CN111228480A - Use of anti-human TNF- α antibody in preparation of medicine for treating virus infection - Google Patents
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Abstract
The invention provides an application of an anti-human TNF- α antibody in preparation of a medicine for treating virus infection for the first time, the invention provides that the anti-human TNF- α antibody is used in virus infection to relieve cytokine storm and inflammatory reaction caused by virus infection, and proved by empirical research, animal experimental research finds that the anti-human TNF- α antibody can obviously reduce the expression level of proinflammatory cytokines in H1N1 influenza virus infected mice, the survival rate of the infected mice is greatly improved, the anti-human TNF- α antibody can relieve immune inflammation caused by acute virus infection by inhibiting the expression of proinflammatory cytokines such as TNF- α, and meanwhile, the anti-human TNF- α antibody can also greatly reduce the mRNA relative expression level of key proteins in a toll-like receptor signal channel in H1N1 influenza virus infected mice, and the anti-human TNF- α antibody can avoid over-activation of an innate immune system.
Description
Technical Field
The invention belongs to the technical field of virus infection treatment, and particularly relates to application of an anti-human TNF- α antibody in preparation of a medicament for treating virus infection.
Background
While Adalimumab (also known as Humira humulimate) can specifically bind to TNF- α, but not to TNF- β and other cytokines, and blocks the interaction of TNF- α with the cell surface TNF receptors of p55 and p75, reducing the inflammatory response caused by the overproduction and release of TNF- α, and has important clinical significance for treating diseases caused by the overproduction of TNF- α.
Adalimumab is a self-injectable biotherapeutic drug which has been approved for 2 indications in the national food and drug administration (CFDA), namely rheumatoid arthritis and ankylosing spondylitis. Rheumatoid arthritis and ankylosing spondylitis are chronic autoimmune diseases.
For example, influenza is a respiratory infectious disease caused by influenza virus infection, and typical clinical symptoms of the influenza are high fever, general pain, obvious weakness and mild respiratory symptoms, some influenza viruses have strong infectivity and can cause severe cytokine storm (cytokine storm) at the initial stage of infection, namely, the phenomenon that a plurality of cytokines in body fluid such as TNF- α -1, IL-6, IL-12, IFN- α - β -gamma, MCP-1, IL-8 and the like are rapidly and massively generated after microorganisms infect organisms.
Cytokine storms occur when the immune system from the human body reacts too aggressively to invaders, thereby synthesizing high levels of cytokines. These cytokines are important signaling compounds that help mobilize immune cells, thereby removing the virion from the body. However, when excessive cytokine production occurs, an inflammatory response occurs and the accumulation of immune cells and associated fluids at the site of infection can prevent normal functioning of tissues and organs, such as the lungs. Cytokine storms are important causes of acute respiratory distress syndrome and multiple organ failure, and can cause acute death in severe cases, such as 2019 novel coronavirus (2019-cov), H7N9 avian influenza virus, H5N1 avian influenza virus, SARS coronavirus and the like.
However, the action mechanism of the traditional antiviral drugs is to inhibit virus replication, prevent large-scale outbreak of virus in vivo, but cannot kill the virus and also cannot relieve systemic cytokine storm and inflammatory reaction.
Disclosure of Invention
The invention aims to provide application of an anti-human TNF- α antibody in preparing a medicament for treating virus infection.
In order to achieve the purpose, the technical scheme of the invention is as follows:
use of an anti-human TNF- α antibody in the manufacture of a medicament for the treatment of viral infections.
Preferably, in the use of the anti-human TNF- α antibody for the manufacture of a medicament for the treatment of viral infections, the virus is one which causes a cytokine storm and inflammatory response in the body following infection, and the cytokine comprises at least a pro-inflammatory cytokine.
The virus comprises 2019 novel coronavirus (2019-cov), H7N9 avian influenza virus, H5N1 avian influenza virus, SARS coronavirus, H1N1 influenza virus and the like.
The invention discloses a method for treating acute viral infection, which comprises the steps of providing a virus, wherein the virus can cause a systemic cytokine storm and inflammatory reaction of an organism after infecting the organism, and in the cytokine storm caused by different virus infections, the expression levels of proinflammatory cytokines such as TNF- α and IL6 are obviously increased, and the expression level of TNF- α is positively correlated with the severity of diseases.
Meanwhile, the anti-human TNF- α antibody can also greatly reduce the mRNA relative expression levels of MyD88, TLR3, TLR4 and TLR7 in a mouse infected by H1N1 influenza virus, and shows that the anti-human TNF- α antibody can avoid the excessive activation of the innate immune system by reducing the mRNA expression level of key protein in a toll-like receptor signal pathway.
In the application of the anti-human TNF- α antibody in preparing a medicament for treating virus infection, the anti-human TNF- α antibody is adalimumab;
or the anti-human TNF- α antibody is obtained by secreting an anti-human TNF- α stable cell strain CHO K1, and the preservation number of the anti-human TNF- α stable cell strain CHO K1 is CCTCC No: C2019183.
The adalimumab is the most effective anti-human TNF- α antibody in the current market, and experiments prove that the adalimumab can effectively relieve cytokine storm and inflammatory reaction caused by virus infection, and the anti-human TNF- α antibody secreted by the anti-human TNF- α stable cell strain CHO K1 with the preservation number of CCTCC No: C2019183 has better relieving effect than the adalimumab.
The invention also provides the application of the anti-human TNF- α antibody and anti-human IL6 antibody composition in preparing medicaments for treating virus infection, and the combined use of the anti-human TNF- α antibody and the anti-human IL6 antibody has better relieving effect on cytokine storm and inflammatory reaction caused by virus infection, and the anti-human TNF- α antibody and the anti-human IL6 antibody supplement each other.
Similarly, in the application of the anti-human TNF- α antibody and anti-human IL6 antibody composition in the preparation of a medicament for treating viral infection, the virus is a virus which causes a cytokine storm and an inflammatory response of a body after infection, and the cytokine at least comprises a proinflammatory cytokine.
The virus comprises 2019 novel coronavirus (2019-cov), H7N9 avian influenza virus, H5N1 avian influenza virus, SARS coronavirus, H1N1 influenza virus and the like.
Similarly, in the application of the anti-human TNF- α antibody and anti-human IL6 antibody composition in preparing a medicament for treating virus infection, the anti-human TNF- α antibody is adalimumab, or the anti-human TNF- α antibody is obtained by secreting an anti-human TNF- α stable cell strain CHO K1, and the preservation number of the anti-human TNF- α stable cell strain CHO K1 is CCTCC No: C2019183.
Preferably, in the application of the anti-human TNF- α antibody and anti-human IL6 antibody composition in preparing a medicament for treating viral infection, the anti-human IL6 antibody is truzumab.
The invention also provides a medicament for treating viral infection, which at least comprises an anti-human TNF- α antibody.
Preferably, the above-mentioned medicament for treating viral infection comprises at least one anti-human TNF- α antibody and one anti-human IL6 antibody.
Compared with the prior art, the invention has the beneficial effects that:
animal experiment researches show that the anti-human TNF- α antibody can obviously reduce the expression level of proinflammatory cytokines (including TNF- α, IL6, IFN-gamma and the like) in a mouse infected by H1N1 influenza virus, the survival rate of the infected mouse is greatly improved, the anti-human TNF- α antibody can relieve immune inflammation caused by acute virus infection by inhibiting the expression of proinflammatory cytokines such as TNF- α and the like, and meanwhile, the anti-human TNF- α antibody can also greatly reduce the mRNA relative expression level of MyD88, TLR3, TLR4 and TLR7 in the mouse infected by H1N 8295 influenza virus, so that the anti-human TNF- α antibody can avoid the excessive activation of an innate immune system by reducing the mRNA expression level of key proteins in a toll-like receptor signal channel.
Drawings
FIG. 1 is a graph showing the effect of anti-human TNF- α antibody treatment on the survival rate of H1N1 influenza virus infected mice;
wherein "Days Post Infection" represents the Days after Infection, "Percent survivor" represents the survival (%), "Placebo" represents the negative control group injected intraperitoneally with PBS, "ZXBio Anti-TNF α" represents the experimental group ① injected intraperitoneally with Anti-human TNF- α antibody, "Humira" represents the experimental group ② injected intraperitoneally with adalimumab;
FIG. 2 is a graph showing the effect of anti-human TNF- α antibody treatment on proinflammatory cytokine concentrations in H1N1 influenza virus infected mice;
wherein "Cytokines" indicates Cytokines, 1 indicates a blank control group, 2 indicates a negative control group, 3 indicates an experimental group ①, 4 indicates an experimental group ②, Protein Concentration in BALF (pg/ml) indicates the Concentration of the relevant Protein (cytokine) (Concentration unit is pg/ml) in the experimental mice, p indicates p < 0.01, the same as the following;
FIG. 3 is a graph showing the effect of anti-human TNF- α antibody treatment on the relative expression levels of the mRNAs of TLR3, TLR4, TLR7, MyD88 in H1N1 influenza virus-infected mice;
here, "Relative mRNA Level to GAPDH" indicates the Relative expression levels of the mRNAs of TLR3, TLR4, TLR7 and MyD88 with respect to the housekeeping gene GAPDH.
Detailed Description
The technical solution of the present invention will be further described in detail with reference to the accompanying drawings and the detailed description.
Example 1
This example describes the alleviating effect of anti-human TNF- α antibody on cytokine storm and inflammatory response caused by virus-infected organism, using Adamantimab and anti-human TNF- α antibody (hereinafter referred to as "orthoxi anti-human TNF- α antibody") secreted by anti-human TNF- α stable cell strain CHO K1 with CCTCC No. C2019183 as examples of H1N1 influenza virus.
The H1N1 influenza virus (strain A/FM/1/47) is a highly virulent and rat-infectable influenza virus extracted from Fort Monmouth patients in the United states in the national outbreak of influenza of 1947, which causes pneumonia and death in BALB/c mice (ATCC VR-97), and is offered by Ningming boat Biotech Ltd. The H1N1 influenza virus was amplified by Madin-Darby Canine kidney (MDCK) cells (ATCC CCL-34). Will be 1 × 103PFU virus was dissolved in 20ul PBS and 6-8 week old sex matched BALB/C mice were infected intranasally.
The mice infected by the H1N1 influenza virus are divided into a negative control group, an experimental group ① and an experimental group ②, each group of ten mice has three repeated experiments, wherein the experimental group ① carries out intraperitoneal injection of Anti-human TNF- α antibody (ZXBio Anti-TNFa, dose: 5mg/kg) on the experimental group within 1 hour of the mice infected by the influenza virus systemically, the mice are injected every other day until 25 days after the mice are infected, the experimental group ② is injected with adalimumab (Humira) with the same dose, the negative control group is injected with 250ul PBS, the uninfected mice are simultaneously set as a blank control group, and the survival conditions of the infected mice in each group after 25 days are all the three repeated experiments are shown in figure 1.
As can be seen from FIG. 1, the mice in the negative control group died completely on day 6 after infection and died completely on day 15 after infection, while the mice in the experimental group ② died only on day 9 after infection and maintained survival rate of more than 50% after infection by day 25, and the mice in the experimental group ① died only on day 12 after infection and maintained survival rate of more than 60% after infection by day 25.
Randomly selecting mice in each group after the fifth day of mouse infection, taking lung Bronchus Alveolar Lavage Fluid (BALF) of each mouse, and detecting the concentration of cytokines in the lung bronchus alveolar lavage fluid by ELISA; the results are shown in FIG. 2.
As can be seen from FIG. 2, the concentration of proinflammatory cytokines (TNF- α, IL6 and IFN-gamma) in the lung bronchoalveolar lavage fluid of mice in the blank control group is low, while the lung bronchoalveolar lavage fluid of mice in the negative control group contains a large amount of proinflammatory cytokines, wherein the concentration of IL6 is as high as 800pg/ml, the concentration of TNF- α is as high as 1100pg/ml, and the concentration of IFN-gamma is as high as 1200 pg/ml. compared with the negative control group, the concentration of proinflammatory cytokines in the lung bronchoalveolar lavage fluid of mice in the experimental group ① and the experimental group ② is significantly reduced (p is less than 0.01), and the concentration of TNF- α and IL6 in the lung bronchoalveolar lavage fluid of mice in the experimental group ① is lower than that in the experimental group ②.
Meanwhile, on the 5 th day after mouse infection, mice were randomly selected from each group, and mouse lung tissues were taken, homogenized, and then RNA was extracted using Qiagen Rneasy Mini Kit. The relative expression levels of the mrnas for TLR3, TLR4, TLR7, MyD88 (compared to the mRNA for housekeeping gene GAPDH) were compared by RT-qPCR after cDNA synthesis, the results of which are shown in figure 3.
As can be seen from FIG. 3, the mRNA relative expression levels of MyD88, TLR3, TLR4 and TLR7 were greatly up-regulated in the mice of the negative control group compared to the mice of the blank control group, indicating that acute infection caused a large amount of innate immune inflammation, whereas the mRNA relative expression levels of MyD88, TLR3, TLR4 and TLR7 were greatly down-regulated in the mice of experimental group ① and experimental group ②.
TLR3, TLR4 and TLR7 are Toll-like receptors (Toll-like receptors), the Toll-like receptors are important protein molecules participating in nonspecific immunity, and when microorganisms break through physical barriers of organisms such as skin, mucosa and the like, the Toll-like receptors can recognize the proteins and activate the organisms to generate immune cell responses, so that the up-regulation of mRNA of the Toll-like receptors is the characteristic of activated innate immune systems.
Similarly, MyD88 (myeloid differentiation factor 88) is a key linker molecule in the Toll-like receptor signaling pathway, and upregulation of its mRNA implies activation of the Toll-like receptor signaling pathway, which is also one of the features of innate immune system activation.
And the adalimumab and the n-xi anti-human TNF- α antibody down-regulate mRNA of MyD88, TLR3, TLR4 and TLR7, which shows that the anti-human TNF- α antibodies such as the adalimumab and the n-xi anti-human TNF- α antibody can avoid over-activation of the body innate immune system.
Claims (10)
1. Use of an anti-human TNF- α antibody in the manufacture of a medicament for the treatment of viral infections.
2. The use of an anti-human TNF- α antibody of claim 1 in the manufacture of a medicament for the treatment of viral infections, wherein the virus is one that causes a cytokine storm and inflammatory response in the body following infection, and wherein the cytokine comprises at least a pro-inflammatory cytokine.
3. The use of an anti-human TNF- α antibody of claim 1 or 2 in the preparation of a medicament for the treatment of a viral infection, wherein the anti-human TNF- α antibody is adalimumab.
4. The use of the anti-human TNF- α antibody of claim 1 or 2 in the preparation of a medicament for treating viral infection, wherein the anti-human TNF- α antibody is secreted from anti-human TNF- α stably transfected cell line CHO K1, and the collection number of the anti-human TNF- α stably transfected cell line CHO K1 is CCTCC No. C2019183.
5. Use of a combination of an anti-human TNF- α antibody and an anti-human IL6 antibody in the manufacture of a medicament for the treatment of a viral infection.
6. The use of a combination of anti-human TNF- α antibody and anti-human IL6 antibody of claim 5 in the manufacture of a medicament for the treatment of viral infections, wherein the virus is one that causes the body to experience a cytokine storm and inflammatory response following infection, and wherein the cytokines include at least pro-inflammatory cytokines.
7. The use of the combination of anti-human TNF- α antibody and anti-human IL6 antibody of claim 5 in the preparation of a medicament for treating viral infection, wherein the anti-human TNF- α antibody is adalimumab, or the anti-human TNF- α antibody is secreted from anti-human TNF- α stably transformed cell line CHO K1, and the anti-human TNF- α stably transformed cell line CHO K1 has the preservation number of CCTCC No: C2019183.
8. The use of the combination of anti-human TNF- α antibody and anti-human IL6 antibody of claim 5 in the manufacture of a medicament for the treatment of viral infections, wherein the anti-human IL6 antibody is truzumab.
9. A medicament for the treatment of viral infections comprising at least one anti-human TNF- α antibody.
10. The medicament according to claim 5, comprising at least one anti-human TNF- α antibody and one anti-human IL6 antibody.
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