Pulmonary Macrophage Cell Death in Lung Health and Disease

Shotland, Abigail M.; Fontenot, Andrew P.; McKee, Amy S.

doi:10.1165/rcmb.2020-0420tr

Cited by 21 publications

(9 citation statements)

References 50 publications

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“…Epitheliums are the main barrier cells against the invasion of pathogens and macrophages are the major immune cells in the lung that determine the resolution of inflammation ( 17 , 18 ). In particular, macrophage polarization involves and influences the orientation and the magnitude of inflammatory responses ( 19 ).…”

Section: Discussionmentioning

confidence: 99%

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Chen

Fan

et al. 2022

Front. Immunol.

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Extracellular vesicles (EVs)-mediated epithelium-macrophage crosstalk has been proved to maintain lung homeostasis in cigarette smoke-induced lung diseases such as chronic obstructive pulmonary disease (COPD). In our previous study, we found that EVs derived from cigarette smoke extract (CSE) treated BEAS-2B promoted M1 macrophage polarization, which probably accelerated the development of inflammatory responses. Naringenin has been proved to suppress M1 macrophage polarization, but whether naringenin regulates macrophage polarization mediated by EVs has not been reported. In this study, we firstly found that EVs derived from naringenin and CSE co-treated BEAS-2B significantly inhibited the expression of CD86 and CD80 and the secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS), and IL-12 in macrophage induced by EVs derived from CSE-treated BEAS-2B. Further research revealed that naringenin downregulated BEAS-2B-derived EVs miR-21-3p which targeted phosphatase and tensin homolog deleted on chromosome ten/protein kinase B (PTEN/AKT) cascade in macrophages and then suppressed M1 macrophage polarization. Subsequent proteomics suggested that naringenin decreased BEAS-2B-derived EVs poly ADP-ribose polymerase (PARP)1 expression thereby suppressing M1 macrophage polarization probably. Our study provides novel pharmacological references for the mechanism of naringenin in the treatment of cigarette smoke-induced lung inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Chen

Fan

et al. 2022

Front. Immunol.

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“…Growing evidence suggests that pyroptosis of macrophages plays a key role in ALI pathogenesis [16,47]. Currently, inhibition of inflammasome to initiate pyroptosis is the main strategy employed to treat ALI [48].…”

Section: Discussionmentioning

confidence: 99%

Sacubitril/valsartan alleviates sepsis‐induced acute lung injury via inhibiting GSDMD‐dependent macrophage pyroptosis in mice

Wang

Lou

et al. 2023

The FEBS Journal

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Sepsis-induced acute lung injury (ALI) is a life-threatening disorder with intricate pathogenesis. Macrophage pyroptosis reportedly plays a vital role in ALI. Although it has been established that angiotensin receptor blockers (ARBs) can reduce sepsis-induced organ injury, the efficacy of sacubitril/valsartan (SV) for sepsis has been largely understudied. Here, we aimed to investigate the role of SV in sepsis-induced ALI. Caecal ligation and puncture (CLP) were used to induce polymicrobial sepsis and related ALI. The therapeutic effects of SV in CLP mice were subsequently assessed. Gasdermin D (GSDMD) À/À mice were used to validate the signalling pathways affected by SV. In vitro, mouse bone marrow-derived macrophages (BMDMs) and Raw264.7 cells were treated with SV following exposure to lipopolysaccharide and adenosine triphosphate. Finally, the serum obtained from 42 septic patients was used for biochemical analysis. Compared to the other ARBs, SV yielded more pronounced anti-inflammatory effects on macrophages. In vivo, SV decreased mortality rates, significantly reduced lung damage and prevented the inflammatory response in CLP mice. In addition, SV suppressed GSDMD-mediated macrophage pyroptosis in mice. In BMDMs and Raw264.7 cells, the anti-inflammatory and anti-pyroptosis properties of SV were verified. SV treatment effectively inhibited NLRP3 inflammasome activation and prevented macrophage pyroptosis in a GSDMD-dependent manner. Furthermore, we found that septic individuals had considerably higher serum angiotensin II levels. Overall, we found that SV might prevent ALI in CLP mice by inhibiting GSDMD-mediated pyroptosis of macrophages. Thus, SV might be a viable drug for sepsis-induced ALI.

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“…The reasons for the loss of TR-AMs are not clear, but it was not preventable by ECP or anti–TGF-β Ab treatment. Therefore, their loss could be potentially explained by their programmed cell death following airway inflammation ( 78 ). We recognized that targeting CCR2 + monocyte–mediated Mo-AM depletion could also result in the defective generation of other CCR2 + monocyte–derived cells that may contribute to BOS, such as iMacs and CD11b + DCs ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome

Liu¹,

Liao²,

Zhu³

et al. 2022

Journal of Clinical Investigation

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Bronchiolitis obliterans syndrome (BOS) is a major impediment to lung transplant survival and is generally resistant to medical therapy. Extracorporeal photophoresis (ECP) is an immunomodulatory therapy that shows promise in stabilizing BOS patients, but its mechanisms of action are unclear. In a mouse lung transplant model, we show that ECP blunts alloimmune responses and inhibits BOS through lowering airway TGF-β bioavailability without altering its expression. Surprisingly, ECP-treated leukocytes were primarily engulfed by alveolar macrophages (AMs), which were reprogrammed to become less responsive to TGF-β and reduce TGF-β bioavailability through secretion of the TGF-β antagonist decorin. In untreated recipients, high airway TGF-β activity stimulated AMs to express CCL2, leading to CCR2 + monocyte-driven BOS development. Moreover, we found TGF-β receptor 2–dependent differentiation of CCR2 + monocytes was required for the generation of monocyte-derived AMs, which in turn promoted BOS by expanding tissue-resident memory CD8 + T cells that inflicted airway injury through Blimp-1–mediated granzyme B expression. Thus, through studying the effects of ECP, we have identified an AM functional plasticity that controls a TGF-β–dependent network that couples CCR2 + monocyte recruitment and differentiation to alloimmunity and BOS.

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Pulmonary Macrophage Cell Death in Lung Health and Disease

Cited by 21 publications

References 50 publications

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Sacubitril/valsartan alleviates sepsis‐induced acute lung injury via inhibiting GSDMD‐dependent macrophage pyroptosis in mice

Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome

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