| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T37 |
0-227 |
Sentence |
denotes |
A second possibility involves the collateral effects of recognition pathways required for the activation of antiviral immunity that may, paradoxically, contribute to an inflammatory environment that favors secondary infections. |
| T38 |
228-402 |
Sentence |
denotes |
ACE2 is not well expressed on immune cells and SARS-CoV are recognized by TLR4 and TLR3, leading to the activation of MyD88- or TRIF-mediated signaling, respectively [20,21]. |
| T39 |
403-543 |
Sentence |
denotes |
Of note, this may be potentiated in the presence of Aspergillus spp. which activate TLR4/MyD88/TRIF through the cleavage of fibrinogen [22]. |
| T40 |
544-684 |
Sentence |
denotes |
It is likely that SARS-CoV-2 may elicit, to a large extent, overlapping signaling pathways towards the production of inflammatory cytokines. |
| T41 |
685-860 |
Sentence |
denotes |
In addition, the activation of the inflammasome by SARS-CoV and the consequent production of IL-1β is an event that contributes further to the hyperinflammatory response [23]. |
| T42 |
861-1044 |
Sentence |
denotes |
A transcriptome analysis of COVID-19 patients revealed an early immune response characterized by a marked upregulation of the IL-1 pathway, even after respiratory function nadir [24]. |
| T43 |
1045-1331 |
Sentence |
denotes |
The possibility that IL-1 and related pro-inflammatory pathways could serve as therapeutic targets was demonstrated by the favorable responses in severe COVID-19 patients with secondary hemophagocytic lymphohistiocytosis treated with the interleukin-1 receptor antagonist anakinra [25]. |
| T44 |
1332-1415 |
Sentence |
denotes |
Similar findings were also disclosed in acute leukemia patients with COVID-19 [26]. |
| T45 |
1416-1661 |
Sentence |
denotes |
Likewise, IL-1 blockade with anakinra has also been found to ameliorate inflammation in both chronic granulomatous disease [27] and cystic fibrosis [28], and in either case, to restrain susceptibility to infection or colonization by Aspergillus. |
| T46 |
1662-1867 |
Sentence |
denotes |
Therefore, the early hyperactivation of the IL-1 pathway induced by the SARS-CoV-2 infection may be a major factor establishing a highly permissive inflammatory environment that favors fungal pathogenesis. |
