1.Regulation and mechanism of up-regulated lncRNA MALAT1 on macrophage inflammation in negative sputum for tuberculous bacterium
Limei HAN ; Shunping LIU ; Aierken AIKEDANMU ; Wurina AXIAN ; Jing GUAN ; Xin LI ; Tieliwaerdi NUERAMINA ; Yilihamu NIGELA ; Jingjing LI ; Wushouer QIMANGULI
Chinese Journal of Immunology 2025;41(3):589-594
Objective:To explore the expression and mechanism of lncRNA MALAT1 in negative sputum for tuberculous bac-terium.Methods:Expression of lncRNA MALAT1 in peripheral blood mononuclear cells(PBMC)of patients with positive sputum bacteria(Positive group)and negative sputum bacteria(Negative group)and healthy volunteers(HC group)was detected by RT-PCR.ELISA was used to detect expression levels of TNF-α,IL-1β and IL-6 in plasma.Expression of lncRNA MALAT1 in mice macro-phages RAW264.7 was silenced by siRNA interference,and RAW264.7 cells were infected with mycobacterium tuberculosis(MTB)H37Rv.Cells were divided into four groups:Control group,Control+MTB group,MTB+si-NC group and MTB+si-MALAT1 group.Proliferation activity of RAW264.7 cells in each group was detected by CCK-8 method.The number of MTB in each group was detected by CFU.Expressions of TNF-α,IL-1β and IL-6 in supernatant of RAW264.7 cells were detected by ELISA.Results:Compared with HC group,expressions of lncRNA MALAT1 in PBMC,and TNF-α,IL-1β and IL-6 in plasma were significantly increased in Positive group and Negative group(P<0.01).Compared with Control group,expression level of lncRNA MALAT1,proliferation activity,CFU value,and concentrations of TNF-α,IL-1β and IL-6 in supernatant of Control+MTB group,MTB+si-NC group and MTB+si-MALAT1 group were significantly increased(P<0.05).Compared with MTB+si-NC group,the above detection indexes in MTB+si-MALAT1 group were significantly decreased(P<0.05),while there was no significant difference in Control+MTB group(P>0.05).Conclusion:The significantly increased expression of MALAT1 in patients with negative sputum for tuberculous bacterium is positively correlated with expression of plasma inflammatory factors,while the silence of MALAT1 expression can reduce MTB induced inflammatory response by inhibiting the proliferation and phagocytosis of MTB infected macrophages.
2.Regulation and mechanism of up-regulated lncRNA MALAT1 on macrophage inflammation in negative sputum for tuberculous bacterium
Limei HAN ; Shunping LIU ; Aierken AIKEDANMU ; Wurina AXIAN ; Jing GUAN ; Xin LI ; Tieliwaerdi NUERAMINA ; Yilihamu NIGELA ; Jingjing LI ; Wushouer QIMANGULI
Chinese Journal of Immunology 2025;41(3):589-594
Objective:To explore the expression and mechanism of lncRNA MALAT1 in negative sputum for tuberculous bac-terium.Methods:Expression of lncRNA MALAT1 in peripheral blood mononuclear cells(PBMC)of patients with positive sputum bacteria(Positive group)and negative sputum bacteria(Negative group)and healthy volunteers(HC group)was detected by RT-PCR.ELISA was used to detect expression levels of TNF-α,IL-1β and IL-6 in plasma.Expression of lncRNA MALAT1 in mice macro-phages RAW264.7 was silenced by siRNA interference,and RAW264.7 cells were infected with mycobacterium tuberculosis(MTB)H37Rv.Cells were divided into four groups:Control group,Control+MTB group,MTB+si-NC group and MTB+si-MALAT1 group.Proliferation activity of RAW264.7 cells in each group was detected by CCK-8 method.The number of MTB in each group was detected by CFU.Expressions of TNF-α,IL-1β and IL-6 in supernatant of RAW264.7 cells were detected by ELISA.Results:Compared with HC group,expressions of lncRNA MALAT1 in PBMC,and TNF-α,IL-1β and IL-6 in plasma were significantly increased in Positive group and Negative group(P<0.01).Compared with Control group,expression level of lncRNA MALAT1,proliferation activity,CFU value,and concentrations of TNF-α,IL-1β and IL-6 in supernatant of Control+MTB group,MTB+si-NC group and MTB+si-MALAT1 group were significantly increased(P<0.05).Compared with MTB+si-NC group,the above detection indexes in MTB+si-MALAT1 group were significantly decreased(P<0.05),while there was no significant difference in Control+MTB group(P>0.05).Conclusion:The significantly increased expression of MALAT1 in patients with negative sputum for tuberculous bacterium is positively correlated with expression of plasma inflammatory factors,while the silence of MALAT1 expression can reduce MTB induced inflammatory response by inhibiting the proliferation and phagocytosis of MTB infected macrophages.
3.Association of copy number variation of exon 11 of IL-23 receptor gene with susceptibility to tuberculosis among Chinese Uygurs.
Daobin JIANG ; Xin HU ; Shuang LI ; AbuduJilili JULAITI ; Yu XIA ; Jing WANG ; Wenbao ZHANG ; Qimanguli WUSHOUER
Chinese Journal of Medical Genetics 2016;33(1):97-100
OBJECTIVETo assess the association of copy number variations (CNVs) of exon 11 of IL-23 receptor gene with susceptibility to active pulmonary tuberculosis among Chinese Uygurs.
METHODSIn this study, 250 subjects with active pulmonary tuberculosis (PTB) and 250 normal controls were recruited. A paired case-control study was conducted in the Chinese Uygur population in Xinjiang and the CNV of IL-23R was analyzed using Taqman real-time PCR.
RESULTSThe study showed that the frequencies of different copy number in exon 11 of IL-23R between PTB and control groups were statistically significant (χ(2)=13.35, P<0.01). There were significant difference in CNV of exon 11 in IL-23R between PTB patients and controls (χ(2)=14.95, P<0.01, OR=2.875, 95%CI: 1.655-4.994). The increase of copy number in exon 11 of IL-23R showed significantly different between PTB and control groups (χ(2)=10.475, P=0.0012, OR=2.611, 95%CI: 1.437-4.744).
CONCLUSIONThe CNV of exon 11 in IL-23R is associated with PTB in the Chinese Uygur population. The increase of the copy number in exon 11 of IL-23R may be a risk factor for PTB in Chinese Uygurs.
Adult ; Aged ; Asian Continental Ancestry Group ; ethnology ; genetics ; Case-Control Studies ; China ; ethnology ; DNA Copy Number Variations ; Exons ; Female ; Genetic Predisposition to Disease ; ethnology ; Humans ; Male ; Middle Aged ; Receptors, Interleukin ; genetics ; Tuberculosis, Pulmonary ; ethnology ; genetics ; Young Adult

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