tetano
Editor, Senior Moderator
Hum Vaccin Immunother. 2015 Sep 11:0. [Epub ahead of print]
[h=1]Hygrothermal environment may cause influenza pandemics through immune suppression.[/h] Wu XL[SUP]1,[/SUP][SUP]2[/SUP], Luo YH[SUP]1,[/SUP][SUP]3[/SUP], Chen J[SUP]2[/SUP], Yu B[SUP]2[/SUP], Liu KL[SUP]4[/SUP], He JX[SUP]2[/SUP], Lu SH[SUP]2[/SUP], Li JX[SUP]1,[/SUP][SUP]3[/SUP], Wu S[SUP]5[/SUP], Jiang ZY[SUP]5[/SUP], Chen XY[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Over the past few decades, climate warming has caused profound changes in our living environment, and human diseases, including infectious diseases, have also been influenced by these changes. However, it remains unclear if a warm-wet climate can influence the infectivity of influenza and result in influenza pandemics. This study focused on observations of how the hydrothermal environment influences the infectivity of the influenza virus and the resulting immunoreactions of the infected mice. We used a manual climatic box to establish the following three environments with different temperatures and humidity: normal environment (T: 24?1?C, RH: 50%? 4%), wet environment (T: 24?1?C, RH: 95%? 4%) and warm-wet environment (T: 33?1?C, RH: 95%? 4%), and the mice were fed and maintained in these three different environments. After 14 days, half of the mice were infected with H1N1 (A/FM1/1/47, a lung adapted strain of the flu virus specific for the mouse lung) virus for 4 days. After establishing the animal model, we observed the microstructure of the lung tissue, the Th1/Th2 T cell subsets, the Th17/Treg balance, the expression of cytokines in the peripheral blood serum and the expression of the immune recognition RLH signal pathway. The results showed that mice in different environments have different reaction. Results showed that after infection, the proportion of Th1/Th2 and Th17/Treg cells in the spleen was significantly increased, and these proportions were increased the most in the infected group kept in wet-hot conditions. After infection, the mRNA levels and protein expression of the RLH (RIG-1-like helicases) signal pathway components were up-regulated while the uninfected animals in the three diverse environments showed no significant change. The infected mice kept in the wet and warm-wet environments showed a slight elevation in the expression of RLH pathway components compared to infected mice maintained in the normal environment. Our study suggested that the warm-wet environment may have interfered with the immune response and balance. The mice kept in the warm-wet environment displayed immune tolerance when they were exposed to the influenza virus, and the body was not able to effectively clear the virus, leading to a persistent infection. A warm-wet climate may thus be a factor that contributes to influenza pandemics, people should focus on the warm-wet climate coming and advance prepare to vaccine manufacture.
[h=4]KEYWORDS:[/h] FM1; Immunity; RLH; Warm-wet climate; influenza
PMID: 26359946 [PubMed - as supplied by publisher]
[h=1]Hygrothermal environment may cause influenza pandemics through immune suppression.[/h] Wu XL[SUP]1,[/SUP][SUP]2[/SUP], Luo YH[SUP]1,[/SUP][SUP]3[/SUP], Chen J[SUP]2[/SUP], Yu B[SUP]2[/SUP], Liu KL[SUP]4[/SUP], He JX[SUP]2[/SUP], Lu SH[SUP]2[/SUP], Li JX[SUP]1,[/SUP][SUP]3[/SUP], Wu S[SUP]5[/SUP], Jiang ZY[SUP]5[/SUP], Chen XY[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Over the past few decades, climate warming has caused profound changes in our living environment, and human diseases, including infectious diseases, have also been influenced by these changes. However, it remains unclear if a warm-wet climate can influence the infectivity of influenza and result in influenza pandemics. This study focused on observations of how the hydrothermal environment influences the infectivity of the influenza virus and the resulting immunoreactions of the infected mice. We used a manual climatic box to establish the following three environments with different temperatures and humidity: normal environment (T: 24?1?C, RH: 50%? 4%), wet environment (T: 24?1?C, RH: 95%? 4%) and warm-wet environment (T: 33?1?C, RH: 95%? 4%), and the mice were fed and maintained in these three different environments. After 14 days, half of the mice were infected with H1N1 (A/FM1/1/47, a lung adapted strain of the flu virus specific for the mouse lung) virus for 4 days. After establishing the animal model, we observed the microstructure of the lung tissue, the Th1/Th2 T cell subsets, the Th17/Treg balance, the expression of cytokines in the peripheral blood serum and the expression of the immune recognition RLH signal pathway. The results showed that mice in different environments have different reaction. Results showed that after infection, the proportion of Th1/Th2 and Th17/Treg cells in the spleen was significantly increased, and these proportions were increased the most in the infected group kept in wet-hot conditions. After infection, the mRNA levels and protein expression of the RLH (RIG-1-like helicases) signal pathway components were up-regulated while the uninfected animals in the three diverse environments showed no significant change. The infected mice kept in the wet and warm-wet environments showed a slight elevation in the expression of RLH pathway components compared to infected mice maintained in the normal environment. Our study suggested that the warm-wet environment may have interfered with the immune response and balance. The mice kept in the warm-wet environment displayed immune tolerance when they were exposed to the influenza virus, and the body was not able to effectively clear the virus, leading to a persistent infection. A warm-wet climate may thus be a factor that contributes to influenza pandemics, people should focus on the warm-wet climate coming and advance prepare to vaccine manufacture.
[h=4]KEYWORDS:[/h] FM1; Immunity; RLH; Warm-wet climate; influenza
PMID: 26359946 [PubMed - as supplied by publisher]