Mycoplasma genitalium infection in the female reproductive system: Diseases and treatment.

Mycoplasma genitalium is a newly emerged sexually transmitted disease pathogen and an independent risk factor for female cervicitis and pelvic inflammatory disease. The clinical symptoms caused by M. genitalium infection are mild and easily ignored. If left untreated, M. genitalium can grow along the reproductive tract and cause salpingitis, leading to infertility and ectopic pregnancy. Additionally, M. genitalium infection in late pregnancy can increase the incidence of preterm birth. M. genitalium infections are often accompanied by co-infection with other sexually transmitted pathogens (Chlamydia trachomatis, Neisseria gonorrhoeae, and Trichomonas vaginalis) and viral infections (Human Papilloma Virus and Human Immunodeficiency Virus). A recent study suggested that M. genitalium plays a role in tumor development in the female reproductive system. However, few studies endorsed this finding. In recent years, M. genitalium has evolved into a new "superbug" due to the emergence of macrolide-and fluoroquinolone-resistant strains leading to frequent therapy failures. This review summarizes the pathogenic characteristics of M. genitalium and the female reproductive diseases caused by M. genitalium (cervicitis, pelvic inflammatory disease, ectopic pregnancy, infertility, premature birth, co-infection, reproductive tumors, etc.), as well as its potential relationship with reproductive tumors and clinical treatment.

Pushing the envelope: Immune mechanism and application landscape of macrophage-activating lipopeptide-2.

Mycoplasma fermentans can cause respiratory diseases, arthritis, genitourinary tract infections, and chronic fatigue syndrome and have been linked to the development of the human immunodeficiency virus. Because mycoplasma lacks a cell wall, its outer membrane lipoproteins are one of the main factors that induce inflammation in the organism and contribute to disease development. Macrophage-activating lipopeptide-2 (MALP-2) modulates the inflammatory response of monocytes/macrophages in a bidirectional fashion, indirectly enhances the cytotoxicity of NK cells, promotes oxidative bursts in neutrophils, upregulates surface markers on lymphocytes, enhances antigen presentation on dendritic cells and induces immune inflammatory responses in sebocytes and mesenchymal cells. MALP-2 is a promising vaccine adjuvant for this application. It also promotes vascular healing and regeneration, accelerates wound and bone healing, suppresses tumors and metastasis, and reduces lung infections and inflammation. MALP-2 has a simple structure, is easy to synthesize, and has promising prospects for clinical application. Therefore, this paper reviews the mechanisms of MALP-2 activation in immune cells, focusing on the application of MALP-2 in animals/humans to provide a basis for the study of pathogenesis in Mycoplasma fermentans and the translation of MALP-2 into clinical applications.

Community-Acquired Respiratory Distress Syndrome Toxin: Unique Exotoxin for M. pneumoniae.

Mycoplasma pneumoniae infection often causes respiratory diseases in humans, particularly in children and adults with atypical pneumonia and community-acquired pneumonia (CAP), and is often exacerbated by co-infection with other lung diseases, such as asthma, bronchitis, and chronic obstructive pulmonary disorder. Community-acquired respiratory distress syndrome toxin (CARDS TX) is the only exotoxin produced by M. pneumoniae and has been extensively studied for its ADP-ribosyltransferase (ADPRT) activity and cellular vacuolization properties. Additionally, CARDS TX induces inflammatory responses, resulting in cell swelling, nuclear lysis, mucus proliferation, and cell vacuolization. CARDS TX enters host cells by binding to the host receptor and is then reverse transported to the endoplasmic reticulum to exert its pathogenic effects. In this review, we focus on the structural characteristics, functional activity, distribution and receptors, mechanism of cell entry, and inflammatory response of CARDS TX was examined. Overall, the findings of this review provide a theoretical basis for further investigation of the mechanism of M. pneumoniae infection and the development of clinical diagnosis and vaccines.

Correlation and Diagnostic Value of Serum Cys-C, RBP4, and NGAL with the Condition of Patients with Traumatic Acute Kidney Injury.

There is a lack of targeted biomarkers that can diagnose Acute Kidney Injury (AKI) early and accurately, which leads to deterioration of renal function and even death in patients who do not receive timely and effective treatment. In recent years, an increasing number of studies have shown that AKI-related markers such as cystatin C (Cys-C) and retinol-binding protein (RBP) can be used for early diagnosis of AKI to a certain extent. A total of 262 subjects were included in this study, of which 132 patients with traumatic AKI were enrolled in one group and named as the AKI group; 130 healthy subjects were enrolled in another group and named as the healthy group. AKI patients with different conditions were classified into AKI phase I, II, and III according to the KDIGO AKI diagnostic criteria, with 45, 59, and 28 in each group. In this study, we examined and compared serum Cys-C, RBP4, and neutrophil gelatinase-associated lipid transport protein (NGAL) levels between the AKI and healthy groups and between patients with AKI of different conditions, and the correlation and diagnostic value of three serum markers with the condition of traumatic AKI patients were also analyzed. The results showed that serum Cys-C, RBP4, and NGAL were significantly higher in the AKI group compared with the healthy group (P < 0.05), and the mean concentrations of the three serum markers increased as the severity of the disease increased, while correlation analysis showed that all three serum markers were positively correlated with serum Scr levels (P < 0.001). Further ROC curve analysis was performed, and the diagnostic values of serum Cys C, RBP4, and NGAL alone and in combination for traumatic AKI were 0.769, 0.741, 0.771, and 0.905, respectively. In short, serum Cys C, RBP4, NGAL have important value for the assessment and diagnosis of traumatic AKI patients.

Resveratrol protects cardiomyocytes from doxorubicin-induced apoptosis through the AMPK/P53 pathway.

Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it has severe cardiotoxic side effects. The aim of the present study was to investigate the effects of resveratrol on the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway in mediating DOX-induced cytotoxicity. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX-induced cardiotoxicity. DOX administration amplified P53 and B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) expression and decreased Bcl-2 expression in H9c2 cells. Resveratrol increased the cell viability and decreased the apoptotic rate. In addition, resveratrol markedly increased the phosphorylation of AMPK. Of note, resveratrol protected against DOX-induced increases of P53 and Bax and also prevented the downregulation of Bcl-2 in H9c2 cells. Furthermore, AMPK inhibitor Compound C abolished the protective effects of resveratrol. The results of the present study therefore indicated that resveratrol protected H9c2 cells from DOX-induced apoptosis via the AMPK/P53 pathway.