Clinical symptoms and immune injury reflected by low CD4/CD8 ratio should increase the suspicion of HIV coinfection with tuberculosis.

Background: Patients who are coinfected with human immunodeficiency virus 1 (HIV) and Mycobacterium tuberculosis (TB) benefit from timely diagnosis and treatment. In the present study frequencies of CD3+, CD4+, and CD8+ T cells among peripheral blood mononuclear cells (PBMCs) of patients in the Kashi region of China infected with HIV, TB, and both HIV and TB (HIV-TB) were investigated to provide a basis for rapid identification of coinfected patients. Methods: A total of 62 patients with HIV, TB, or HIV-TB who were first hospitalized at our institution were included in the study, as were 30 controls. PBMCs were isolated, and the frequencies of CD3+, CD4+, and CD8+ T cells were determined via flow cytometry. Results: The frequency of CD4+ T cells and the CD4/CD8 ratio were significantly lower in the HIV-TB group than in the other three groups. In fever patients the frequency of CD4+ T cells and the CD4/CD8 ratio were significantly lower in the HIV-TB group than in the HIV group and the TB group. In patients who exhibited rapid weight loss there were no significant differences in the frequency of CD4+ T cells or the CD4/CD8 ratio between the groups. The results of treatment were compared in the HIV, TB, and HIV-TB groups after 7 days, and there were obvious improvements in the frequency of CD4+ T cells and the CD4/CD8 ratio. Conclusion: Clinical symptoms and the degree of immune injury can heighten suspicion for HIV-TB coinfection.

Protective effect of astaxanthin on tuberculosis-associated inflammatory lung injury.

Mycobacterium tuberculosis (MTB) invades the lungs and is the key cause of tuberculosis (TB). MTB induces immune overreaction and inflammatory damage to lung tissue. There is a lack of protective drugs against pulmonary inflammatory damage. Herein, the protective roles and mechanisms of Astaxanthin (ASTA), a natural compound, in inflammatory injured lung epithelial cells were investigated. Lipopolysaccharide (LPS) was used to establish inflammatory injury model in the murine lung epithelial (MLE)-12 cells. Cell counting kit-8 was used for screening of compound concentrations. Cell proliferation was observed real-time with a high content analysis system. Flow cytometry assessed apoptosis. The changes of apoptotic proteins and key proteins in nuclear factor kappa-B (NF-κB) pathway were measured with the western blot. LPS was used to establish an animal model of pulmonary injury. The pathological changes and degree of inflammatory injury in lung tissue were observed with hematoxylin and eosin (HE) staining. The levels of inflammatory mediators were detected with enzyme-linked immunosorbent assay. The results showed that ASTA reduced lung inflammation and attenuated inflammatory damage in lung tissues. ASTA reduced apoptosis stimulated by LPS through suppressing the NF-κB pathway in MLE-12 cells. We believe that ASTA may have great potential for protection against inflammatory damage to lung tissue.

Astaxanthin Prevents Tuberculosis-Associated Inflammatory Injury by Inhibiting the Caspase 4/11-Gasdermin-Pyroptosis Pathway.

Pyroptosis is a programmed cell death caused by inflammation. Multiple studies have suggested that Mycobacterium tuberculosis infection causes tissue pyroptosis. However, there are currently no protective drugs against the inflammatory damage caused by pyroptosis. In this study, anti-pyroptotic effects of the natural compound astaxanthin (ASTA) were explored in a simulated pulmonary tuberculosis-associated inflammatory environment. The results showed that ASTA maintained the stability of MLE-12 lung epithelial cell numbers in the inflammatory environment established by lipopolysaccharide. The reason is not to promote cell proliferation but to inhibit lipopolysaccharide-induced pyroptosis. The results showed that ASTA significantly inhibited the expression of key proteins in the caspase 4/11-gasdermin D pathway and the release of pyroptosis-related inflammatory mediators. Therefore, ASTA inhibits inflammation-induced pyroptosis by inhibiting the caspase 4/11-gasdermin D pathway and has the potential to protect lung tissue from tuberculosis-related inflammatory injury. ASTA, a functional food component, is a promising candidate for protection against tuberculosis-associated inflammatory lung injury.

Decabromodiphenyl ether causes insulin resistance and glucose and lipid metabolism disorders in mice.

BACKGROUND: Decabromodiphenyl ether (BDE-209) is the most commonly used brominated flame retardant. Recently, BDE-209 has been suspected of being an environmental risk factor for metabolic diseases such as obesity, insulin resistance (IR), type 2 diabetes mellitus, and hypertension. AIM: To investigate the effects of BDE-209 on IR and glucose and lipid metabolism in C57BL/6 mice. METHODS: Adult male C57BL/6 mice were randomly divided into high, medium-high, medium, medium-low, and low dose BDE-209 groups, and a control group (n = 6 per group), which received 1000, 800, 600, 450, 300, and 0 mg/kg BDE-209, respectively. After BDE-209 exposure for 60 d, the mice were fasted overnight, and then sacrificed to obtain tissues. An automatic biochemical analyzer was used to detect serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C); enzyme-linked immunosorbent assay kits were used to detect fasting serum insulin (FINS), leptin (LEP), and adiponectin (Adp) levels; a blood glucose meter was used to detect fasting blood glucose (FBG). Morphological changes of the liver were observed by hematoxylin and eosin staining. Real-time quantitative polymerase chain reaction and Western blot were used to determine the messenger ribonucleic acid (mRNA) and protein levels, respectively, of LEP, Adp, and peroxisome proliferators activated receptor-γ (PPARγ) in mouse liver and adipose tissues. RESULTS: There was a statistically significant difference in the weight of mice in each group after 45 and 60 d of exposure (P < 0.05). After 60 d of exposure, the weight of liver and adipose tissues in the exposure groups were greater than that of the control group (P < 0.05). The liver tissue structure was disordered and the liver tissues were accompanied by local inflammatory cell infiltration in the high, medium-high, and medium dose BDE-209 groups. The levels of FINS, insulin sensitivity index, Adp, and HDL-C were decreased in the BDE-209 group compared with the control group, as were the mRNA and protein levels of Adp in liver and adipose tissues (P < 0.05). Serum level of FBG and LEP were higher in the BDE-209 group than in controls. TC, TG, and LDL-C levels as well as the mRNA and protein expression of LEP and PPARγ in liver and adipose tissues were higher than those in the control group (P < 0.05). Homeostatic assessment model of IR was higher in the medium and medium-low dose BDE-209 groups (P < 0.05). CONCLUSION: BDE-209 increases the body weight, fat and liver tissue weight, TC, TG, and LDL-C, reduces HDL-C, and causes IR in mice, which may be related to activating the PPARγ receptor.

[Effects of decabromodiphenyl ether on glucose and lipid metabolism and adipocyte factors in C57BL/6 mice].

OBJECTIVE: To investigate the effect of decabromodiphenyl ether(BDE-209) on glucose and lipid metabolism and adipocytokines in mice. METHODS: A total of 36 adult male C57 BL/6 mice were randomly divided into 6 groups, 1000, 800, 600, 450 and 300 mg/kg groups and the control group, with 6 in each group. 60 days after gavage, fasting overnight, the mice were killed and the corresponding test materials were taken. Using an automatic biochemical analyzer to detect triglycerides(TG), total cholesterol(cholesterol, TC), low-density lipoprotein(LDL-C), and high-density lipoprotein(HDL-C). Detected rat fasting blood glucose(FBG) with Roche blood glucose meter. Observed the morphological changes of mouse liver tissue using HE staining. Determined leptin(LEP), the mRNA and protein expression levels of adiponectin(ADP) and peroxisome proliferators-activated receptors(PPAR)-γ with Real-time fluorescent quantitative PCR and Western blotting. RESULTS: The levels of fasting serum lisulin(FINS), insulin sensitivity index(ISI), ADP and HDL-C in the serum of the BDE-209 exposure group decreased(P& lt; 0. 05). The levels of FBG, LEP, TC, TG and LDL-C in the serum of the BDE-209 exposure group increased(P& lt; 0. 05). mRNA and protein expression levels of LEP and PPAR-γ in the liver increased(P& lt; 0. 05), and ADP mRNA and protein expression levels decreased(P& lt; 0. 05). Adipocyte factor LEP was positively correlated with the content of FBG, TG, TC and LDL-C, with r values of 0. 775, 0. 767, 0. 716 and 0. 812(P& lt; 0. 05), and negatively correlated with FINS and HDL-C, with r values of-0. 919 and-0. 817(P& lt; 0. 05). ADP was positively correlated with FINS and HDL-C, with r values of 0. 824 and 0. 832(P& lt; 0. 05), and negatively correlated with FBG, TG, TC and LDL-C, with r values of-0. 883, -0. 686, -0. 704 and-0. 772, respectively(P& lt; 0. 05). BDE-209 exposure to each dose group could change the morphology of mouse liver tissue to a certain extent. CONCLUSION: Decabromodiphenyl ether can disturb the metabolism of glucose and lipids. Among them, the disorder in the high and high dose groups of BDE-209 is more obvious. The low dose of BDE-209 can also change the morphology of liver tissue.