Application of an immunomodulatory peptide in the preparation of drugs for preventing and treating bacterial infections

Abstract

The present invention discloses an application of an immunomodulatory peptide in the preparation of a drug for preventing and treating bacterial infection, and belongs to the field of biomedical technology; the rice-derived immunomodulatory peptide RDP3 can inhibit bacterial infection in mice, and can alleviate the inflammatory damage of the lung tissue of infected mice and reduce the level of inflammatory factor protein in the serum of infected mice to a certain extent, and can also improve the survival rate of sepsis model mice. RDP3 exerts an antibacterial effect by recruiting phagocytes to the infected site. In view of the unique antibacterial mechanism of RDP3, it can provide a basis for the research and development of RDP3 as a polypeptide anti-infective drug, and provide candidate molecules for the research and development of peptide antibiotics.

Description

Technical Field

[0001] The invention belongs to the field of biomedical technology, and specifically relates to the application of an immunomodulatory peptide in the preparation of a drug for preventing and treating bacterial infection. Background Art

[0002] Classic sepsis is often caused by a systemic response induced by bacterial infection. The bacteria in the body then release endotoxins (such as LPS and LTA). These molecules interact with cellular toll-like receptors (TLRs) and induce the body's immune and inflammatory responses.

[0003] The infectious pathogens of sepsis are complex and diverse, mainly bacterial infections, such as E. coli , Burkholderia pseudomallei and Francisella tularensis , Salmonella , S. pneumoniae etc., can induce bacterial sepsis in the body. Gram-positive bacterial sepsis accounts for 57% of all sepsis cases each year. Sepsis can be caused by infection in various parts of the body and often occurs after severe trauma, burns, and surgery. The patient's immune response continues to be excessive, and inflammatory cytokines (TNF-α, IL1-β, IL-6, etc.) act on organs such as lung tissue, causing lung damage, edema, and fibrosis.

[0004] Intravenous antibiotic therapy and intravenous infusion therapy are currently the main treatments for sepsis. However, the causes of sepsis vary greatly, the drug resistance rate is high, and the limited antibiotic selection and insufficient microbial data make the management and treatment of patients difficult. The use of combined antibiotic therapy and broad-spectrum antibiotics increases the risk of microbial resistance. Therefore, the treatment of sepsis urgently needs a more targeted approach with fewer side effects. Summary of the invention

[0005] In view of the deficiencies of the prior art, the purpose of the present invention is to provide an application of an immunomodulatory peptide in the preparation of a drug for preventing and treating bacterial infection, thereby solving the problems in the prior art.

[0006] The purpose of the present invention can be achieved through the following technical solutions:

[0007] Application of RDP3 in the preparation of medicines for preventing and treating bacterial infections.

[0008] Furthermore, the bacteria include Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus or methicillin-resistant Staphylococcus aureus.

[0009] Furthermore, the drug includes RDP3 and RDP3 derivatives.

[0010] A drug for preventing and treating bacterial infections, including RDP3.

[0011] Furthermore, the drug also includes RDP3 derivatives.

[0012] Application of RDP3 in the preparation of drugs for treating sepsis.

[0013] Furthermore, the sepsis is caused by Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus or methicillin-resistant Staphylococcus aureus.

[0014] Furthermore, the drug includes RDP3 and RDP3 derivatives.

[0015] Beneficial effects of the present invention:

[0016] 1. The rice-derived immunomodulatory peptide RDP3 of the present invention can inhibit bacterial (Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, methicillin-resistant Staphylococcus aureus) infection in mice, and can alleviate the inflammatory damage of the lung tissue of infected mice and reduce the level of inflammatory factor protein in the serum of infected mice to a certain extent, and can also improve the survival rate of sepsis model mice.

[0017] 2. RDP3 cannot inhibit the growth of bacteria, has no killing effect on bacteria, and does not affect the metabolic activity of bacteria. In other words, RDP3 has no direct antibacterial effect, but exerts its antibacterial effect by recruiting phagocytes to the infection site. Given the unique antibacterial mechanism of RDP3, it can provide a basis for the research and development of RDP3 as a polypeptide anti-infective drug and provide candidate molecules for the research and development of peptide antibiotics. BRIEF DESCRIPTION OF THE DRAWINGS

[0018] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings required for use in the embodiments or the description of the prior art will be briefly introduced below. Obviously, for ordinary technicians in this field, other drawings can be obtained based on these drawings without paying any creative work.

[0019] Figure 1 This is a graph showing the experimental results of the effect of RDP3 on the bacterial load in the peritoneal cavity of mice in Example 1;

[0020] Figure 2 This is a graph showing the experimental results of the effect of RDP3 on the bacterial load in the peripheral blood of mice in Example 2;

[0021] Figure 3 This is a graph showing the experimental results of the effect of RDP3 on bacterial infection-induced lung inflammation damage in mice in Example 3;

[0022] Figure 4This is a graph showing the experimental results of the effect of RDP3 in Example 4 on the production of pro-inflammatory cytokines in the peripheral blood of mice infected with bacteria;

[0023] Figure 5 This is a graph showing the experimental results of the effect of RDP3 on the survival rate of mice infected with lethal doses of bacteria in Example 5;

[0024] Figure 6 This is a graph showing the experimental results of the effect of RDP3 on the survival rate of mice with sepsis induced by cecal ligation and puncture (CLP) in Example 6;

[0025] Figure 7 is a graph showing the bactericidal kinetics experimental results of RDP3 in Example 8;

[0026] Figure 8 is a graph showing the experimental results of the effect of RDP3 on bacterial metabolic activity in Example 9;

[0027] Fig. 9 This is a graph showing the experimental results of the effect of intraperitoneal injection of RDP3 on the number of peritoneal phagocytes in mice in Example 10. DETAILED DESCRIPTION

[0028] The following will be combined with the drawings in the embodiments of the present invention to clearly and completely describe the technical solutions in the embodiments of the present invention. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without creative work are within the scope of protection of the present invention.

[0029] At present, rice-derived peptides have different forms and functions. They can be roughly divided into three categories according to the processing methods and sources: Rice bran derived peptide (RBP), Rice peptide (RP) and Rice-derived peptide (RDP).

[0030] RDP3 (Rice-derived peptide 3, RDP3) is a new type of immunomodulatory peptide derived from rice, which can inhibit xanthine oxidase activity, reduce the production of uric acid, and reduce the production of proinflammatory cytokine IL1-β in hyperuricemia model mice. Unlike the general processing technology of rice active peptides, RDP3 does not undergo rice proteolysis, but is directly isolated and purified from the supernatant of rice homogenate. RDP3 has similar functions to RDP1 and RDP2 discovered at the same time. The three rice-derived active peptides have only 9 amino acids, but there are differences in the hydrophilic end of the structure (RDP1, RDP2). In addition, RDP3 has the best thermal stability and serum stability.

[0031] The following examples are used to study and illustrate the application of RDP3 in antibacterial applications;

[0032] Example 1

[0033] In this example, it is shown that RDP3 significantly reduces the bacterial load in the peritoneal cavity of mice;

[0034] The bacterial infection model was established by intraperitoneal injection of C57BL / 6J mice (divided into 5 groups of female mice, 6 mice in each group). The infected mice were injected intraperitoneally (2×10 7 CFU / mouse, 200 μL) of bacteria. The five groups of mice were: intraperitoneal injection of RDP3 (10 mg / kg) 8 h before bacterial infection (-8 h), 4 h (-4 h), and 4 h after infection (+4 h), a control group (intraperitoneal injection of 200 μL of sterile PBS) and a model group (intraperitoneal injection of 200 μL of sterile PBS after infection with the tested bacteria). 18 h after the mice were infected with bacteria, the mice were killed by cervical dislocation. On a sterile workbench, 2 mL of sterile PBS was injected into the mouse peritoneal cavity. The mouse abdomen was slowly kneaded to allow the PBS to fully irrigate the mouse peritoneal cavity, and then 1 mL of irrigating fluid was extracted. The irrigating fluid was diluted by the 10-fold gradient dilution method to a final multiple of 10 -4 , spread the gradient diluted peritoneal lavage fluid (100 μL) evenly on the LB plate, culture in a 37°C incubator for 16-18 hours, and then count the number of colonies.

[0035] in, Figure 1 AD in Figure 2 respectively represent the effects of RDP3 on Escherichia coli ( E. coli ), Acinetobacter baumannii ( A. baumannii ), Staphylococcus aureus ( S. aureus ) and methicillin-resistant Staphylococcus aureus Staphylococcus aureus , MRSA)-infected mice with bacterial load in the peritoneal cavity; Figure 1 The results showed that the bacterial load in the peritoneal cavity of mice in the RDP3-treated group was significantly reduced compared with that in the model group. Among the mice infected with E. coli, the colony count (CFU) of the model group was 4.62×10 6 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at 8 h before infection (-8 h), 4 h before infection (-4 h), and 4 h after infection (+4 h) were 1.4×10 5 , 1.70×10 6 and 2.78×10 6, the load of Escherichia coli in the peritoneal cavity of the RDP3-treated group was significantly reduced; in mice infected with Acinetobacter baumannii, the colony count (CFU) of the model group was 1.19×10 5 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 3.0×10 3 , 2.0×10 3 and 6×10 3 The load of Acinetobacter baumannii in the peritoneal cavity of the RDP3-treated group was significantly reduced; in the mice infected with Staphylococcus aureus, the colony count (CFU) of the model group mice was 1.71×10 7 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 3.0×10 5 , 2.0×10 5 and 9.4×10 6 , the load of Staphylococcus aureus in the peritoneal cavity of the RDP3-treated group was significantly reduced; in mice infected with methicillin-resistant Staphylococcus aureus, the colony count (CFU) of the model group mice was 2.76×10 6 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 1.81×10 6 , 2.10×10 6 and 1.45×10 6 , the load of methicillin-resistant Staphylococcus aureus in the peritoneal cavity of the RDP3-treated group was significantly reduced.

[0036] Example 2

[0037] In this example, it was shown that RDP3 significantly reduced the bacterial load in the peripheral blood of mice;

[0038] C57BL / 6J mice (divided into 5 groups of female mice, 6 mice in each group) were injected intraperitoneally with 2×10 7 CFU / mouse, 200 μL) of bacteria. The five groups of mice were: intraperitoneal injection of RDP3 (10 mg / kg) 8 h before (-8h), 4 h (-4 h), and 4 h after infection (+4 h), a control group (intraperitoneal injection of 200 μL of sterile PBS), and a model group (intraperitoneal injection of 200 μL of sterile PBS after infection with the tested bacteria). 18 h after infection with bacteria, blood was collected from the mouse orbital vein, and 100% of the blood was diluted with sterile PBS. -3 The diluted blood (100 μL) was evenly spread on the LB plate and cultured in a 37°C incubator for 16-18 h, and then the number of colonies was counted.

[0039] in, Figure 2 AD in the figure represent the effects of RDP3 on the bacterial load in the peripheral blood of mice infected with Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, and methicillin-resistant Staphylococcus aureus, respectively; Figure 2 The results showed that the bacterial load in the blood of mice treated with RDP3 was significantly reduced compared with that of mice in the model group. Among the mice infected with E. coli, the colony count (CFU) of mice treated with PBS was 5.93×10 5 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at 8 h before infection (-8 h), 4 h before infection (-4 h), and 4 h after infection (+4 h) were 2.0×10 3 , 1.0×10 4 and 5.10×10 5 The load of Escherichia coli in the peripheral blood of the RDP3-treated group was significantly reduced; in mice infected with Acinetobacter baumannii, the colony count (CFU) of the model group was 2.06×10 5 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 5.0×10 2 , 7.0×10 3 and 1.0×10 3 The load of Acinetobacter baumannii in the peripheral blood of the RDP3-treated group was significantly reduced; in the mice infected with Staphylococcus aureus, the colony count (CFU) of the model group mice was 6.92×10 5 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 9.8×10 4 , 4.7×10 4 and 5.29×10 5 , the load of Staphylococcus aureus in the peripheral blood of the RDP3-treated group was significantly reduced; in mice infected with methicillin-resistant Staphylococcus aureus, the colony count (CFU) of the model group mice was 9.34×10 5 , while the colony counts (CFU) of mice injected intraperitoneally with RDP3 at -8 h, -4 h, and +4 h were 6.26×10 5 ,7.10×10 5 and 4.58×10 5 , the load of methicillin-resistant Staphylococcus aureus in the peripheral blood of the RDP3-treated group was significantly reduced.

[0040] Example 3

[0041] In this example, it is shown that RDP3 alleviates inflammatory damage in the lungs of mice caused by bacterial infection;

[0042] The bacterial infection model was established by intraperitoneal injection of C57BL / 6J mice (female mice, 6 mice in each group). The infected mice were injected intraperitoneally (2×10 7 CFU / mouse, 200 μL) of bacteria, and intraperitoneal injection of RDP3 (10 mg / kg) 8 h (-8 h), 4 h (-4 h) and 4 h (+4 h) before bacterial infection. The model group was: intraperitoneal injection of 200 μL of sterile PBS after infection with the tested bacteria, and a non-infected PBS treatment group was set as the control group. 18 h after the mice were infected with bacteria, the mice were killed by cervical dislocation, and the lung tissues of the mice were taken, dehydrated, paraffin-embedded, sectioned, and HE-stained to observe the lesions in the lungs.

[0043] The results show Figure 3 As shown, compared with the control group, after infection with Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus or methicillin-resistant Staphylococcus aureus, the PBS-treated group mice had increased lung inflammatory cell infiltration (blue dots) and alveolar wall thickening, while intraperitoneal injection of RDP3 8 h before (-8 h), 4 h (-4 h) and 4 h after infection (+4 h) reduced the inflammatory cell infiltration in the mouse lungs and alleviated the thickening of the alveolar wall caused by bacterial infection. The results showed that RDP3 alleviated the lung inflammatory damage caused by bacterial infection.

[0044] Example 4

[0045] In this example, it is shown that RDP3 inhibits the production of pro-inflammatory cytokines caused by bacterial infection;

[0046] The bacterial infection model was established by intraperitoneal injection of C57BL / 6J mice (female mice, 6 mice in each group). The infected mice were injected intraperitoneally (2×10 7 CFU / mouse, 200 μL) of bacteria, RDP3 (10 mg / kg) was intraperitoneally injected 8 h (-8 h) and 4 h (-4 h) before bacterial infection and 4 h (+4 h) after infection. The model group was intraperitoneally injected with 200 μL of sterile PBS after infection with the tested bacteria, and a non-infected PBS treatment group was set as the control group. 18 h after infection with bacteria, blood was collected from the orbital vein of mice, and the levels of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in serum were detected by ELISA.

[0047] in, Figure 4 AD in the figure represent: the effect of RDP3 on the production of proinflammatory cytokines in peripheral blood of Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and methicillin-resistant Staphylococcus aureus infection; Figure 4The results showed that compared with the mice in the control group, the levels of proinflammatory cytokines TNF-α, IL-1β and IL-6 in the peripheral blood of the model group mice were significantly increased after infection with Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and methicillin-resistant Staphylococcus aureus, while intraperitoneal injection of RDP3 8 h (-8 h), 4 h (-4 h) and 4 h (+4 h) before bacterial infection inhibited the increase of proinflammatory cytokines TNF-α, IL-1β and IL-6 in the peripheral blood of mice caused by bacterial infection.

[0048] Example 5

[0049] In this example, it was shown that RDP3 increased the survival rate of mice infected with lethal doses of bacteria;

[0050] C57BL / 6J mice (female mice, 8 mice per group) were infected by intraperitoneal injection (4×10 7 The mice were intraperitoneally injected with RDP3 (10 mg / kg) 8 h before (-8 h) and 4 h after (+4 h) bacterial infection. The survival rate of mice in each group was monitored within 7 days after infection with a lethal dose of bacteria.

[0051] like Figure 5 A and B in the figure represent the effects of RDP3 on the survival rate of mice infected with lethal doses of Escherichia coli and Staphylococcus aureus, respectively; Figure 5 The results showed that after infection with lethal doses of Escherichia coli and Staphylococcus aureus, the survival rate of mice infected with Escherichia coli treated with PBS within 7 days was only 15%, and all mice infected with Staphylococcus aureus treated with PBS died on the second day, with a survival rate of 0 within 7 days. Intraperitoneal injection of RDP3 into mice at - 8 h and + 4 h increased the survival rate of mice with sepsis induced by lethal doses of bacteria.

[0052] Example 6

[0053] In this example, it was demonstrated that RDP3 improved the survival rate of mice with cecal ligation and puncture (CLP)-induced sepsis;

[0054] Sepsis was induced in mice by cecal ligation and puncture (CLP). A single dose of 10 mg / kg RDP3 was intraperitoneally injected 8 h before surgery to observe the effect of RDP3 on the survival rate of mice with CLP-induced sepsis. Mice in the sham operation group served as normal controls.

[0055] The results are as follows Figure 6As shown, there was no death in the sham-operated mice. Compared with the sham-operated mice, the survival rate of CLP mice in the PBS-treated group was significantly decreased, while intraperitoneal injection of RDP3 into mice 8 h before CLP significantly increased the survival rate of CLP mice. The results showed that RDP3 improved the survival rate of mice with sepsis induced by cecal ligation and puncture (CLP).

[0056] Example 7

[0057] In this example, it is demonstrated that RDP3 is unable to inhibit bacterial growth;

[0058] Next, this example explored the antibacterial mechanism of the small molecule peptide RDP3. First, the minimum inhibitory concentration (MIC) of RDP3 against the tested bacteria was determined to explore whether RDP3 could inhibit the growth of bacteria. The bacteria were diluted to 10 5 CFU / mL. A series of two-fold dilutions of RDP3 (50 μL / well) were prepared in a 96-well plate, and then an equal volume of bacterial dilutions was added to make the concentrations of RDP3 tested 200, 100, 50, 25, 12.5, 6.25, 3.125, and 1.5625 μg / mL, respectively, and cultured at 37°C for 18 hours. The antimicrobial peptide Hc-CATH was used as a positive control.

[0059] The results are shown in Table 1. RDP3 cannot inhibit the growth of Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and methicillin-resistant Staphylococcus aureus at a concentration of up to 200 μg / mL, while the reported positive control antimicrobial peptide Hc-CATH can inhibit the growth of Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and methicillin-resistant Staphylococcus aureus at 4.69, 4.69, 2.34 and 2.34 μg / mL, respectively. The results show that RDP3 cannot inhibit the growth of bacteria.

[0060] Table 1 Minimum inhibitory concentration of RDP3

[0061]

[0062] Example 8

[0063] In this example, it is shown that RDP3 has no killing effect on bacteria;

[0064] In this example, the killing effect of RDP3 on the tested bacteria was determined by a bactericidal kinetics experiment, the antimicrobial peptide Hc-CATH was used as a positive control, and PBS was used as a negative control. The tested bacteria were diluted to 10 5CFU / mL. RDP3 (200 μg / mL), Hc-CATH (1×MIC) or an equal volume of PBS were incubated with the diluted test bacterial solution at 37°C for 0, 1, 2, 3 and 4 hours. At each time point, the bacterial solution was aspirated, diluted 1000 times in LB broth, and the mixture (50 μL) was spread on LB agar plates. After incubation at 37°C for 12 hours, the colonies were counted.

[0065] Figure 7 AD in the figure represent the bactericidal experimental data of RDP3 against Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and methicillin-resistant Staphylococcus aureus, respectively. Figure 7 The results in the results showed that RDP3 at a concentration of up to 200 µg / mL could not kill Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, and MRSA after incubation for 4 hours. The positive control Hc-CATH at a concentration of 1×MIC killed Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, and MRSA after incubation for 1 hour. The results showed that RDP3 had no killing effect on bacteria.

[0066] Example 9

[0067] In this example, it is demonstrated that RDP3 does not affect the metabolic activity of bacteria;

[0068] In this example, the effect of RDP3 on bacterial metabolic activity was further determined, and the antimicrobial peptide Hc-CATH was used as a positive control, and PBS was used as a negative control. The bacteria were diluted to 10 5 CFU / mL, RDP3 (200 μg / mL), Hc-CATH (1×MIC) or an equal volume of PBS was added. After incubation at 37°C for 1, 2, 3, and 4 h, the incubated bacterial solution (100 μL / well) was pipetted into a 96-well plate, CCK-8 (10 μL / well) was added, and the absorbance at 450 nm was monitored. Metabolic activity was expressed as a percentage of the PBS incubation group.

[0069] like Figure 8 AD in the figure respectively reflects the effects of RDP3 on the metabolic activities of Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and MRSA; Figure 8The results in the results showed that at a concentration of up to 200 µg / mL, after incubation with Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus and MRSA for 4 h, there was no significant effect on the metabolic activity of the bacteria; while the positive control Hc-CATH at a concentration of 1× MIC significantly inhibited the metabolic activity of the bacteria after incubation with Escherichia coli for 1 h, and significantly inhibited the metabolic activity of the bacteria after incubation with Acinetobacter baumannii, Staphylococcus aureus and MRSA for 2 h. The results showed that RDP3 did not affect the metabolic activity of the bacteria.

[0070] Example 10

[0071] In this example, it is demonstrated that RDP3 can recruit phagocytes to the site of infection;

[0072] In the early stage of bacterial infection, the number of local phagocytes in the body is crucial for the clearance of local bacteria. It was previously found that RDP3 could not inhibit bacterial growth, had no killing effect on bacteria, and did not affect the metabolic activity of bacteria, indicating that RDP3 does not have a direct antibacterial effect like traditional antimicrobial peptides. RDP3 lacks direct antibacterial effect. In order to explore whether RDP3 exerts its antibacterial effect by regulating the number of local phagocytes in the body, mice were intraperitoneally injected with RDP3 (10 mg / kg). 4 h and 8 h after injection, the peritoneal lavage fluid of the mice was collected for cell counting, and 0.5 μL of APC-Cy7-CD45 (Biolegend), PE-CD11b (Biolegend), PE-Cy7-Ly6G (Biolegend), FITC-Ly6C (Biolegend), and APC-F4 / 80 (Biolegend) were added, and incubated at 4°C in the dark for 25 min. Lymphoid system: 0.5 μL each of APC-CD45 (Biolegend), FITC-CD3 (Biolegend), APC-Cy7-CD4 (Biolegend), PE-Cy7-CD8 (Biolegend), and PE-B220 (Biolegend), incubated at 4°C in the dark for 25 min. After staining, the proportion of each phagocyte subset was detected by flow cytometry. At the same time, the PBS treatment group was set as the control group.

[0073] Fig. 9 A in the figure is the proportion of myeloid-derived cell subsets in the mouse peritoneal lavage fluid. Fig. 9 B in the figure is the absolute number of white blood cells, myeloid cells, neutrophils, and monocytes / macrophages in peritoneal lavage.

[0074] Fig. 9The results showed that RDP3 could recruit neutrophils and monocytes / macrophages to the peritoneal cavity. Compared with the control group, the number of neutrophils in the peritoneal cavity increased by about 2.98×10-1 at 4 h and 8 h after RDP3 injection. 4 , 1.24×10 4 , the proportion of neutrophils increased by 6.17% and 6.44% respectively. Ly6C high The number of monocytes increased by 1.36×10 4 , 1.58×10 4 , Ly6C low The number of monocytes increased by 6.77×10 4 , 4.5×10 4 ; This indicates that RDP3 can recruit macrophages to the site of infection.

[0075] In the description of this specification, the description with reference to the terms "one embodiment", "example", "specific example", etc. means that the specific features, structures, materials or characteristics described in conjunction with the embodiment or example are included in at least one embodiment or example of the present invention. In this specification, the schematic representation of the above terms does not necessarily refer to the same embodiment or example. Moreover, the specific features, structures, materials or characteristics described can be combined in any one or more embodiments or examples in a suitable manner.

[0076] The above shows and describes the basic principles, main features and advantages of the present invention. Those skilled in the art should understand that the present invention is not limited to the above embodiments, and the above embodiments and descriptions are only for explaining the principles of the present invention. Without departing from the spirit and scope of the present invention, the present invention may have various changes and improvements, and these changes and improvements all fall within the scope of the present invention to be protected.

Claims

1. Application of rice-derived immunomodulatory peptide RDP3 in the preparation of drugs for preventing and treating bacterial infections.

2. The use according to claim 1, characterized in that: The bacteria include Escherichia coli, Acinetobacter baumannii or Staphylococcus aureus.

3. The use according to claim 1, characterized in that: The drug includes RDP3.

4. Application of rice-derived immunomodulatory peptide RDP3 in the preparation of drugs for treating sepsis; The sepsis is caused by Escherichia coli, Acinetobacter baumannii or Staphylococcus aureus.

5. The use according to claim 4, characterized in that: The drug includes RDP3.

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