngwoo; Ryu, Min Sook; Park, Hae‐Sim

doi:10.1016/j.alit.2023.06.004

Cited by 9 publications

(6 citation statements)

References 46 publications

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“…M1 macrophages could release ETs (M1ETs) underlying the stimulation of LPS, IFN-γ, and TNF-α, which were more elevated in patients with SA than in those with non-SA. 52 55 56 Functional studies have recently demonstrated that M1ETs activated neutrophils, ILC1, and ILC3. 56 These findings suggest that macrophage function could be considered in novel therapies for SA.…”

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

“… 52 55 56 Functional studies have recently demonstrated that M1ETs activated neutrophils, ILC1, and ILC3. 56 These findings suggest that macrophage function could be considered in novel therapies for SA.…”

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

“…, B cell-activating chemokine 1) and induce B cell maturation, proliferation, and survival; and 3) the activation of neutrophils and macrophages. 56 57 58 59 60 Macrophages release a range of proinflammatory cytokines ( e.g. , IL-1β, IL-6, TNF-α, and ROS), resulting in local and systemic inflammation and promoting fibrosis and degradation of cartilage.…”

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

“… 53 Moreover, M1ETs could directly induce the release of neutrophil activation-related cytokines from AECs and simulate neutrophils to release NETs, further aggravating neutrophilic inflammation in SA. 56 Clinical efficacy and limitations of anti-IL-1, anti-TNF-α, and anti-IL-6 antibodies have been reported in clinical trials on patients with pulmonary diseases. 61 62 63 Novel therapeutics targeting upstream signaling in the pathway of the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) have been focused on investigation [ e.g.…”

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

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Immune Cell-Mediated Autoimmune Responses in Severe Asthma

Cao,

Quoc,

Jang

et al. 2024

Yonsei Med J

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Severe asthma (SA) has heterogeneous inflammatory phenotypes characterized by persistent airway inflammation (eosinophilic and/or neutrophilic inflammation) and remodeling. Various immune cells (eosinophils, neutrophils, and macrophages) become more activated and release inflammatory mediators and extracellular traps, damaging the protective barrier of airway epithelial cells and further activating other immune and structural cells. These cells play a role in autoimmune responses in asthmatic airways, where the adaptive immune system generates autoantibodies, inducing immunoglobulin G-dependent airway inflammation. Recent studies have suggested that adult asthmatics had high titers of autoantibodies associated with asthma severity, although pathogenic factors or diagnostic criteria are not well-defined. This challenge is further compounded by asthmatics with the autoimmune responses showing therapy insensitivity or failure to current pharmacological and biological treatment. This review updates emerging mechanisms of autoimmune responses in asthmatic airways and provides insights into their roles, proposing potential biomarkers and therapeutic targets for SA.

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Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

Section: Autoimmune Mechanism Possible Biomarkers and Noble Treatment...mentioning

confidence: 99%

See 2 more Smart Citations

Immune Cell-Mediated Autoimmune Responses in Severe Asthma

Cao,

Quoc,

Jang

et al. 2024

Yonsei Med J

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“…Furthermore, they have immunomodulatory effects and can activate monocytes, macrophages, and dendritic cells, thereby enhancing immune surveillance and antigen presentation. However, the unregulated release or persistence of NETs can exacerbate autoimmune diseases, thrombosis, tissue damage, and conditions such as NA or MGA [ 50 ]. Importantly, the presence of NETs may damage AECs and activate eosinophils.…”

Section: Na and Mga: Mechanisms And Therapeutic Targetsmentioning

confidence: 99%

New targets for type 2-low asthma

Quoc,

Choi,

Hur

et al. 2024

Korean J Intern Med

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Asthma is characterized by airway obstruction and inflammation, and presents significant diagnostic and treatment challenges. The concept of endotypes has improved understanding of the mechanisms of asthma and has stimulated the development of effective treatment strategies. Sputum profiles may be used to classify asthma into two major inflammatory types: type 2-high (T2H) and type 2-low (T2L) asthma. T2H, characterized by elevated type 2 inflammation, has been extensively studied and several effective biologic treatments have been developed. However, managing T2L is more difficult due to the lack of reliable biomarkers for accurate diagnosis and classification. Additionally, conventional anti-inflammatory therapy does not completely control the symptoms of T2L; therefore, further research is needed to identify effective biologic treatments. This review provides new insights into the clinical characteristics and underlying mechanisms of severe T2L and investigates potential therapeutic approaches to control the disease.

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