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Long term adverse effect of polyinosinic-polycytidylic acid on lung antibacterial defence mechanism

A technology of polyinosinic acid and defense mechanism, which is used in preparations for in vivo experiments, pharmaceutical formulations, etc.

Inactive Publication Date: 2017-05-31
宁波美丽人生医药生物科技发展有限公司
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

Furthermore, the deleterious effects of polyino

Method used

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  • Long term adverse effect of polyinosinic-polycytidylic acid on lung antibacterial defence mechanism
  • Long term adverse effect of polyinosinic-polycytidylic acid on lung antibacterial defence mechanism
  • Long term adverse effect of polyinosinic-polycytidylic acid on lung antibacterial defence mechanism

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0060] Polyinosinogenic acid increases susceptibility of lung tissue to bacteria

[0061] We first examined the effect of polysinosinate administration on bacterial clearance following bacterial infection. Experimental animals receive intranasal administration of polyinosine or imiquimod for two consecutive days (eg, double dose). On the third day (ie, 24 hours after the last polyinosinate dose), animals were injected intrathecally with S. pneumoniae. We found a significant increase in bacterial counts in the lungs of animals administered nasal polyinosinosinate. Interestingly, imiquimod or gademotel (TLR7 agonists such as figure 1 A) There was no significant difference in bacterial clearance between the treatment groups. But both groups showed robust clearance during the initial challenge phase. Administration of TLR7 ligand alone was therefore not sufficient to reduce bacterial clearance.

[0062] Second, we examined whether polyinosinogenic acid also reduced the clear...

Embodiment 2

[0064] The degree of impairment of bacterial clearance is directly proportional to the duration of polyinosarglycine administration

[0065] We observed a time point at which the rate of bacterial clearance in animals decreased after administration of polyinosinogenic acid. Since viral infections, such as influenza, usually last for several days or even longer, we conducted related experimental studies, taking polyinosinogenic acid in 1 dose or 3 doses to simulate the effect of viral infection. After 24 hours of intranasal administration of polyinosinogenic acid or saline once or three times, the experimental animals were intrathecally injected with Streptococcus pneumoniae. At 48h, the amount of bacteria in the body was recorded. We found that the dose of polysarcocytate correlates with the rate of bacterial clearance. The bacterial clearance rate in the experimental animals with one-time administration of polyinosinic acid will tend to decrease (the average CFU value is 8 ...

Embodiment 3

[0067] TLR3 and Cardif pathways enhance host susceptibility to bacteria induced by polyinosinogenic acid

[0068] Since polysinosine activates both TLR3 and the Cardif-dependent helicases RIG-I and MDA5, we sought to determine whether either or both pathways are involved in polysinosine impairing host bacterial clearance. For such studies, we use polyinosinocytosine in animals lacking TLR3 (Tlr3- / -), Cardif (Cardif- / -), or both (double knockout). Cardif acts as an adapter molecule for RIG-I and MDA5 signaling early in the antiviral response [25][26][27][28] . We found that TLR3 (Tlr3- / -) deletion or Cardif (Cardif- / -) experimental animals had improved bacterial clearance rate after administration of polyinosinogenic acid. Compared with the normal saline group, the double-knockout (Cardif- / - / Tlr3- / -) group was administered polyinosinogenic acid under the environment of secondary bacterial infection, and the bacterial clearance rate in the body was significantly improved ( i...

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Abstract

The invention discloses a long term adverse effect of polyinosinic-polycytidylic acid on a lung antibacterial defence mechanism, relates to the field of biomedicine, and particularly relates to a use of polyinosinic-polycytidylic acid in increasing of an Ifnar animal neutrophile granulocyte aggregation amount. The inventor has explored the role of a type I interferon in mediation of polyinosinic-polycytidylic acid. Polyinosinic-polycytidylic acid can increase the mortality of secondary bacterial infected hosts dependent on the type I interferon. It is found that the type I interferon induced by polyinosinic-polycytidylic acid causes stimulation of TLR3 and Cardif-dependent signaling pathways so that the defence of host lung tissue to two clinically important Gram-positive bacteria (such as Streptococcus pneumoniae and methicillin-resistant Staphylococcus aureus) is impaired and the susceptibility of animal bodies to Gram-positive bacteria is increased. It is confirmed that polyinosinic-polycytidylic acid has the effect of increasing the Ifnar animal neutrophile granulocyte aggregation amount.

Description

technical field [0001] The invention relates to the field of biomedicine, in particular to the effect of polysinosinate on increasing the aggregation of neutrophils in Ifnar- / - animals. Background technique [0002] Viral infections of the respiratory tract are common respiratory diseases and often present with a benign clinical course. However, a significant proportion of patients develop concomitant or secondary bacterial infections [1][2][3] , this complication can lead to respiratory failure or death. Although children, the elderly, and the immunocompromised population are at high risk for outbreaks of these complications, viral bacterial pneumonia can also occur in healthy adults and result in a significant disease burden. Viral-bacterial pneumonia has been repeatedly reported following the prevalence of influenza infection. It was the leading cause of death in patients during the influenza epidemics of the 20th century and the 2009 H1N1 influenza pandemic [4][5][6]...

Claims

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Application Information

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IPC IPC(8): A61K49/00
Inventor 田晓丽
Owner 宁波美丽人生医药生物科技发展有限公司
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