Редактирование: CXCL11

C-X-C motif chemokine 11 precursor (Beta-R1) (H174) (Interferon gamma-inducible protein 9) (IP-9) (Interferon-inducible T-cell alpha chemoattractant) (I-TAC) (Small-inducible cytokine B11) [ITAC] [SCYB11] [SCYB9B]

==Publications==

{{medline-entry
|title=Endothelial cells under therapy-induced senescence secrete [[CXCL11]], which increases aggressiveness of breast cancer cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659248
|abstract=The effects of senescence associated secretory phenotype (SASP) from therapy-induced senescent endothelial cells on tumor microenvironment (TME) remains to be clarified. Here, we investigated effects of ionizing radiation (IR)- and doxorubicin-induced senescent HUVEC on TME. MDA-[[MB]]-231 cancer cells treated with conditioned medium (CM) from senescent HUVEC or co-cultured with senescent HUVEC significantly increased cancer cell proliferation, migration, and invasion. We found that [[CXCL11]] plays a principal role in the senescent CM-induced aggressive activities of MDA-[[MB]]-231 cells. When we treated HUVEC with a neutralizing anti-[[CXCL11]] antibody or [[CXCL11]] SiRNA, or treated MDA-[[MB]]-231 cells with [[CXCR3]] SiRNA, we observed synergistic diminution of the ability of the HUVEC SASP to alter the migration and spheroid invasion of cancer cells. ERK activation was involved in the HUVEC SASP-induced aggressive activity of MDA-[[MB]]-231 cells. Finally, we observed the in vivo effect of [[CXCL11]] from the senescent HUVEC in tumor-bearing mice. Together, our results demonstrate that SASP from endothelial cells experiencing therapy-induced senescence promotes the aggressive behavior of cancer cells, and that [[CXCL11]] can potentially be targeted to prevent the adverse effects of therapy-induced senescent endothelial cells on the tumor microenvironment.

|keywords=* CXCL11
* Endothelial cells
* Therapy-induced senescence
* Tumor microenvironment
|full-text-url=https://sci-hub.do/10.1016/j.canlet.2020.06.019
}}
{{medline-entry
|title=Prebiotic supplementation in frail older people affects specific gut microbiota taxa but not global diversity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30867067
|abstract=There are complex interactions between aging, frailty, diet, and the gut microbiota; modulation of the gut microbiota by diet could lead to healthier aging. The purpose of this study was to test the effect of diets differing in sugar, fat, and fiber content upon the gut microbiota of mice humanized with microbiota from healthy or frail older people. We also performed a 6-month dietary fiber supplementation in three human cohorts representing three distinct life-stages. Mice were colonized with human microbiota and then underwent an 8-week dietary intervention with either a high-fiber/low-fat diet typical of elderly community dwellers or a low-fiber/high-fat diet typical of long-stay residential care subjects. A cross-over design was used where the diets were switched after 4 weeks to the other diet type to identify responsive taxa and innate immunity changes. In the human intervention, the subjects supplemented their normal diet with a mix of five prebiotics (wheat dextrin, resistant starch, polydextrose, soluble corn fiber, and galactooligo-saccharide) at 10 g/day combined total, for healthy subjects and 20 g/day for frail subjects, or placebo (10 g/day maltodextrin) for 26 weeks. The gut microbiota was profiled and immune responses were assayed by T cell markers in mice, and serum cytokines in humans. Humanized mice maintained gut microbiota types reflecting the respective healthy or frail human donor. Changes in abundance of specific taxa occurred with the diet switch. In mice with the community type microbiota, the observed differences reflected compositions previously associated with higher frailty. The dominance of Prevotella present initially in community inoculated mice was replaced by Bacteroides, Alistipes, and Oscillibacter. Frail type microbiota showed a differential effect on innate immune markers in both conventional and germ-free mice, but a moderate number of taxonomic changes occurring upon diet switch with an increase in abundance of Parabacteroides, Blautia, Clostridium cluster IV, and Phascolarctobacterium. In the human intervention, prebiotic supplementation did not drive any global changes in alpha- or beta-diversity, but the abundance of certain bacterial taxa, particularly Ruminococcaceae (Clostridium cluster IV), Parabacteroides, Phascolarctobacterium, increased, and levels of the chemokine [[CXCL11]] were significantly lower in the frail elderly group, but increased during the wash-out period. Switching to a nutritionally poorer diet has a profound effect on the microbiota in mouse models, with changes in the gut microbiota from healthy donors reflecting previously observed differences between elderly frail and non-frail individuals. However, the frailty-associated gut microbiota did not reciprocally switch to a younger healthy-subject like state, and supplementation with prebiotics was associated with fewer detected effects in humans than diet adjustment in animal models.
|mesh-terms=* Adult
* Aged
* Aging
* Animals
* Bacteria
* Biodiversity
* Chemokine CXCL11
* Cross-Over Studies
* Feces
* Female
* Frail Elderly
* Gastrointestinal Tract
* Germ-Free Life
* Humans
* Immunity, Innate
* Male
* Mice
* Microbiota
* Middle Aged
* Models, Animal
* Prebiotics
* Treatment Outcome
* Up-Regulation
* Young Adult
|keywords=* Aging
* Elderly
* Gut microbiota
* Innate immune response
* Microbiome
* Prebiotics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417215
}}
{{medline-entry
|title=[Signal molecules of endometrium: gerontological and general pathhological aspects].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28509480
|abstract=The review describes neuro-immuno-endocrine signal molecules expression in human endometrial cells in the normal conditions, in the pathology and during aging. Human endometrial cells synthesizes estrogen, progesterone, estradiol, progestin, cell adhesion molecules (integrines α1β1, α4β1, αVβ3, L-selectin, Е-catgerin, MUC1), grow factors (TGF, [[EGF]], HB-[[EGF]], IGF), cytokines (IL-1, IL-2, INF-α, IL-12, СХСL10, [[CXCL11]], CXCR3), various immune cells markers (CD68, CD105, [[CD163]], CD16, CD56, [[CD4]], CD8), heat shock proteins (HSP60, HSP70, HSP90, V[[EGF]], MMP). Changes of this molecules expression level are the base of the social significant diseases as endometriosis, endometrial cancer and infertility. Thus, the investigation of neuro-immuno-endocrine interactions in endometrial cells can be used for new drugs creating, in differential diagnostics of endometrial cancer and increasing of extracorporal fertilization success.
|mesh-terms=* Aging
* Biological Factors
* Cellular Senescence
* Cytokines
* Endometrium
* Female
* Heat-Shock Proteins
* Hormones
* Humans
* Signal Transduction
|keywords=* aging
* endometrium
* neuro-immuno-endocrine interactions
* pathology
* signal molecules

}}