LitCovid-sentences  

PMC:7456455 / 8914-14147 JSONTXT 13 Projects

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Id Subject Object Predicate Lexical cue
T56 0-31 Sentence denotes 3.2 Co-morbidities and the mps
T57 32-207 Sentence denotes Macrophage activities contribute to many co- morbidities [8,9], including aging [28], obesity [29], diabetes [30], exposure to pollutants [31], and microbiome properties [32].
T58 208-348 Sentence denotes Macrophage functions alter with age, together with adaptive immune processes such as thymic involution, which deplete T lymphocyte reserves.
T59 349-444 Sentence denotes Chronic, low grade inflammation (INFLAMMAGING) has been proposed as a predisposing factor [33].
T60 445-665 Sentence denotes This may result from failure of macrophages and NK cells to clear increasing accumulation of senescent cells, that enhance basal levels of inflammation and interfere with subsequent adaptive immunity upon infection [28].
T61 666-836 Sentence denotes Baseline inflammation may not be detrimental in itself, but can initiate an inflammatory cascade that amplifies excessive inflammation occurring in response to pathogens.
T62 837-1029 Sentence denotes Age-related metabolic correlates of macrophage dysfunction include innate lymphoid cell interactions with adipose tissue and associated macrophages, as well as inflammasome activation [34,35].
T63 1030-1231 Sentence denotes This affects thermogenesis, part of a wider metabolic syndrome involving glucose and lipid metabolism [36], elevated body mass index (BMI), type 1 and type 2 diabetes, obesity and atherosclerosis [37].
T64 1232-1383 Sentence denotes These correlate with macrophage metabolic and mitochondrial activities [38] and, possibly, ACE2 expression and hypertension, another co-morbidity [37].
T65 1384-1632 Sentence denotes ACE2, the COVID-19 entry receptor, is widely expressed on microvascular endothelium and binds the SARS-CoV2 spike glycoprotein implicated in angiotensin regulation by its competition with ACE1, and potential role as an anti-inflammatory agent [39].
T66 1633-1861 Sentence denotes Macrophages in tuberculosis and sarcoidosis express ACE1 [40], but expression of ACE2 by monocytes and tissue macrophages has not been validated [41]; evidence for productive infection of macrophages via ACE2 is incomplete [15].
T67 1862-2247 Sentence denotes Macrophages express scavenger receptors including Axl and MERTK, tyrosine kinase receptors implicated in phosphatidyl serine recognition and phagocytosis of apoptotic cells [21]; Axl is a coreceptor for ACE2+ dependent infection of other cell types by COVID-19 and other enveloped viruses via surface or endocytic routes [42], the basis for a clinical trial involving an Axl inhibitor.
T68 2248-2417 Sentence denotes Alveolar macrophages [43] are close to Type 1 pneumocytes, involved in gas exchange, Type 2 surfactant-producing pneumocytes, and capillary endothelium, all ACE 2+ [43].
T69 2418-2690 Sentence denotes They take up and store atmospheric pollutants and poorly-degradable pro-inflammatory particles; host DNA from dying cells can induce the innate STING pathway after uptake and also activate inflammasomes in lung macrophages after exposure to ozone and cigarette smoke [31].
T70 2691-2891 Sentence denotes Other airway predisposing conditions involving macrophages [8,9], include genetic disorders such as fibrocystic disease and structural abnormalities associated with chronic inflammation and infection.
T71 2892-3072 Sentence denotes Chronic infections in which TH1-activated macrophages play a major role, tuberculosis and AIDS, enhance the risk of severe infection, with odds ratios of 1.7 and 2.3– respectively.
T72 3073-3195 Sentence denotes TH2-dependent asthma may not enhance COVID-19 susceptibility, possibly correlated with low levels of ACE2 expression [44].
T73 3196-3298 Sentence denotes IL-13 also reduces ACE2 expression, suggesting that M2-macrophages may contribute to viral resistance.
T74 3299-3420 Sentence denotes BCG and other immunisations may transiently promote non-specific resistance to SARS-CoV2 [45], to be confirmed in trials.
T75 3421-3623 Sentence denotes Mononuclear phagocytes are implicated in selected genetic [46] or acquired systemic immunodeficiency, immunosuppression and autoimmunity, including chronic renal disease requiring organ transplantation.
T76 3624-3796 Sentence denotes Tumor associated macrophages (TAM) and Myeloid derived suppressor cells (MDSC) promote malignancy and metastasis, and with chemo-and radiotherapy may enhance COVID-19 risk.
T77 3797-3927 Sentence denotes Microglia contribute to neurodegeneration through interaction with neurons in Alzheimer disease, a comorbidity independent of age.
T78 3928-4236 Sentence denotes Comorbidities are likely to be multifactorial, and not all display an obvious macrophage link; for example, the ACE2 locus on the X chromosome [47] may contribute to the decreased risk of females [48], but genetic and environmental factors underlying gender, racial and individual disparities remain unclear.
T79 4237-4496 Sentence denotes Therapeutics for many comorbidities impact on macrophage inflammatory and metabolic functions, including statins, sugar stabilizers, anti-hypertensives and anti-inflammatory agents; control of diabetes and obesity are important in preventing severe infection.
T80 4497-4708 Sentence denotes Glucocorticoids, which have potent anti-inflammatory effects on macrophages, are contra-indicated in early infection, while protecting against severe disease; timing of administration is therefore critical [49].
T81 4709-4851 Sentence denotes The use of anti-TNF antibody in treatment of rheumatoid arthritis, protects against subsequent severe COVID-19 requiring hospitalization [50].
T82 4852-4988 Sentence denotes In conclusion, the present evidence for a common macrophage contribution to a range of comorbidities is correlative, rather than causal.
T83 4989-5073 Sentence denotes Nor is it clear whether they increase the risk as well as the severity of infection.
T84 5074-5233 Sentence denotes Macrophages are central to inflammation, immunity and metabolic diseases, but further genetic and cellular studies are needed to provide a unifying hypothesis.