ABSTRACT
Infectious diseases are still one of the leading causes of morbidity and death globally, affecting public health and life, social and economic development, and even national security. Early detection focuses on detecting the abnormal information of infectious disease outbreaks or epidemics in a timely and sensitive way to conduct field investigation and verification. It is also a precursor to effective surveillance and early warning system. The effective surveillance and early warning system can fully and accurately understand the real conditions, driving forces, and transmission chain of the occurrence of a specific infectious disease outbreak and epidemic and put forward scientific and effective prevention and control strategies and measures. Due to the measurement of the resources support and the particular data collection value, it is not easy to obtain epidemiological, etiological, and other data information in a timely, complete and accurate manner. This paper summarized the theory and technology on early detection, effective surveillance, and early warning information on infectious diseases. It also integrated and utilized the multi-source data, including effective infectious disease surveillance and the country's early warning system, to better understand the outbreak epidemic, causes, risks, processes, and driving forces. Thus, it is possible to set up a sensitive, specific staging measurement innovative technical system to monitor, early warning, and timely respond to acute infectious diseases through multidisciplinary cooperation in China. It provides the basis for strengthening the surveillance and early warning of new emerging and major infectious diseases and public health emergencies, avoiding the spread of inadequate response to infectious disease, and preventing the resources waste of over-response.
Subject(s)
Communicable Diseases , Epidemics , China/epidemiology , Communicable Diseases/diagnosis , Communicable Diseases/epidemiology , Disease Outbreaks , Humans , Population SurveillanceABSTRACT
Objective: To investigate the damage and mechanism of artemisia annua pollen on tight junction of human nasal mucosa epithelial cells (HNEpC). Methods: HNEpC were cultured in vitro. Different concentrations of artemisia annua pollen (0, 20, 40, 80, 100, 160, 200 µg/ml) were used to intervene the cells for 24 h, and the cell proliferation activity was detected by the CCK-8 method. The expression and phosphorylation of p38MAPK signaling pathway were detected by Western Blot before and after the intervention of SB203580, a p38MAPK inhibitor in HNEpC. Immunofluorescence chemical staining, Western Blot and quantitative real-time PCR (qPCR) were used to observe the expression and distribution of tight junctions Occludin and Claudin-1. SPSS 21.1 software was used for statistical analysis. Results: CCK-8 results showed that, compared with the control group, the proliferation activity of HNEpC increased after 6 h intervention with different concentrations of artemisia annua pollen (all P<0.05). After 12 h of intervention, the proliferation activity of HNEpC in the 20, 40, 80, 100 and 160 µg/ml groups was not significantly changed (all P>0.05), while that in the 200 µg/ml group was decreased (P<0.05). After the intervention for 24 h, the proliferation activity of cells in the 20 and 40 µg/ml groups was not significantly changed (all P>0.05), while that in the 80, 100, 160 and 200 µg/ml groups was decreased (all P<0.05). Immunofluorescence staining showed that the Occludin and Claudin-1 proteins in the normal control group were localized on the cell membrane and expressed more and formed a ring structure around the cell membrane. However, under the intervention of high concentration artemisia annua pollen, its expression level decreased, appeared broken, fuzzy, and nonuniform distribution. Western Blot and qPCR results showed that after 24 h of intervention, the expression levels of HNEpC Claudin-1 protein and its mRNA in the pollen groups (40, 80, 100, 160, 200 µg/ml) of artemisia annua decreased compared with those of those of the control group (mRNA expression levels were 0.567±0.214, 0.443±0.109, 0.462±0.160, 0.497±0.134, 0.388±0.076 compared with 1.001±0.067, respectively, all P<0.05). However, the mRNA of Occludin protein and its mRNA only decreased in the 200 µg/ml treatment group (mRNA expression level was 0.631±0.109 compared with 1.016±0.026, P<0.05), while all the other treatment groups increased (mRNA expression levels were 1.258±0.134, 1.827±0.103, 2.429±0.077, 1.707±0.085, 1.477±0.066 compared with 1.016±0.026, respectively, all P<0.05). Western Blot showed that p-p38MAPK expression increased after intervention with 100, 160, 200 µg/ml artemisia annua pollen for 24 h. SB203580 could inhibit the decreasing expression of Occludin caused by artemisinin pollen (mRNA expression was 1.255±0.179 compared with 0.631±0.109, P<0.05), but had no effect on Claudin-1 protein expression. Conclusion: Pollen from artemisia annua may activate p38MAPK signaling pathway and destroy the close connection of HNEpC.