scholarly journals Capillasterin A, a Novel Pyrano[2,3-f]chromene from the Australian Crinoid Capillaster multiradiatus

Marine Drugs ◽  
2019 ◽  
Vol 17 (1) ◽  
pp. 26 ◽  
Author(s):  
Kah Yean Lum ◽  
Anthony R. Carroll ◽  
Merrick G. Ekins ◽  
Silven Read ◽  
Zahra Haq ◽  
...  

Capillasterin A (1), a novel pyrano[2,3-f]chromene, together with seven known naphthopyrones including comaparvin (2), TMC-256C1 (3), 6-methoxycomaparvin-5- methyl ether (4), 5,8-dihydroxy-6-methoxy-2-propyl-4H-naphtho[2,3-b]pyran-4-one (5), 5,8-dihydroxy-6,10-dimethoxy-2-propyl-4H-naphtho[2,3-b]pyran-4-one (6), TMC-256A1 (7) and 6-methoxycomaparvin (8) were isolated from an EtOH/H2O extract from the Australian crinoid Capillaster multiradiatus. The structures of all the compounds were determined by detailed spectroscopic (1D/2D NMR and MS) data analysis. This is the first report of a natural product that contains the pyrano[2,3-f]chromene skeleton. Compounds 2–6 were observed to display moderate inhibition of in vitro HIV-1 replication in a T cell line with EC50 values ranging from 7.5 to 25.5 µM without concomitant cytotoxicity.

2016 ◽  
Vol 11 (12) ◽  
pp. 1934578X1601101
Author(s):  
Wasana Prapalert ◽  
Dammrong Santiarworn ◽  
Saisunee Liawruangrath ◽  
Boonsom Liawruangrath ◽  
Stephen G. Pyne

Two carotenoids, lutein (1) and lutein 3′-methyl ether (2), have been isolated from the EtOAc fraction of the MeOH extract of Peristrophe lanceolaria, growing in Thailand. The structures of these compounds were elucidated from their 1D and 2D NMR spectroscopic data and from comparisons made with the literature data. This is the first report of the isolation of lutein-3′-methyl ether as a natural product.


1998 ◽  
Vol 187 (9) ◽  
pp. 1439-1449 ◽  
Author(s):  
Shinichiro Sawada ◽  
Kavitha Gowrishankar ◽  
Rui Kitamura ◽  
Misao Suzuki ◽  
Gen Suzuki ◽  
...  

T cell line–tropic (T-tropic) HIV type 1 strains enter cells by interacting with the cell-surface molecules CD4 and CXCR4. We have generated transgenic mice predominantly expressing human CD4 and CXCR4 on their CD4-positive T lymphocytes (CD4+ T cells). Their primary thymocytes are susceptible to T-tropic but not to macrophage-tropic HIV-1 infection in vitro, albeit with a viral antigen production less efficient than human peripheral blood mononuclear cells. Interestingly, even without HIV infection, transgenic mice display a CD4+ T cell depletion profile of peripheral blood reminiscent of that seen in AIDS patients. We demonstrate that CD4+ T cell trafficking in transgenic mice is biased toward bone marrow essentially due to CXCR4 overexpression, resulting in the severe loss of CD4+ T cells from circulating blood. Our data suggest that CXCR4 plays an important role in lymphocyte trafficking through tissues, especially between peripheral blood and bone marrow, participating in the regulation of lymphocyte homeostasis in these compartments. Based on these findings, we propose a hypothetical model in which the dual function of CXCR4 in HIV-1 infection and in lymphocyte trafficking may cooperatively induce progressive HIV-1 infection and CD4+ T cell decline in patients.


Author(s):  
Elahe Akbari ◽  
Kimia Kardani ◽  
Ali Namvar ◽  
Soheila Ajdary ◽  
Esmat Mirabzadeh Ardakani ◽  
...  

2014 ◽  
Vol 38 (5) ◽  
pp. 608-612 ◽  
Author(s):  
Dai Chihara ◽  
Yoshitoyo Kagami ◽  
Harumi Kato ◽  
Noriaki Yoshida ◽  
Tohru Kiyono ◽  
...  

Viruses ◽  
2017 ◽  
Vol 9 (5) ◽  
pp. 105 ◽  
Author(s):  
Jiwei Ding ◽  
Jianyuan Zhao ◽  
Zhijun Yang ◽  
Ling Ma ◽  
Zeyun Mi ◽  
...  

2003 ◽  
Vol 77 (1) ◽  
pp. 291-300 ◽  
Author(s):  
L. Musey ◽  
Y. Ding ◽  
J. Cao ◽  
J. Lee ◽  
C. Galloway ◽  
...  

ABSTRACT Induction of adaptive immunity to human immunodeficiency virus type 1 (HIV-1) at the mucosal site of transmission is poorly understood but crucial in devising strategies to control and prevent infection. To gain further understanding of HIV-1-specific T-cell mucosal immunity, we established HIV-1-specific CD8+ cytotoxic T-lymphocyte (CTL) cell lines and clones from the blood, cervix, rectum, and semen of 12 HIV-1-infected individuals and compared their specificities, cytolytic function, and T-cell receptor (TCR) clonotypes. Blood and mucosal CD8+ CTL had common HIV-1 epitope specificities and major histocompatibility complex restriction patterns. Moreover, both systemic and mucosal CTL lysed targets with similar efficiency, primarily through the perforin-dependent pathway in in vitro studies. Sequence analysis of the TCRβ VDJ region revealed in some cases identical HIV-1-specific CTL clones in different compartments in the same HIV-1-infected individual. These results clearly establish that a subset of blood and mucosal HIV-1-specific CTL can have a common origin and can traffic between anatomically distinct compartments. Thus, these effectors can provide immune surveillance at the mucosa, where rapid responses are needed to contain HIV-1 infection.


1991 ◽  
Vol 173 (3) ◽  
pp. 589-597 ◽  
Author(s):  
G Poli ◽  
A L Kinter ◽  
J S Justement ◽  
P Bressler ◽  
J H Kehrl ◽  
...  

The pleiotropic immunoregulatory cytokine transforming growth factor beta (TGF-beta) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-beta significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-beta suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-beta did not significantly affect the expression of HIV induced by tumor necrosis factor alpha (TNF-alpha). These suppressive effects were not mediated via the induction of interferon alpha (IFN-alpha). TGF-beta also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-beta were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-beta may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals.


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