Pulmonary macrophages and SARS-Cov2 infection

Bain, Calum C.; Rossi, Adriano G.; Lucas, Christopher D.

doi:10.1016/bs.ircmb.2022.01.001

Cited by 18 publications

(14 citation statements)

References 113 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SARS-CoV-2 can replicate inside alveolar macrophages, alter their normal function, and drive them into a pro-inflammatory state [ 15 ]. Tissue-resident alveolar macrophages can be diminished in number, even after a mild case of COVID-19 [ 16 ]. On the other hand, this patient could have had pre-existing PAP, and COVID-19 infection and corticosteroid treatment resulted in the flare-up.…”

Section: Discussionmentioning

confidence: 99%

Post-COVID-19 Pulmonary Alveolar Proteinosis Treated Successfully with Whole Lung Lavage: A Rare Case Report

Le-Khac,

Tran-Le,

Nguyen-Ho

et al. 2023

Pulm Ther

View full text Add to dashboard Cite

Pulmonary alveolar proteinosis (PAP) is an uncommon disease and its diagnosis remains challenging. During the COVID-19 pandemic, it has been difficult to distinguish between PAP and post-COVID-19 pulmonary sequelae. Here we present a case of a 44-year-old male patient who experienced exertional dyspnea after recovering from COVID-19. He was initially diagnosed with post-COVID-19 syndrome and treated with systemic corticosteroid without improvement. Chest computed tomography (CT) showed crazy-paving pattern with ground-glass opacities. Fibreoptic bronchoscopy with bronchial lavage fluid (BLF) analysis confirmed the final diagnosis of PAP. The patient underwent left lung lavage in combination with conventional therapy and experienced significant improvement in his respiratory condition and overall health during follow-up. Hence, PAP could occur after a COVID-19 infection. This case highlights the importance of considering PAP as a potential diagnosis in patients with persistent respiratory symptoms after COVID-19. The high suspicion indicators of PAP revealed by chest-CT and BLF may be a key to differentiating PAP from post-COVID-19 pulmonary sequelae. Moreover, it is plausible that SARS-CoV-2 plays a role in the development of proteinosis, either by inducing a flare-up or by directly causing the condition.

show abstract

Section: Discussionmentioning

confidence: 99%

Post-COVID-19 Pulmonary Alveolar Proteinosis Treated Successfully with Whole Lung Lavage: A Rare Case Report

Le-Khac,

Tran-Le,

Nguyen-Ho

et al. 2023

Pulm Ther

View full text Add to dashboard Cite

show abstract

“…A cell census from the COVID-19 lung autopsies also showed increased levels of dendritic cells (DCs) and natural killer (NK) cells [ 44 ]. In severe COVID-19, in the setting of inflammation, tissue resident AMφs in the bronchoalveolar space are diminished in number, a phenomenon described as the macrophage “disappearance reaction” [ 46 ]. Infected tissue resident AMφs express higher levels of proinflammatory chemokines, which leads to an excessive monocyte recruitment through a positive feedback loop [ 46 ].…”

Section: Biological Mechanisms For In Situ Pulmonary Immunothrombosismentioning

confidence: 99%

“…In severe COVID-19, in the setting of inflammation, tissue resident AMφs in the bronchoalveolar space are diminished in number, a phenomenon described as the macrophage “disappearance reaction” [ 46 ]. Infected tissue resident AMφs express higher levels of proinflammatory chemokines, which leads to an excessive monocyte recruitment through a positive feedback loop [ 46 ]. Monocytes, in addition to their role against various pathogens, promote the activation of the extrinsic coagulation pathway during inflammatory states and could be considered a bridge from inflammation to thrombosis [ 47 ].…”

Section: Biological Mechanisms For In Situ Pulmonary Immunothrombosismentioning

confidence: 99%

“…Immune cells, such as macrophages, monocytes, MCs, T cells, DCs, NK cells, and neutrophils, “orchestrate” the crosstalk between proinflammatory and procoagulative networks [ 4 , 18 , 43 , 44 , 45 , 46 , 47 , 48 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 113 , 114 , 115 , 129 , 131 ].…”

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of COVID-19 Associated Pulmonary Thrombosis: A Narrative Review

2023

View full text Add to dashboard Cite

COVID-19, the infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is frequently associated with pulmonary thrombotic events, especially in hospitalized patients. Severe SARS-CoV-2 infection is characterized by a proinflammatory state and an associated disbalance in hemostasis. Immune pathology analysis supports the inflammatory nature of pulmonary arterial thrombi composed of white blood cells, especially neutrophils, CD3+ and CD20+ lymphocytes, fibrin, red blood cells, and platelets. Immune cells, cytokines, chemokines, and the complement system are key drivers of immunothrombosis, as they induce the damage of endothelial cells and initiate proinflammatory and procoagulant positive feedback loops. Neutrophil extracellular traps induced by COVID-19-associated “cytokine storm”, platelets, red blood cells, and coagulation pathways close the inflammation–endotheliopathy–thrombosis axis, contributing to SARS-CoV-2-associated pulmonary thrombotic events. The hypothesis of immunothrombosis is also supported by the minor role of venous thromboembolism with chest CT imaging data showing peripheral blood clots associated with inflammatory lesions and the high incidence of thrombotic events despite routine thromboprophylaxis. Understanding the complex mechanisms behind COVID-19-induced pulmonary thrombosis will lead to future combination therapies for hospitalized patients with severe disease that would target the crossroads of inflammatory and coagulation pathways.

show abstract

“…Macrophages play a role in the physiopathology of COVID-19 as shown by histological examination of tissue sample from patients with severe symptoms ( 11 , 12 ). The accumulation of macrophages in the alveolar lumen has been shown in a humanized mice model of SARS-CoV-2 expressing human angiotensin-converting enzyme 2 (ACE2) ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

Macrophages and γδ T cells interplay during SARS-CoV-2 variants infection

et al. 2022

View full text Add to dashboard Cite

IntroductionThe emergence of several SARS-CoV-2 variants during the COVID pandemic has revealed the impact of variant diversity on viral infectivity and host immune responses. While antibodies and CD8 T cells are essential to clear viral infection, the protective role of innate immunity including macrophages has been recognized. The aims of our study were to compare the infectivity of different SARS-CoV-2 variants in monocyte-derived macrophages (MDM) and to assess their activation profiles and the role of ACE2 (Angiotensin-converting enzyme 2), the main SARS-CoV-2 receptor. We also studied the ability of macrophages infected to affect other immune cells such as γδ2 T cells, another partner of innate immune response to viral infections.ResultsWe showed that the SARS-CoV-2 variants α-B.1.1.7 (United Kingdom), β-B.1.351 (South Africa), γ-P.1 (Brazil), δ-B.1.617 (India) and B.1.1.529 (Omicron), infected MDM without replication, the γ-Brazil variant exhibiting increased infectivity for MDM. No clear polarization profile of SARS-CoV-2 variants-infected MDM was observed. The β-B.1.351 (South Africa) variant induced macrophage activation while B.1.1.529 (Omicron) was rather inhibitory. We observed that SARS-CoV-2 variants modulated ACE2 expression in MDM. In particular, the β-B.1.351 (South Africa) variant induced a higher expression of ACE2, related to MDM activation. Finally, all variants were able to activate γδ2 cells among which γ-P.1 (Brazil) and β-B.1.351 (South Africa) variants were the most efficient.ConclusionOur data show that SARS-CoV-2 variants can infect MDM and modulate their activation, which was correlated with the ACE2 expression. They also affect γδ2 T cell activation. The macrophage response to SARS-CoV-2 variants was stereotypical.

show abstract

Pulmonary macrophages and SARS-Cov2 infection

Cited by 18 publications

References 113 publications

Post-COVID-19 Pulmonary Alveolar Proteinosis Treated Successfully with Whole Lung Lavage: A Rare Case Report

Post-COVID-19 Pulmonary Alveolar Proteinosis Treated Successfully with Whole Lung Lavage: A Rare Case Report

Mechanisms of COVID-19 Associated Pulmonary Thrombosis: A Narrative Review

Macrophages and γδ T cells interplay during SARS-CoV-2 variants infection

Contact Info

Product

Resources

About