Temporal variation in the oral microbiome and the prediction of early childhood caries in different ethnicities.

Globally, early childhood caries (ECC) is a significant public health concern, necessitating effective prediction and prevention strategies. This study aimed to explore variations in the oral microbiome of saliva from pre-school Han and Uyghur children during ECC development and establish a predictive model based on temporal oral microbiome changes. Saliva samples were collected from a single kindergarten every three months over six months.

Histogram analysis of ultrasonographic images in the differentiation of benign and malignant parotid gland tumors.

Objective: We evaluated the diagnostic value of histogram analysis (HA) using ultrasonographic (US) images for differentiation among pleomorphic adenoma (PA), adenolymphoma (AL), and malignant tumors (MT) of the parotid gland.

Study Design: Preoperative US images of 48 patients with PA, 39 patients with AL, and 17 patients with MT were retrospectively analyzed for gray-scale histograms. Nine first-order texture features derived from histograms of the tumors were compared.

IL-27 Signaling Promotes Th1 Response by Downregulating IL-10 Production in DCs during Chlamydial Respiratory Infection.

usually causes mucosal infections, bringing considerable morbidity and socioeconomic burden worldwide. We previously revealed that IL-27/IL-27R mediates protection against chlamydial invasion by promoting a protective Th1 response and suppressing neutrophilic inflammation. Here, we used the mouse model of () respiratory infections to further investigate the impact of IL-27 signaling in the DCs-regulated immune response, since an elevated IL-27/IL-27R expression in DCs was identified following chlamydial infection.

Identification of active compounds in Ophiopogonis Radix from different geographical origins by UPLC-Q/TOF-MS combined with GC-MS approaches.

Ophiopogonis Radix, also known as Maidong in Chinese, is largely produced in the Sichuan and Zhejiang provinces: "Chuan-maidong (CMD)" and "Zhe-maidong (ZMD)," respectively. This study aimed to distinguish and evaluate the quality of CMD and ZMD. In this study, the tubers of CMD and ZMD were investigated using UPLC-Q/TOF-MS, GC-MS, and LC-MS methods, respectively.

IL-21/IL-21R Regulates the Neutrophil-Mediated Pathologic Immune Response during Chlamydial Respiratory Infection.

IL-21/IL-21R was documented to participate in the regulation of multiple infection and inflammation. During () respiratory infection, our previous study had revealed that the absence of this signal induced enhanced resistance to infection with higher protective Th1/Th17 immune responses. Here, we use the murine model of respiratory infection and IL-21R deficient mice to further identify a novel role of IL-21/IL-21R in neutrophilic inflammation.

IL-27/IL-27R Mediates Protective Immunity against Chlamydial Infection by Suppressing Excessive Th17 Responses and Reducing Neutrophil Inflammation.

IL-27, a heterodimeric cytokine of the IL-12 family, has diverse influences on the development of multiple inflammatory diseases. In this study, we identified the protective role of IL-27/IL-27R in host defense against respiratory infection and further investigated the immunological mechanism. Our results showed that IL-27 was involved in infection and that IL-27R knockout mice (WSX-1 mice) suffered more severe disease, with greater body weight loss, higher chlamydial loads, and more severe inflammatory reactions in the lungs than C57BL/6 wild-type mice.

IL-21/IL-21R Signaling Aggravated Respiratory Inflammation Induced by Intracellular Bacteria through Regulation of CD4 T Cell Subset Responses.

The IL-21/IL-21R interaction plays an important role in a variety of immune diseases; however, the roles and mechanisms in intracellular bacterial infection are not fully understood. In this study, we explored the effect of IL-21/IL-21R on chlamydial respiratory tract infection using a chlamydial respiratory infection model. The results showed that the mRNA expression of IL-21 and IL-21R was increased in -infected mice, which suggested that IL-21 and IL-21R were involved in host defense against lung infection.

Chlamydia muridarum infection induces CD4+ T cells apoptosis via PI3K/AKT signal pathway.

Apoptosis is essential for the homeostatic control of the lymphocytes number during the development of an immune response to an invasive microorganism. CD4+ T cells play a major role in homeostasis of the immune system and are sufficient to confer protection against Chlamydia muridarum (Cm) infection in mice. The present study demonstrated that phosphatidylinositol 3-kinase (PI3K) p110δ mRNA and phosphorylation of protein kinase B (p-AKT) level were significantly increased in lung cells and spleen cells at day 3 and day 7 post-infection, p-AKT level was inhibited when adding PI3K inhibitor LY294002.

Endogenous IL-17A mediated neutrophil infiltration by promoting chemokines expression during chlamydial lung infection.

Chlamydia is an obligate intracellular bacteria, which can infect cervix, urethra, conjunctiva, joints, lungs and so on. Neutrophils are important in host protection against microbial invasion during the early phase of infection. Here, to investigate the mechanism of IL-17A in recruiting neutrophils during Chlamydia muridarum (Cm) lung infection, we introduced IL-17A antibodies and IL-17 mice to confirm the effect of IL-17A on influencing neutrophil attractants expressions.

V4+ T Cells: A Novel IL-17-Producing T Subsets during the Early Phase of Chlamydial Airway Infection in Mice.

Our previous studies showed that T cells provided immune protection against Chlamydial (Cm), an obligate intracellular strain of chlamydia trachomatis, lung infection by producing abundant IL-17. In this study, we investigated the proliferation and activation of lung T cell subsets, specifically the IL-17 and IFN production by them following Cm lung infection. Our results found that five T cell subsets, V1+ T, V2+ T, V4+ T, V5+ T, and V6+ T, expressed in lungs of naïve mice, while Cm lung infection mainly induced the proliferation and activation of V4+ T cells at day 3 p.