A human intestinal saliva-associated lactobacillus Ligilactobacillus salivarius MTR-1105 and its application

Abstract

The present application discloses a human intestinal Ligilactobacillus salivarius MTR-1105 and its application, and relates to the field of microorganisms; the strain of the Ligilactobacillus salivarius MTR-1105 has a strain preservation number of GDMCC 65345; the present application further evaluates the biological activity of the Ligilactobacillus salivarius MTR-1105 in combination with an acute gastric mucosal injury rat model, finds that the Ligilactobacillus salivarius MTR-1105 can inhibit alcohol and non-steroidal anti-inflammatory drug-induced gastric mucosal damage and bleeding, down-regulate the expression of inflammatory factors such as IL-6 and IL-1β and the generation of MDA, and up-regulate the expression of antioxidant proteins such as CAT and SOD; the present application provides a Ligilactobacillus salivarius MTR-1105, which can be used for preparing a functional bacterial agent and a drug for protecting gastric mucosa, and has a wide application prospect.

Description

Technical Field

[0001] This invention relates to the field of microbiology, and in particular to a human intestinal saliva-associated lactobacillus (Ligilactobacillus salivarius) MTR-1105 and its applications. Background Technology

[0002] Gastric mucosal injury refers to the disruption of the integrity of the gastric mucosa caused by factors such as chemical factors (e.g., smoking, alcohol, strong tea, coffee, and medications that irritate the gastric mucosa, such as aspirin and indomethacin), physical factors (e.g., excessively cold, hot, or rough food, or overeating), and bacterial or toxin-induced stimulation. Gastroscopy reveals pathological changes such as altered gastric mucosal color, bleeding, congestion, erosion, and ulcers. Gastric mucosal injury initially manifests as the shedding and necrosis of the superficial epithelium of the gastric mucosa due to various pathogenic factors, resulting in superficial mucosal damage. Further damage can destroy microvascular endothelial cells, leading to mucosal ischemia, hypoxia, and tissue necrosis, thus causing deep mucosal damage (erosion or ulceration). Gastric mucosal injury typically causes gastrointestinal symptoms such as stomach pain, bloating, acid reflux, heartburn, nausea, and vomiting. If left untreated, it can lead to serious complications such as gastritis, gastric ulcers, and even gastric bleeding and perforation. Due to the stomach's unique physiological functions and environment, the repeated presence of irritants such as food, microorganisms, and gastric acid leads to the continuous development of gastric mucosal damage, seriously affecting patients' health and quality of life.

[0003] Currently, mild gastric mucosal damage can be improved by removing causative factors (such as eradicating Helicobacter pylori, discontinuing suspected medications, and correcting unhealthy dietary habits) and adjusting lifestyle (such as maintaining good living habits, regular sleep patterns, quitting smoking and limiting alcohol consumption, and avoiding overwork and mental stress). For moderate to severe gastric mucosal damage, interventions such as drugs that inhibit gastric acid secretion and drugs that protect the gastric mucosa can be used to promote gastric mucosal repair. However, drug treatment has many adverse reactions and cannot provide long-term effectiveness or prevent disease recurrence.

[0004] The gut microbiota is crucial for maintaining gastrointestinal homeostasis. A healthy, balanced gut microbiota promotes food digestion, degrades exogenous foreign substances, and secretes mucins, thereby isolating toxic metabolites from the gastric mucosa, maintaining intestinal immune balance, eliminating pathogen invasion, and protecting the gastric mucosa from various pathological factors. Many probiotics have been found to have protective effects on the gastric mucosa, but these strains are mostly isolated from the environment, plants, or animals. Human-derived microbiota mainly exist on the human body surface, in the oral cavity, and in the gastrointestinal tract. Through long-term symbiotic relationships with the human body, they have adapted to the relatively stable internal environment (such as temperature, pH, and nutritional conditions), forming special surface structures that are easier to colonize in the human body; compared with non-human-derived microbiota, they have higher safety and easier colonization. *Lactobacillus salivarius* is mainly found in human saliva and can also be detected in the gastrointestinal tract. It can produce lactase, which helps in the digestion and absorption of lactose. However, there are no reports or applications of *Lactobacillus salivarius* protecting against gastric mucosal damage. This invention provides a healthy human gut-derived Lactobacillus saliva MTR-1105. We are the first to comprehensively utilize microbiological and pharmacological experimental techniques to discover that Lactobacillus saliva MTR-1105 alleviates acute gastric mucosal damage in rats induced by alcohol and nonsteroidal anti-inflammatory drugs, and has broad application prospects in the field of clinical application development. Summary of the Invention

[0005] This invention provides a human intestinal saliva combined with Lactobacillus MTR-1105 and its application, in order to solve the problems existing in the prior art.

[0006] To achieve the above objectives, the present invention provides a human intestinal Lactobacillus salivae MTR-1105, the strain preservation number of which is GDMCC 65345.

[0007] The present invention also provides the application of the aforementioned Lactobacillus saliva-associated MTR-1105 in the preparation of products for the prevention and treatment of acute gastric mucosal injury.

[0008] Furthermore, the gastric mucosal damage was induced by chemical factors.

[0009] Furthermore, the gastric mucosal damage can be induced by alcohol or nonsteroidal anti-inflammatory drugs.

[0010] Furthermore, the chemical factors include alcohol or nonsteroidal anti-inflammatory drugs.

[0011] Furthermore, the strain may be in the form of cream, dried form, lyophilized form, or paste.

[0012] Furthermore, the composition comprising the strain, and derivatives thereof, wherein the derivatives are selected from: live cells, inactivated cells, lyophilized bacterial powder, strain metabolites, cell lysates, or cell autolyses.

[0013] Furthermore, the composition is a functional microbial agent (such as a probiotic preparation) or a drug.

[0014] Furthermore, the functional microbial agent is a probiotic preparation.

[0015] Furthermore, the drug also contains a pharmaceutically acceptable carrier.

[0016] This invention discloses the following technical effects: This invention isolates and identifies a species of *Lactobacillus salivarius*, MTR-1105, from fecal samples of healthy individuals. Further evaluation of its bioactivity using a rat model of acute gastric mucosal injury revealed that *Lactobacillus salivarius* MTR-1105 can inhibit gastric mucosal damage and bleeding, downregulate the expression of inflammatory factors such as IL-6 and IL-1β and the production of peroxidation products such as MDA, and upregulate the expression of antioxidant functional proteins such as CAT and SOD, thus preventing or treating acute gastric mucosal injury. This invention not only clarifies the important role of this bacterium in acute gastric mucosal injury but also reveals its broad application prospects in the prevention and treatment of acute gastric mucosal injury. Attached Figure Description

[0017] To more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the drawings used in the embodiments will be briefly introduced below. Obviously, the drawings described below are only some embodiments of the present invention. For those skilled in the art, other drawings can be obtained based on these drawings without creative effort.

[0018] Figure 1 The figure shows the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced gastric mucosal damage in rats in Example 2 (*, P<0.05; ***, P<0.001).

[0019] Figure 2 Figure 2 shows the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced HE and PAS staining of rat gastric mucosa.

[0020] Figure 3 This is a diagram illustrating the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced expression of MUC5AC and MUC6 in the gastric mucosa of rats in Example 2.

[0021] Figure 4 Figure 2 shows the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced ZO-1 expression in rat gastric mucosa.

[0022] Figure 5The graph shows the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced gastric mucosal tissue and plasma CAT, MDA, and SOD levels in rats in Example 2 (*, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001).

[0023] Figure 6 The graph shows the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced IL-1β and IL-6 levels in rat gastric mucosa in Example 2 (***, P<0.001).

[0024] Figure 7 The figure shows the effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced gastric mucosal damage in rats in Example 3 (**, P<0.01).

[0025] Figure 8 Figure 3 shows the effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced HE and PAS staining of rat gastric mucosa.

[0026] Figure 9 Figure 3 shows the effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced expression of MUC5AC and MUC6 in rat gastric mucosa.

[0027] Figure 10 The figure shows the effect of saliva combined with Lactobacillus MTR-1105 on the levels of CAT, MDA, and SOD in rat gastric mucosa and plasma induced by indomethacin in Example 3 (*, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001).

[0028] Specific embodiments of the present invention

[0029] The technical solutions of the embodiments of the present invention will be clearly and completely described below with reference to the accompanying drawings. Obviously, the described embodiments are only some embodiments of the present invention, and not all embodiments. All other embodiments obtained by those skilled in the art based on the embodiments of the present invention without creative effort are within the scope of protection of the present invention.

[0030] To make the above-mentioned objects, features and advantages of the present invention more apparent and understandable, the present invention will be further described in detail below with reference to the accompanying drawings and specific embodiments.

[0031] Example 1: Isolation and Identification of Strains

[0032] In a clean environment, fresh fecal samples from healthy individuals were collected, diluted with sterile water, and spread onto lactic acid bacteria (MRS) medium. The samples were incubated at 37°C for 2–3 days. When significant bacterial colonies were observed, morphologically different colonies were picked and inoculated onto freshly prepared MRS medium. Incubation at 37°C was continued for 2 days. When monoclonal colonies were observed, these were further inoculated onto freshly prepared MRS medium and incubated at 37°C for 2 days to obtain purified colonies, designated MTR-1105. The bacterial cells were then placed in a 20% glycerol aqueous solution and stored at -80°C. Simultaneously, the samples were entrusted to a cultural heritage center for identification. Reverse transcription polymerase chain reaction (RT-PCR) was performed using 16S rDNA primers, and 16S rRNA gene sequencing analysis was performed on the isolated strain. BLAST comparison with the National Center for Biotechnology Information (NCBI) nucleic acid database confirmed the species as *Ligilactobacillus salivarius* (99.57% homology). The strain of *Lactobacillus salivarius* MTR-1105 has been deposited at the Guangdong Provincial Center for Microbial Culture Collection (accession number GDMCC 65345, address: No. 100, Xianlie Middle Road, Yuexiu District, Guangzhou, Guangdong Province).

[0033] Nucleotide sequence of 16S rRNA:

[0034] TCTGTCGTCTGCCTATACTGCAAGTCGAACGAAACTTTCTTACACCGAATGCTTGCATTCACCGTAAGAAGTTGAGTGGCGGACGGGTGAGTAACACGTGGGTAACCTGCCTAAAAGAAGGGGATAACACTTGGAAACAGGTGCTAATACCGTATATCTCTAAGGATCGCATGATCCTTAGATGAAAGATGGTTCTGCTATCGCTTTTAGATGGACCCGCGGCGTATTAACTAGTTGGTGGGGTAACGGCCTACCAAGGTGATGATACGTAGCCGAACTGAGAGGTTGATCGGCCACATTGGGACTGAGACACGGCCCAAACTCCTACGGGAGGCAGCAGTAGGGAATCTTCCACAATGGACGCAAGTCTGATGGAGCAACGCCGCGTGAGTGAAGAAGGTCTTCGGATCGTAAAACTCTGTTGTTAGAGAAGAACACGAGTGAGAGTAACTGTTCATTCGATGACGGTATCTAACCAGCAAGTCACGGCTAACTACGTGCCAGCAGCCGCGGTAATACGTAGGTGGCAAGCGTTGTCCGGATTTATTGGGCGTAAAGGGAACGCAGGCGGTCTTTTAAGTCTGATGTGAAAGCCTTCGGCTTAACCGGAGTAGTGCATTGGAAACTGGAAGACTTGAGTGCAGAAGAGGAGAGTGGAACTCCATGTGTAGCGGTGAAATGCGTAGATATATGGAAGAACACCAGTGGCGAAAGCGGCTCTCTGGTCTGTAACTGACGCTGAGGTTCGAAAGCGTGGGTAGCAAACAGGATTAGATACCCTGGTAGTCCACGCCGTAAACGATGAATGCTAGGTGTTGGAGGGTTTCCGCCCTTCAGTGCCGCAGCTAACGCAATAAGCATTCCGCCTGGGGAATACGACCGCAAGGTTGAAACTCAAAGGAATTGACGGGGGCCCGCACAAGGGGGGAACA

[0035] Example 2: Mitigation effect of Lactobacillus salivarius MTR-1105 on alcohol-induced gastric mucosal injury in rats

[0036] Male SD rats aged 6-8 weeks were randomly divided into 5 groups (control group, Lactobacillus saliva-associated MTR-1105 control group, alcohol model group, Lactobacillus saliva-associated MTR-1105 treatment group, and ranitidine treatment group) after 1 week of acclimatization, with 5 rats in each group.

[0037] From day 1 to 14, rats in the saliva-containing Lactobacillus MTR-1105 control group and the saliva-containing Lactobacillus MTR-1105 treatment group were administered saliva-containing Lactobacillus MTR-1105 bacterial suspension (5 × 10⁻⁶) by gavage. 9 Rats in the ranitidine group were administered ranitidine (20 mg / kg, suspended in physiological saline) by gavage; rats in the control group and the alcohol model group were administered the same volume of physiological saline by gavage.

[0038] On day 15, rats in the alcohol model group, the saliva-combined Lactobacillus MTR-1105 treatment group, and the ranitidine treatment group were administered 1 ml of anhydrous ethanol by gavage to induce acute gastric mucosal injury. Two hours later, the stomachs of rats in each group were harvested, cut open along the greater curvature to expose the gastric mucosa, and photographs were taken. Simultaneously, the length and width of bleeding points and bleeding bands were measured using calipers, and a gastric mucosal injury score was calculated. The criteria are shown in the table below. Because the width represents a much greater degree of injury severity than the length, the width index was given double the score.

[0039]

[0040] Gastric mucosal damage and scoring results as follows Figure 1 As shown in the figure. The results showed that the gastric mucosa of rats in the control group and the saliva-combined Lactobacillus MTR-1105 control group exhibited normal gastric tissue structure and morphology, without damage, with a glossy and smooth surface, and numerous and neatly arranged gastric folds. The gastric mucosa of rats in the alcohol model group was severely damaged, showing a red congested state and a certain number of ulcers and bleeding points, with fewer gastric tissue folds, and significantly increased gastric mucus compared with the control group. The gastric mucosa of rats in the saliva-combined Lactobacillus MTR-1105 treatment group and the ranitidine treatment group showed a light pink congested state and a few ulcers and bleeding points, with a slightly glossy gastric wall surface and clearer folds; compared with the alcohol model group, the degree of gastric mucosal damage in rats was significantly alleviated.

[0041] Tissue samples from the most severely hemorrhagic rat gastric mucosa were excised, fixed in 10% formalin solution, and stained with hematoxylin-eosin (HE) and periodic acid Schiff (PAS) for microscopic observation. Figure 2As shown, the gastric mucosa of rats in the control group and the saliva-treated group combined with Lactobacillus MTR-1105 showed intact structure, with tightly packed epithelial cells and no bleeding, inflammatory cell infiltration, or submucosal edema. The alcohol-induced model group exhibited significant pathological changes in the gastric mucosa, with disordered gastric gland structure, severe epithelial cell loss, widespread mucosal congestion, inflammatory cell infiltration, and severe submucosal edema. Compared with the alcohol-induced model group, the gastric mucosal damage in the saliva-treated group combined with Lactobacillus MTR-1105 and the ranitidine-treated group was relatively mild, with reduced gastric gland structural loss and disorder, and improved epithelial cell shedding and inflammatory cell infiltration. The results indicate that saliva-treated group combined with Lactobacillus MTR-1105 inhibits alcohol-induced pathological changes in the rat gastric mucosa.

[0042] PAS staining showed that the gastric mucosa of rats in the control group and the saliva-treated Lactobacillus MTR-1105 control group was covered with a complete and uninterrupted purplish-red mucus layer. In the alcohol-induced model group, a large number of epithelial cells sloughed off, the mucosal structure was destroyed, and a complete mucus layer could not be observed. The gastric mucosa of rats in the saliva-treated Lactobacillus MTR-1105 and ranitidine treatment groups showed intact structure and increased mucus distribution, similar in morphology to the gastric mucosa of healthy control rats. The results indicate that saliva-treated Lactobacillus MTR-1105 inhibits alcohol-induced loss of mucus protein in the rat gastric mucosa and improves the mucus barrier function of the gastric mucosa.

[0043] Mucin 5AC (MUC5AC) and mucin 6 (MUC6) are important components of gastric mucus proteins. Further immunofluorescence staining of gastric mucosal tissue was performed to observe the expression of MUC5AC and MUC6 in the gastric mucosa. Figure 3 As shown, the control group and the saliva-combined Lactobacillus MTR-1105 control group rats had a higher number of MUC5AC and MUC6 positive cells; the model group showed gastric mucosal surface damage, with low expression of MUC5AC and MUC6; the saliva-combined Lactobacillus MTR-1105 treatment group and the ranitidine treatment group rats had basically intact gastric mucosal structure, with significantly increased expression of MUC5AC and MUC6. These results further demonstrate that saliva-combined Lactobacillus MTR-1105 reverses the alcohol-induced reduction in MUC5AC and MUC6 expression, thereby maintaining the integrity of the mucus layer and enhancing the mucus barrier function.

[0044] Further immunohistochemical staining of gastric mucosal tissue was performed to observe the expression of the tight junction protein ZO-1 in the gastric mucosal epithelial barrier. Figure 4As shown, compared with the control group and the control group treated with Lactobacillus saliva combined with MTR-1105, the expression of ZO-1 protein in the gastric mucosa of rats in the alcohol-induced model group was significantly decreased. The expression of ZO-1 in the gastric mucosa of rats treated with Lactobacillus saliva combined with MTR-1105 and ranitidine was significantly restored. The results indicate that Lactobacillus saliva combined with MTR-1105 upregulates the expression of tight junction-related proteins in the gastric mucosa, maintaining the mechanical barrier function of the gastric mucosa.

[0045] Gastric mucosal tissue from each group of rats was weighed, added to pre-cooled physiological saline, homogenized, and centrifuged for 10 minutes (1000 × g, 4°C). The supernatant was collected. The levels of SOD, MDA, and CAT in the gastric tissue of each group were detected according to the instructions of the superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) kits. Figure 5 As shown, the alcohol-induced model group exhibited increased MDA production and decreased CAT and SOD levels in the gastric mucosa of rats. Compared to the model group, the saliva-treated group combined with Lactobacillus MTR-1105 and the ranitidine-treated group showed significantly reduced MDA content and significantly increased CAT and SOD activities in the gastric mucosa of rats. These results further demonstrate that the saliva-treated group combined with Lactobacillus MTR-1105 alleviates gastric mucosal damage by reducing oxidative stress levels.

[0046] Gastric mucosal tissues from rats in each group were weighed, total RNA was extracted, reverse transcribed, and the expression levels of inflammatory factors such as interleukin-1β (IL-1β) and interleukin-6 (IL-6) were measured using real-time quantitative PCR (qPCR) to evaluate the inflammatory response of the rat gastric mucosa. Figure 6 As shown, the expression of IL-1β and IL-6 in the gastric mucosa of rats in the alcohol-induced model group was significantly increased. Compared with the model group, the level of inflammation in the gastric mucosa of rats treated with saliva combined with Lactobacillus MTR-1105 and ranitidine was significantly reduced. The results indicate that saliva combined with Lactobacillus MTR-1105 inhibits the inflammatory response and alleviates gastric mucosal damage.

[0047] Gastric mucosal tissues from rats in each group were weighed and proteins were extracted. Western blot analysis was used to detect the expression of oxidative stress-related proteins Nrf2 and heme oxygenase-1 (HO-1), apoptosis-related proteins B-cell lymphoma-2 (Bcl-2) and apoptosis regulator (Bax), and inflammation-related protein cyclooxygenase-2 (COX-2). The results showed that saliva combined with Lactobacillus MTR-1105 colonization improved the alcohol-induced decrease in Nrf2, HO-1, and Bcl-2 expression in rat gastric mucosa and alleviated the alcohol-induced increase in COX-2 and Bax expression. This indicates that saliva combined with Lactobacillus MTR-1105 inhibits oxidative stress, inflammation, and apoptosis in gastric mucosa and alleviates gastric mucosal damage.

[0048] Example 3: Alleviating effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced gastric mucosal damage in rats

[0049] Male SD rats aged 6-8 weeks were randomly divided into 4 groups (control group, indomethacin model group, saliva combined with Lactobacillus MTR-1105 treatment group, and ranitidine treatment group) after 1 week of acclimatization, with 5 rats in each group.

[0050] Days 1-14, saliva combined with Lactobacillus MTR-1105 treatment group: Rats were administered saliva combined with Lactobacillus MTR-1105 bacterial suspension (5×10⁻⁶) by gavage. 9 Rats in the ranitidine group were administered ranitidine (20 mg / kg, suspended in physiological saline) by gavage; rats in the control group and the alcohol model group were administered the same volume of physiological saline by gavage.

[0051] On day 15, rats in the indomethacin model group, the saliva-combined Lactobacillus MTR-1105 treatment group, and the ranitidine treatment group were administered indomethacin (25 mg / kg) by gavage to induce acute gastric mucosal injury. Two hours later, the stomachs of rats in each group were harvested, cut open along the greater curvature to expose the gastric mucosa, and photographs were taken. Simultaneously, the length and width of bleeding points and bleeding bands were measured using calipers, and the gastric mucosal injury score was calculated. The gastric mucosal and pathological scores of rats in each group are shown below. Figure 7 As shown, the gastric mucosa of rats in the indomethacin model group exhibited a red congested state and linear hemorrhages, with fewer gastric tissue folds. The gastric mucosa of rats treated with saliva combined with Lactobacillus MTR-1105 and ranitidine showed a light pink congested state and a few hemorrhages, with a slightly glossy gastric wall surface, clearer folds, and significantly reduced gastric mucosal injury scores, indicating a significant alleviation of gastric mucosal damage.

[0052] Tissue samples from the most severely hemorrhagic gastric mucosa of rats were excised, fixed in 10% formalin solution, and stained with hematoxylin and eosin (HE) and eosin (PAS) for microscopic observation. Figure 8 As shown, treatment with saliva combined with Lactobacillus MTR-1105 and ranitidine significantly reversed indomethacin-induced pathological changes in rat gastric mucosa, restored the number and structural arrangement of gastric glands, and reduced epithelial cell shedding and inflammatory cell infiltration. The results indicate that saliva combined with Lactobacillus MTR-1105 inhibits alcohol-induced pathological changes in rat gastric mucosa.

[0053] PAS staining showed that the gastric mucosa of rats treated with saliva combined with Lactobacillus MTR-1105 and ranitidine recovered structural integrity, with increased mucus distribution and a relatively continuous purplish-red mucus layer re-covering the gastric mucosal surface. The results indicated that saliva combined with Lactobacillus MTR-1105 inhibited indomethacin-induced loss of mucus protein in rat gastric mucosa and improved the mucus barrier function of the gastric mucosa.

[0054] Simultaneously, the expression of MUC5AC and MUC6 in gastric mucosal tissue was observed by immunofluorescence staining, and the results were as follows: Figure 9 As shown, *Lactobacillus saliva-associated* MTR-1105 and ranitidine significantly reversed the indomethacin-induced decrease in MUC5AC and MUC6 expression in rat gastric mucosa. These results further demonstrate that *Lactobacillus saliva-associated* MTR-1105 upregulates MUC5AC and MUC6 expression, enhances mucus barrier function, and alleviates indomethacin-induced gastric mucosal damage in rats.

[0055] Further analysis was conducted to detect the levels of SOD, MDA, and CAT in the gastric tissue of each group. Figure 10 As shown, compared with the indomethacin-induced model group, the MDA content and CAT and SOD activities in the gastric mucosa of rats treated with saliva combined with Lactobacillus MTR-1105 and ranitidine were significantly reduced. These results further demonstrate that saliva combined with Lactobacillus MTR-1105 alleviates gastric mucosal damage by reducing oxidative stress levels.

[0056] The above description of the disclosed embodiments enables those skilled in the art to make or use the invention. Various modifications to these embodiments will be readily apparent to those skilled in the art, and the general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of the invention. Therefore, the invention is not to be limited to the embodiments shown herein, but is to be accorded the widest scope consistent with the principles and novel features disclosed herein.

Claims

1. A strain of human intestinal saliva-associated lactobacillus (Ligilactobacillus salivarius) MTR-1105, deposited at Guangdong Provincial Microbial Culture Collection Center, accession number GDMCC 65345.

2. A composition, characterized in that, It includes the strain described in claim 1.

3. The composition according to claim 2, characterized in that, The composition is a functional microbial agent.

4. The composition according to claim 3, characterized in that, The functional microbial agent is a probiotic preparation.

5. The composition according to claim 2, characterized in that: The composition is a drug and contains a pharmaceutically acceptable carrier.

6. Use of the composition according to any one of claims 2-5 in the preparation of an agent for the prevention or treatment of acute gastric mucosal injury caused by alcohol or indomethacin.

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