CN112121068A - Use of lactobacillus johnsonii for the prevention and/or treatment of inflammatory bowel disease - Google Patents

Use of lactobacillus johnsonii for the prevention and/or treatment of inflammatory bowel disease Download PDF

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CN112121068A
CN112121068A CN202011051237.4A CN202011051237A CN112121068A CN 112121068 A CN112121068 A CN 112121068A CN 202011051237 A CN202011051237 A CN 202011051237A CN 112121068 A CN112121068 A CN 112121068A
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inflammatory bowel
lactobacillus johnsonii
bowel disease
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武振龙
张云常
杨鹰
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China Agricultural University
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Abstract

The invention belongs to the field of biomedicine, and discloses application of Lactobacillus johnsonii (Lactobacillus johnsonii) in preparing a medicament for preventing and/or treating inflammatory bowel diseases and an oral microecological preparation for preventing and/or treating inflammatory bowel diseases, wherein the microecological preparation comprises the Lactobacillus johnsonii such as UMNLJ22 strain. According to the invention, spleen hyperplasia, colon shortening, colon mucosa hyperplasia and colon inflammation reaction in a mouse model of inflammatory bowel disease induced by lactobacillus johnsonii (Citrobacter rodentium) can be remarkably improved, and the lactobacillus johnsonii is found to be capable of remarkably relieving the inflammatory bowel disease of mice, so that the lactobacillus johnsonii can be used for developing and preparing medicines for preventing and/or treating the inflammatory bowel disease.

Description

Use of lactobacillus johnsonii for the prevention and/or treatment of inflammatory bowel disease
Technical Field
The invention belongs to the field of biological medicine, and relates to application of Lactobacillus johnsonii (Lactobacillus johnsonii) in preparation of a medicine for preventing and/or treating inflammatory bowel diseases and an oral microecological preparation containing the Lactobacillus johnsonii.
Background
Inflammatory Bowel Disease (IBD) is a chronic, recurrent Inflammatory bowel disease. The clinical symptoms are mainly manifested by abdominal pain, abdominal distension, diarrhea and hematochezia. The worldwide incidence of inflammatory bowel disease has increased year by year over the past few decades, making inflammatory bowel disease a significant public health problem worldwide.
Although the research on inflammatory bowel disease has been more complete and systematic in recent years, the causes and pathogenesis of inflammatory bowel disease are not well understood. Recent studies have shown that factors affecting inflammatory bowel disease mainly include genetic factors, environmental factors and the intestinal microflora. Intestinal microorganisms and their products can act as a promoter of intestinal inflammation, inducing inflammatory bowel disease, and disorders of the intestinal microflora are also a major condition of inflammatory bowel disease. Thus, the homeostasis of the gut microflora may be a major factor affecting the development and progression of inflammatory bowel disease.
Currently, the drugs for clinically treating inflammatory bowel disease mainly include: traditional anti-inflammatory drugs, immunosuppressants, antibiotics, and the like. However, these therapeutic agents are associated with certain side effects, are not suitable for long-term use, or are relatively expensive.
With the further development of the study of intestinal microorganisms, probiotics are applied for the treatment of inflammatory bowel diseases. Compared with other treatment methods, the microecological preparation such as probiotic preparation and prebiotic preparation has the advantages of small side effect, easy implementation, low treatment cost and the like. Numerous studies have shown that various probiotics such as lactic acid bacteria and bifidobacteria can alleviate inflammatory bowel disease, but certain disadvantages still exist, such as not obvious therapeutic effect.
Thus, there is a need in the art for a safe, highly effective treatment for inflammatory bowel disease without side effects.
Disclosure of Invention
As described above, there is a need in the art for a safe, highly effective, non-side-effect therapy for inflammatory bowel disease that can effectively prevent, alleviate and/or cure inflammatory bowel disease, and that is easy to implement, has few side effects, and has low treatment cost.
The inventors surprisingly found that the abundance of Lactobacillus johnsonii (Lactobacillus johnsonii) is significantly reduced in the intestine of mice with colitis induced by Citrobacter (Citrobacter rodentium); while the abundance of lactobacillus johnsonii in the intestinal tract of mice was significantly increased after the colitis was alleviated. Based on this finding, the present inventors have completed the present invention.
Accordingly, in a first aspect, the present invention provides the use of Lactobacillus johnsonii (Lactobacillus johnsonii) for the manufacture of a medicament for the prevention and/or treatment of inflammatory bowel disease.
In a second aspect, the present invention provides an oral probiotic for use in the prevention and/or treatment of inflammatory bowel disease, said probiotic comprising lactobacillus johnsonii, e.g. strain UMNLJ 22.
The invention has the beneficial effects that: the lactobacillus johnsonii can remarkably improve symptoms related to inflammatory bowel diseases, such as spleen hyperplasia, colon shortening, colon mucosa hyperplasia and colon inflammatory reaction, thereby preventing, relieving or curing the inflammatory bowel diseases. The invention provides a dominant strain for preventing, relieving or curing inflammatory bowel diseases, which can be used as an oral microecological preparation and can be used for preparing a medicament for preventing and/or treating the inflammatory bowel diseases.
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In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings will be briefly described below. It is obvious that the drawings in the following description relate only to some embodiments of the invention, and that for a person skilled in the art, other embodiments can be obtained on the basis of these drawings without inventive effort.
FIG. 1 shows the result of MegAlign alignment of the isolated nucleic acid sequences of Lactobacillus johnsonii.
FIG. 2 shows the effect of Lactobacillus johnsonii on spleen weight and colon length in a mouse model of Citrobacter-induced inflammatory bowel disease. Wherein, fig. 2A: statistics of spleen weights of mice of each group; FIG. 2B: statistics of colon length for each group of mice; FIG. 2C: schematic colon of mice for each group. Data are expressed as mean ± sem; n is 12; different letters indicate significant differences between groups, P < 0.05.
FIG. 3 shows the effect of Lactobacillus johnsonii on colonic mucosal hyperplasia in a mouse model of Citrobacter-induced inflammatory bowel disease. Wherein, fig. 3A: a graphical representation of colon morphology of mice for each group; FIG. 3B: statistics of colonic mucosal thickness of mice for each group. Data are expressed as mean ± sem; n is 12; different letters indicate significant differences between groups, P < 0.05; white scale represents 100 μm.
FIG. 4 shows the effect of Lactobacillus johnsonii on the citrate-induced proliferation of colon cells in a mouse model of inflammatory bowel disease. Wherein, fig. 4A: colon Ki67 of mice in each group+Staining results of cells (red); FIG. 4B: colon Ki67 of mice in each group+Statistics of cell numbers. Data are expressed as mean ± sem; n is 12; different letters indicate significant difference between groups, P<0.05; white scale represents 20 μm.
Figure 5 shows the effect of lactobacillus johnsonii on colonic inflammatory cell infiltration in a mouse model of citric acid bacteria induced inflammatory bowel disease. Wherein, fig. 5A: staining results of colonic inflammatory cells (red) in mice of each group; FIG. 5B: statistical results of colonic inflammatory cell infiltration in mice of each group. Data are expressed as mean ± sem; n is 6; different letters indicate significant differences between groups, P < 0.05; white scale represents 20 μm.
Detailed Description
The present invention will now be described more fully hereinafter. It is to be understood that the described embodiments are merely a subset of the present invention and not all embodiments. All other embodiments are available to the person skilled in the art based on the embodiments of the invention and are within the scope of protection of the invention.
As described above, there is a need in the art for a safe, highly effective, non-side-effect therapy for inflammatory bowel disease that can effectively prevent, alleviate and/or cure inflammatory bowel disease, and that is easy to implement, has few side effects, and has low treatment cost.
As mentioned in the background section, by "inflammatory bowel disease" is meant a chronic, recurrent inflammatory bowel disease, the clinical manifestations of which are mainly abdominal pain, abdominal distension, diarrhea and hematochezia. In addition, patients with inflammatory bowel disease also have the manifestations of spleen hyperplasia, colon shortening, colon mucosa hyperplasia, colon inflammatory reaction and the like.
The inventors surprisingly found that in the intestinal tract of mice with colitis induced by citrobacter, the abundance of lactobacillus johnsonii was significantly reduced; while the abundance of lactobacillus johnsonii in the intestinal tract of mice was significantly increased after the colitis was alleviated. Based on this finding, the present inventors have completed the present invention.
Accordingly, in a first aspect, the present invention provides the use of Lactobacillus johnsonii (Lactobacillus johnsonii) for the manufacture of a medicament for the prevention and/or treatment of inflammatory bowel disease.
As used herein, "prevention" refers to prophylactic intervention in a normal or susceptible individual, thereby protecting the individual from a disease or disorder. In the present invention, the preventive effect is exhibited in the following aspects: compared with the control group, the spleen is not proliferated, the colon length is not shortened, the colon mucosa is not proliferated, and the colon inflammatory response is not generated.
In this context, "treatment" is a therapeutic intervention administered to a diseased individual whereby the disease or condition of the diseased individual is not progressed, alleviated, or cured relative to the disease or condition of the diseased individual prior to the administration of the therapeutic intervention. In the present invention, the effect of the treatment is shown in the following aspects: the spleen hyperplasia of the mice in the treatment group is inhibited relative to the diseased group (i.e. the citrobacter gavage group), and the level is recovered to be equivalent to that of the control group; the shortening of the colon length is inhibited, and the colon length is equivalent to that of a control group; colonic mucosa hyperplasia was inhibited, returning to a level comparable to the control group, and colonic inflammatory response was significantly inhibited.
In addition, the inventors also performed sequence alignment analysis on the Lactobacillus johnsonii isolated from intestinal tracts of colitis mice. As a result, it was found that the isolate was Lactobacillus johnsonii strain UMNLJ 22. Thus, in one embodiment, the lactobacillus johnsonii is the UMNLJ22 strain.
As described above, the lactobacillus johnsonii was isolated from the intestine of mice with citrobacter induced colitis. In other words, the colitis is induced by intestinal microorganisms such as Citrobacter. Thus, in one embodiment, the colitis is an inflammatory bowel disease induced by intestinal microbes, for example an inflammatory bowel disease induced by citrobacter.
As discussed in the background section, inflammatory bowel disease can be divided into ulcerative colitis and crohn's disease.
Ulcerative colitis was first described by Willks and Moxon in 1875, was named ulcerative colitis by Willks and Boas in 1903, and was formally named chronic nonspecific ulcerative colitis by the World Health Organization (WHO) international committee for medical science, in 1973. The disease is a chronic nonspecific inflammatory disease that mainly invades the colonic mucosa, often starting from the left half colon, and progressing gradually in a continuous manner towards the proximal colon and even the entire colon. The clinical symptoms are different, the alleviation and the attack are alternated, and the patients only have colon symptoms and also have the accompanied general symptoms.
Crohn's disease, also known as Crohn's disease, granulomatous enteritis, also translated as Crohn's disease, is an inflammatory disease of the intestinal tract of unknown cause. Crohn's disease occurs in any part of the entire gastrointestinal tract, but often occurs in the terminal ileum and right colon, with abdominal pain, diarrhea, and ileus as the main symptoms, and with extra-intestinal manifestations such as fever and malnutrition. The disease course is prolonged and repeated, and the disease is not easy to be cured.
In one embodiment, the inflammatory bowel disease comprises ulcerative colitis and crohn's disease.
As will be appreciated by those skilled in the art, the lactobacillus johnsonii may also be used in combination with other drugs for the prevention and/or treatment of inflammatory bowel disease. The other drug may be 5-aminosalicylic acid.
In a second aspect, the present invention provides an oral probiotic for use in the prevention and/or treatment of inflammatory bowel disease, said probiotic comprising lactobacillus johnsonii.
In one embodiment, the lactobacillus johnsonii is lactobacillus johnsonii UMNLJ22 strain.
In this context, the term "probiotic" is intended to mean a live microbial preparation made of normal microorganisms or substances which promote the growth of microorganisms. That is, all preparations which promote the growth and reproduction of normal microbiota and inhibit the growth and reproduction of pathogenic bacteria are called "probiotics".
In one embodiment, the inflammatory bowel disease is an inflammatory bowel disease induced by intestinal microbes. In a specific embodiment, the inflammatory bowel disease is an inflammatory bowel disease induced by Citrobacter.
In one embodiment, the inflammatory bowel disease is ulcerative colitis or crohn's disease.
The invention has the beneficial effects that: the lactobacillus johnsonii can remarkably improve symptoms related to inflammatory bowel diseases, such as spleen hyperplasia, colon shortening, colon mucosa hyperplasia and colon inflammatory reaction, thereby preventing, relieving or curing the inflammatory bowel diseases. The invention provides a dominant strain for preventing, relieving or curing inflammatory bowel diseases, which can be used as an oral microecological preparation and can be used for preparing a medicament for preventing and/or treating the inflammatory bowel diseases.
Examples
The following examples are provided to better understand the present invention. The test methods in the following examples are conventional methods unless otherwise specified. The test materials used in the following examples were purchased from a conventional reagent store unless otherwise specified. It should be noted that the summary above and the detailed description below are merely intended to specifically illustrate the present invention and are not intended to limit the invention in any way. The scope of the invention is to be determined by the appended claims without departing from the spirit and scope of the invention.
Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. The terminology used in the description of the invention herein is for the purpose of describing particular embodiments only and is not intended to be limiting of the invention.
Test animal
48 SPF-grade 4-week-old female C57BL/6 mice (purchased from Beijing Huafukang laboratory animal technologies Co., Ltd.) were selected for the test, and were bred in a mouse room at 23 + -1 deg.C with an illumination time of 12 hours (8 to 20 points) per day, and the test was started after one week of adaptation to food and water intake.
Reagents and materials
Citrobacter (DBS100) was purchased from American ATCC biological resources center, accession number 51459;
the mouse maintenance ration is purchased from Beijing Huafukang biological experiment animal technology Limited, and the cargo number is 1022;
paraformaldehyde, hematoxylin and eosin dye were purchased from sequoia jinqiao biotechnology limited, beijing;
ki67 antibody was purchased from BD, CD4, CD8, CD11b, F4/80 antibody and Alexa Fluor 594 secondary antibody was purchased from Biolegend;
the UinQ-10 column type gel recovery kit was purchased from Beijing Etdelly Bio-Rad.
Main instrument equipment
A multifunctional microplate reader:
Figure BDA0002709624110000061
m, available from Molecular Devices, USA;
vertical large capacity shake incubator: ZHIY-300s, available from Shanghai ZhiChu instruments, Inc., China;
water-proof electric heating constant temperature incubator: PXY-DHS.500-BS, purchased from Shanghai leap-into group in China;
electrophoresis apparatus: Mini-DNA, available from Bio-Rad, USA;
paraffin slicer: RM2233, available from Leica, Germany;
freezing microtome: CM3050S, available from Leica, Germany;
olympus inverted microscope: CK40-SLP available from Olympus, Japan;
a digital imaging system: DP72, available from OLYMPUS, Japan;
gel imaging split system: gel Doc XR +, available from Bio-Rad, USA;
refrigerated centrifuge, Legend micro 21R, available from Thermo Fisher, USA.
Example 1 isolation, identification and culture of Lactobacillus johnsonii
1.1. Isolation of Lactobacillus johnsonii
The mouse colonic chyme was placed in a 1.5ml centrifuge tube, 500. mu.l PBS was added, and vortexed for 1 minute to completely suspend it. The resulting suspension was diluted with a 10-fold serial gradient and spread on MRS (Man, Rogosa and Sharpe) agar plates and incubated overnight at 37 ℃.
1.2. Identification of Lactobacillus johnsonii
Selecting a single clone of the lactobacillus johnsonii in an MRS liquid culture medium, performing static culture, and amplifying the 16S rDNA full length, wherein the primer sequences are respectively as follows:
27F:5’-AGAGTTTGATCCTGGCTCAG-3’;
1492R:5’-CGGYTACCTTGTTACGACTT-3’。
the PCR reaction system is shown in Table 1:
TABLE 1 PCR reaction System
Figure BDA0002709624110000071
The PCR reaction conditions were as follows:
Figure BDA0002709624110000072
detecting the obtained PCR product by using 1% agarose gel electrophoresis, purifying and recovering by using a UinQ-10 column type gel recovery kit, sequencing by using the Huada gene, and carrying out MegAlign comparison on the sequencing result.
As a result: the results of the nucleic acid sequencing and MegAlign alignment of Lactobacillus johnsonii are shown in FIG. 1. 16S rDNA full-length sequencing and sequence alignment analysis show that the obtained isolate is Lactobacillus johnsonii strain UMNLJ 22.
1.3. Culture of Lactobacillus johnsonii
Activating the lactobacillus johnsonii twice, inoculating the activated lactobacillus johnsonii to a 50mL centrifuge tube containing 50mL MRS liquid culture medium, sealing to form a micro-aerobic environment, and performing static culture in a constant temperature incubator at 37 ℃ for 24 hours for later use.
Example 2 prevention and treatment of mice with inflammatory bowel disease by Lactobacillus johnsonii
2.1. Culture of Citrobacter
After activating Citrobacter (DBS100) twice, inoculating into an Erlenmeyer flask containing 50mL LB (Luria-Bertani) culture medium, sealing to form a micro-aerobic environment, and culturing for 12 hours at 220rpm in a constant temperature shaking table at 37 ℃ for later use.
2.2. Establishment, grouping and administration of inflammatory bowel disease mouse model
After one week of acclimation, mice were randomized into 4 groups of 12 mice per body weight, including:
control group: the group of mice was drenched with PBS once every 2 days;
diseased group (i.e. citrobacter intragastric group): the mice in this group were drenched with PBS once every 2 days and 2X 10 on day 89CFU of Citrobacter, then continuing to feed for a week, wherein PBS is administered every 2 days;
prevention group: the mice were drenched 10 times every 2 days9CFU of Lactobacillus johnsonii, and administered 2X 10 by drenching on day 89CFU of Citrobacter, then continuing to feed for a week, wherein PBS is administered every 2 days;
treatment groups: mice were drenched with PBS once every 2 days and 2X 10 on day 89CFU of citrobacter, followed by one week of continued rearing, wherein lactobacillus johnsonii is administered every 2 days.
The test period was 14 days.
2.3. Sample collection
On day 15 of the experiment, the mice were fasted for 6 hours, and after blood was collected by the eyeball method, the mice were sacrificed by neck-breaking. Taking a mouse spleen and measuring the weight of the spleen; and mouse colon tissue was taken, its length was measured and representative pictures were taken, and then the colon tissue was fixed in 4% paraformaldehyde or embedded in a frozen section embedding medium.
2.4. Colon paraffin section and staining
1) Preparation of paraffin sections of colon tissue:
A. tissue dehydration, transparency and waxing: the colon tissue fixed in 4% paraformaldehyde is taken out, washed 3 times with PBS and stored in 70% ethanol; the tissue was then removed from 70% ethanol and sequentially immersed in 80% ethanol for 40 minutes, 95% ethanol for 1 hour, absolute ethanol I for 30 minutes, absolute ethanol II for 30 minutes, xylene I for 5 minutes, xylene II for 5 minutes, wax solution I for 1 hour, and wax solution II for 1 hour.
B. Embedding: and pouring the wax solution into an embedding box, placing the embedding box into the tissue block, and installing a wax holder.
C. Slicing: the wax block was cut into a wax tape 5 μm thick with a manual microtome, and then the wax tape was immersed in a water bath at 43 ℃ and allowed to adhere to the surface of the slide glass.
D. Baking slices: incubate at 37 ℃ overnight, bake the slide at 62 ℃ for 1 hour.
2) Hematoxylin-eosin staining:
A. dewaxing: the slices were sequentially immersed in xylene I10 minutes, xylene II 10 minutes, absolute ethanol 8 minutes, 95% ethanol 5 minutes, 70% ethanol 5 minutes, 50% ethanol 5 minutes, and distilled water 5 minutes.
B. Dyeing: the resulting mixture was stained by dropping hematoxylin stain for 1 minute, washed with distilled water for 3 times (2 minutes each), differentiated by 1% hydrochloric acid alcoholic solution for 5 seconds, washed with distilled water for 3 times (5 minutes each), stained by dropping eosin stain for 1 minute, and washed with distilled water for 3 times (2 minutes each).
C. Dehydrating, transparent and sealing: the slices were sequentially immersed in 70% ethanol for 2 seconds, 95% ethanol for 5 seconds, absolute ethanol for 5 minutes, xylene I for 5 minutes, and xylene II for 5 minutes, then 1 drop of neutral gum was dropped onto the slide, coverslipped, and dried overnight. The photographs were observed under a microscope. Colonic mucosal thickness was measured with ImageJ software.
2.5. Frozen colon sections and immunofluorescence staining
1) Preparation of frozen sections of colon tissue:
embedding in the frozen section embedding medium, cutting the colon tissue into strips with the thickness of 6 mu m by using a freezing microtome, and adhering the strips to the surface of a glass slide; acetone fixation for 10 minutes and storage at-80 ℃.
2) And (3) immunofluorescence staining:
A. the frozen sections were removed and returned to room temperature and washed 1 time with PBS.
B. Blocking with 3% BSA for 30 min at room temperature and washing 3 times with PBS.
C. Ki67, CD4, CD8, CD11b and F4/80 were diluted 1:200 in PBS to antibody dilutions that were dropped onto glass slides and incubated overnight at 4 ℃.
D. Washed 3 times with PBS, Alexa Fluor 594 was diluted 1:200 into antibody dilutions, dropped onto slides, and incubated at 37 ℃ for 1 hour.
E. Washed 3 times with PBS, diluted 1:1000 Hoechst 33258, dropped onto a glass slide, and incubated for 5 minutes at room temperature.
F. 1 drop of the mounting medium is dropped on the glass slide, the glass slide is covered, and the photographing is carried out under the fluorescent microscope and in the dark.
2.6. Statistical analysis
Data are presented as mean ± SEM and analyzed by one-way anova. Duncan's multiple comparisons were performed using GraphPad prism version 7.0 (GraphPad software, san Diego, Calif.) to determine differences, with P <0.05 considered significant.
2.7. Results of the experiment
(1) Effect of Lactobacillus johnsonii on spleen weight in mouse model of Citrobacter-induced inflammatory bowel disease
Spleen weight statistics for each group of mice are shown in FIG. 2A. Compared with the control group, the spleen weight of the mice in the diseased group is obviously increased, and the spleen weight of the mice in the prevention group and the mice in the treatment group are obviously smaller than that of the mice in the diseased group and are equivalent to that of the control group. The result shows that the spleen hyperplasia of the mice caused by the inflammatory bowel disease induced by the citric acid bacillus can be obviously relieved by supplementing the lactobacillus johnsonii.
(2) Effect of Lactobacillus johnsonii on Colon Length in mouse model of Citrobacter induced inflammatory bowel disease
Representative images of colon tissue length and colon length measurements for each group of mice are shown in fig. 2C, and colon length statistics for each group of mice are shown in fig. 2B. As can be seen from the figure, the colon of the mice in the affected group was significantly shortened as compared to the control group, while the colon length of the mice in both the prevention group and the treatment group was significantly longer than that in the affected group and was comparable to that in the control group. The results show that supplementation with Lactobacillus johnsonii can significantly alleviate colonic shortening caused by Citrobacter.
(3) Effect of Lactobacillus johnsonii on Colon mucosal hyperplasia in mouse model of Citrobacter-induced inflammatory bowel disease
Fig. 3A and 3B are a colon morphology diagram and a mucosal thickness statistic of each group of mice, respectively. Compared with the control group, the colon morphology of the mice of the affected group has no significant change, but the colon mucosa thickness is significantly increased, while the colon mucosa thickness of the mice of the prevention group and the treatment group is significantly smaller than that of the affected group and is equivalent to that of the control group. The results show that: lactobacillus johnsonii can significantly alleviate colonic mucosal thickening induced by citrobacter.
(4) Effect of Lactobacillus johnsonii on Colon cell proliferation in mouse model of Citrobacter-induced inflammatory bowel disease
FIGS. 4A and 4B are graphs of colon Ki67 of mice in each group+Cell staining results and statistical results. Colon epithelium Ki67 of mice in the affected group compared to control group+The number of cells is remarkably increased, and the colon epithelium Ki67 of mice in the prevention group and the treatment group+The cell number was significantly smaller than the diseased group and comparable to the control group. The results show that: lactobacillus johnsonii can significantly alleviate colonic mucosal hyperplasia induced by citrobacter.
(5) Effect of Lactobacillus johnsonii on Colon inflammatory cell infiltration in mouse model of Citrobacter-induced inflammatory bowel disease
FIGS. 5A and 5B show the results and system of colon inflammatory cell staining of mice in each groupAnd (6) calculating the result. The mice in the affected group had significantly increased colonic epithelial inflammatory cell infiltration compared to the control group, e.g., CD4+、CD8+T lymphocytes, CD11b+、F4/80+Macrophages, and colonic epithelial inflammatory cell infiltration in mice in the prophylactic and therapeutic groups was significantly less than in the diseased group. The results show that: lactobacillus johnsonii significantly ameliorates the inflammatory response of the mouse colon induced by Citrobacter.

Claims (10)

1. Use of Lactobacillus johnsonii (Lactobacillus johnsonii) for the preparation of a medicament for the prevention and/or treatment of inflammatory bowel disease.
2. The use of claim 1, wherein the lactobacillus johnsonii is strain UMNLJ 22.
3. The use according to claim 1 or 2, wherein the inflammatory bowel disease is an inflammatory bowel disease induced by intestinal microorganisms.
4. The use of claim 3, wherein the inflammatory bowel disease is an inflammatory bowel disease induced by Citrobacter rodentium.
5. The use of any one of claims 1-4, wherein the inflammatory bowel disease comprises ulcerative colitis and Crohn's disease.
6. The use according to any one of claims 1 to 5, wherein Lactobacillus johnsonii is used in combination with other drugs for the prevention and/or treatment of inflammatory bowel diseases.
7. The use of claim 4, wherein the other drug is 5-aminosalicylic acid.
8. An oral probiotic for use in the prevention and/or treatment of inflammatory bowel disease, said probiotic comprising lactobacillus johnsonii, e.g. strain UMNLJ 22.
9. The oral probiotic of claim 8, wherein said inflammatory bowel disease is an inflammatory bowel disease induced by intestinal microorganisms such as Citrobacter rodentium.
10. The oral probiotic of claim 8 or 9, wherein said inflammatory bowel disease is ulcerative colitis or crohn's disease.
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CN115737618A (en) * 2022-10-13 2023-03-07 中国农业大学 Application of alpha-ketoglutaric acid in preventing and/or treating Crohn's disease
CN115992059A (en) * 2022-07-06 2023-04-21 南京财经大学 Lactobacillus johnsonii for producing feruloyl esterase and application thereof in relieving ulcerative colitis

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CN115737618A (en) * 2022-10-13 2023-03-07 中国农业大学 Application of alpha-ketoglutaric acid in preventing and/or treating Crohn's disease

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