The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD

Ween, Miranda P.; White, Jake; Tran, Hai B.; Mukaro, Violet; Jones, Charles H.; Macowan, Matthew; Hodge, G. E.; Trim, Paul J.; Snel, Marten F.; Hodge, Sandra

doi:10.1038/s41598-021-82481-0

Cited by 20 publications

(22 citation statements)

References 87 publications

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“…These oxidation-specific components are recognized as endogenous DAMPs by PRR in phagocytic cells acting as antigen-presenting cells (APCs) to over-stimulate the innate immune cells (26). Recent evidence reported that CD1b in dendritic cells play a role in oxidizing lipids that stimulate NKT cells (27). Leiw et al reported that selfantigenic lipids are associated with CD1d that promotes NKT cell participation in restoring tissue homeostasis after a sterile injury (28).…”

Section: Acute Inflammationmentioning

confidence: 99%

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Old and New Players of Inflammation and Their Relationship With Cancer Development

et al. 2021

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Pathogens or genotoxic agents continuously affect the human body. Acute inflammatory reaction induced by a non-sterile or sterile environment is triggered for the efficient elimination of insults that caused the damage. According to the insult, pathogen-associated molecular patterns, damage-associated molecular patterns, and homeostasis-altering molecular processes are released to facilitate the arrival of tissue resident and circulating cells to the injured zone to promote harmful agent elimination and tissue regeneration. However, when inflammation is maintained, a chronic phenomenon is induced, in which phagocytic cells release toxic molecules damaging the harmful agent and the surrounding healthy tissues, thereby inducing DNA lesions. In this regard, chronic inflammation has been recognized as a risk factor of cancer development by increasing the genomic instability of transformed cells and by creating an environment containing proliferation signals. Based on the cancer immunoediting concept, a rigorous and regulated inflammation process triggers participation of innate and adaptive immune responses for efficient elimination of transformed cells. When immune response does not eliminate all transformed cells, an equilibrium phase is induced. Therefore, excessive inflammation amplifies local damage caused by the continuous arrival of inflammatory/immune cells. To regulate the overstimulation of inflammatory/immune cells, a network of mechanisms that inhibit or block the cell overactivity must be activated. Transformed cells may take advantage of this process to proliferate and gradually grow until they become preponderant over the immune cells, preserving, increasing, or creating a microenvironment to evade the host immune response. In this microenvironment, tumor cells resist the attack of the effector immune cells or instruct them to sustain tumor growth and development until its clinical consequences. With tumor development, evolving, complex, and overlapping microenvironments are arising. Therefore, a deeper knowledge of cytokine, immune, and tumor cell interactions and their role in the intricated process will impact the combination of current or forthcoming therapies.

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Section: Acute Inflammationmentioning

confidence: 99%

Section: Acute Inflammationmentioning

confidence: 99%

Old and New Players of Inflammation and Their Relationship With Cancer Development

et al. 2021

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“…It was proposed that cigarette smoke exposure increases phospholipid oxidation, which hinders its surface tension-lowering ability [138]. Indeed, BALF isolated from mice exposed to cigarette smoke for 2 weeks was found to contain high levels of oxidised PC and in vitro treatment of alveolar macrophages with oxidised lipids and phospholipids led to reduced cell viability, decreased respiratory burst upon LPS stimulation and impaired bacterial killing [94,139]. Similarly, several studies have observed that direct in vitro treatment of surfactant with cigarette smoke led to dose-dependent alterations in surfactant interfacial properties and microstructure leading to reduced surface activity [140][141][142][143].…”

Section: Cigarette Smokingmentioning

confidence: 99%

Revisiting the role of pulmonary surfactant in chronic inflammatory lung diseases and environmental exposure

Milad

Morissette

2021

Eur Respir Rev

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Pulmonary surfactant is a crucial and dynamic lung structure whose primary functions are to reduce alveolar surface tension and facilitate breathing. Though disruptions in surfactant homeostasis are typically thought of in the context of respiratory distress and premature infants, many lung diseases have been noted to have significant surfactant abnormalities. Nevertheless, preclinical and clinical studies of pulmonary disease too often overlook the potential contribution of surfactant alterations – whether in quantity, quality or composition – to disease pathogenesis and symptoms. In inflammatory lung diseases, whether these changes are cause or consequence remains a subject of debate. This review will outline 1) the importance of pulmonary surfactant in the maintenance of respiratory health, 2) the diseases associated with primary surfactant dysregulation, 3) the surfactant abnormalities observed in inflammatory pulmonary diseases and, finally, 4) the available research on the interplay between surfactant homeostasis and smoking-associated lung disease. From these published studies, we posit that changes in surfactant integrity and composition contribute more considerably to chronic inflammatory pulmonary diseases and that more work is required to determine the mechanisms underlying these alterations and their potential treatability.

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“…Tobacco smoke is a complex, not fully studied mixture of several thousand different chemicals, including many free radicals, which can have a significant effect on the lipids of the lungs [ 35 ]. Exposure to cigarette smoke causes lipid peroxidation in the bronchial epithelium and also leads to the redistribution of various lipid fractions [ 36 ].…”

Section: Lipid Metabolism and Its Disorders In Copdmentioning

confidence: 99%

“…It has been shown that exposure to cigarette smoke causes the production of antibodies against oxidized lipids in the lungs of mice, which may contribute to limiting the response to damaged lipids [ 230 ]. Interestingly, the phagocytic function of macrophages was dose-dependent suppressed by the presence of oxidized epithelial lipids [ 36 ].…”

Section: Participation Of Lipids In Phagocytosis Disorders In Copdmentioning

confidence: 99%

Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease

Kotlyarov

Kotlyarova

2021

IJMS

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Exacerbations largely determine the character of the progression and prognosis of chronic obstructive pulmonary disease (COPD). Exacerbations are connected with changes in the microbiological landscape in the bronchi due to a violation of their immune homeostasis. Many metabolic and immune processes involved in COPD progression are associated with bacterial colonization of the bronchi. The objective of this review is the analysis of the molecular mechanisms of lipid metabolism and immune response disorders in the lungs in COPD exacerbations. The complex role of lipid metabolism disorders in the pathogenesis of some infections is only beginning to be understood, however, there are already fewer and fewer doubts even now about its significance both in the pathogenesis of infectious exacerbations of COPD and in general in the progression of the disease. It is shown that the lipid rafts of the plasma membranes of cells are involved in many processes related to the detection of pathogens, signal transduction, the penetration of pathogens into the cell. Smoking disrupts the normally proceeded processes of lipid metabolism in the lungs, which is a part of the COPD pathogenesis.

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The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD

Cited by 20 publications

References 87 publications

Old and New Players of Inflammation and Their Relationship With Cancer Development

Old and New Players of Inflammation and Their Relationship With Cancer Development

Revisiting the role of pulmonary surfactant in chronic inflammatory lung diseases and environmental exposure

Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease

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