LitCovid-sentences  

PMC:7463108 / 43487-47302 JSONTXT 10 Projects

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Id Subject Object Predicate Lexical cue
T664 0-135 Sentence denotes The direct contributions of astrocytes to opioid and HIV interactions have been discussed previously (Dutta and Roy 2012; Hauser et al.
T665 136-154 Sentence denotes 2012; Reddy et al.
T666 155-184 Sentence denotes 2012; Hauser and Knapp 2014).
T667 185-282 Sentence denotes Subsets of astroglia can express MOR, DOR and KOR (Stiene-Martin and Hauser 1991; Eriksson et al.
T668 283-303 Sentence denotes 1992; Ruzicka et al.
T669 304-324 Sentence denotes 1995; Gurwell et al.
T670 325-344 Sentence denotes 1996; Hauser et al.
T671 345-366 Sentence denotes 1996; Peterson et al.
T672 367-393 Sentence denotes 1998; Stiene-Martin et al.
T673 394-459 Sentence denotes 1998, 2001), as well as endogenous opioid peptides (Vilijn et al.
T674 460-480 Sentence denotes 1988; Shinoda et al.
T675 481-500 Sentence denotes 1989; Spruce et al.
T676 501-520 Sentence denotes 1990; Hauser et al.
T677 521-537 Sentence denotes 1990; Low et al.
T678 538-544 Sentence denotes 1992).
T679 545-728 Sentence denotes It appears that the ‘early’ events triggering the release of proinflammatory cytokines (i.e., TNF-α and IL-1β) from astroglia can be mediated by HIV Tat exposure alone (El-Hage et al.
T680 729-752 Sentence denotes 2005, 2006a, b, 2008a).
T681 753-1034 Sentence denotes Opioids enhance HIV-1-induced inflammation later during the inflammatory cascade by exacerbating the sustained release of CCL5 from astrocytes, which subsequently triggers the release of CCL2 thereby enhancing the recruitment and activation of macrophages/microglia (El-Hage et al.
T682 1035-1051 Sentence denotes 2008a) (Fig. 1).
T683 1052-1208 Sentence denotes This is caused by the morphine-dependent exacerbation of Tat-induced increases in intracellular calcium concentration ([Ca2+]i) in astroglia (El-Hage et al.
T684 1209-1372 Sentence denotes 2005), which accelerates the trafficking of NF-κB p65 (RelA) subunits to the nucleus and sustained CCL2, CCL5, and IL-6 transcription in astrocytes (El-Hage et al.
T685 1373-1380 Sentence denotes 2008b).
T686 1381-1584 Sentence denotes Fig. 1 Opioids exacerbate HIV-1-induced CNS inflammation, in part, by augmenting CCL5-dependent increases in CCL2—key sites of opioid-HIV convergent interactions in glial inflammatory signaling cascades.
T687 1585-1859 Sentence denotes Subpopulations of striatal glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes in wildtype mice normally express CCR2 immunoreactivity (a-b; arrows), CCL2 (c; arrow), or μ-opioid receptor (MOR) (d; arrows) immunoreactivity (scale bars a-b = 25 μm; c-d = 15 μm).
T688 1860-2140 Sentence denotes CCR2 deletion (−/−) significantly reduces HIV-1 Tat ± morphine-induced increases in GFAP+ astroglia (e) and F4/80+ macrophages/microglia (f) compared to wild type (+/+) mice at sites near (300 ± 100 μm) the site of Tat injection (*p < 0.05 vs. wild type mice) (see, El-Hage et al.
T689 2141-2148 Sentence denotes 2006a).
T690 2149-2697 Sentence denotes In wild-type mice, Tat ± morphine administration markedly increases the proportion of CCL2 immunoreactive astrocytes (g) or macrophages/microglia (h) [*p < 0.05 vs. other groups in wild-type or CCL5(−/−) mice; bp < 0.05 vs. vehicle- or Tat plus morphine-treated wild-type mice; #p < 0.05 vs. equivalent treatment in wild-type mice], while in CCL5 null mice, significant increases in CCL2 immunoreactivity were only seen in macrophages/microglia co-exposed to Tat and morphine (§p < 0.05 vs. vehicle injected CCL5 knockout mice) (see, El-Hage et al.
T691 2698-2705 Sentence denotes 2008a).
T692 2706-2878 Sentence denotes CCL5 expression in striatal GFAP-immunoreactive astrocytes (arrows) increases following Tat injections (i, j) compared to wild-type control mice (not shown) (El-Hage et al.
T693 2879-2886 Sentence denotes 2008a).
T694 2887-3139 Sentence denotes Opioids exacerbate HIV-1-induced CNS inflammation, in part, by increasing CCL5 and augmenting CCR5-dependent increases in CCL2 production by astrocytes resulting in the activation and recruitment of microglia/macrophages and spiraling inflammation (k).
T695 3140-3245 Sentence denotes Additional factors likely mediate the proinflammatory cascade, but these are less well substantiated (?).
T696 3246-3661 Sentence denotes Moreover, autocrine and reciprocal paracrine (astroglial ↔ macrophage/microglial) intercellular, feedback amplification mechanisms from macrophages/microglia are likely to be operative (dashed red arrow) (also see, Kang and Hebert 2011) and occur elsewhere within the cascade (not shown); effects of HIV-1 Tat/HIV, red arrows; sites of opioid convergence, blue arrows; pro-BDNF:mature BDNF (mBDNF) ratio (Kim et al.
T697 3662-3815 Sentence denotes 2018). (a-f) Modified and reprinted with permission from El-Hage et al. (2006a). (g-k) Modified and reprinted with permission from El-Hage et al. (2008a)