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This study investigates how Lactiplantibacillus plantarum 6.2 can reduce inflammation in acute lung injury.

June 20, 2026Open Access

Oral administration of Lactiplantibacillus plantarum 6.2 mitigates acute lung injury via immunostaining of the TLR4/NF-κB pathway and reduction of IL-17 in lung tissue

Key Points

This study investigates how Lactiplantibacillus plantarum 6.2 can reduce inflammation in acute lung injury.
Thirty male Swiss mice (N = 30) were randomly assigned to five groups (n = 6).
Lactiplantibacillus plantarum 6.2 was administered orally for one week at a dose of 10⁹ CFU/mL.
Acute lung injury was induced by LPS, and lung tissues were analyzed for inflammation and biomarker levels.
Lactiplantibacillus plantarum 6.2 reduced IL-1β release in bronchoalveolar lavage fluid (BALF), with significant differences (p < 0.05).
There was a notable decrease in the activation of TLR4 and NF-κB, resulting in reduced inflammatory infiltration in lung tissues.
Macroscopic lung lesions were less severe in Lp62-treated mice compared to those with acute lung injury.

Abstract

Abstract Background Acute lung injury (ALI) is an inflammatory condition that compromises the lungs and is associated with substantial morbidity and mortality. In the absence of effective therapeutic options, the search for alternative treatments, such as probiotics, has intensified. Objective: This study investigated the anti-inflammatory potential of Lactiplantibacillus plantarum 6.2 (Lp62), administered orally in a murine ALI model. Materials and Methods Thirty male Swiss mice (N = 30) were randomly assigned to five groups (n = 6): negative control, healthy supplemented with Lp62 (Lp62), ALI, ALI supplemented with Lp62 (ALI+Lp62), and ALI treated with Dexamethasone (Dexa). Lp62 (10⁹ CFU/mL) was administered daily by oral gavage for one week. ALI was induced by intranasal instillation of LPS under anesthesia. Lungs were collected 24 h later for macroscopic examination. Histological evaluation used hematoxylin–eosin staining, and immunohistochemistry included anti-TLR4, anti-NF-κB, and anti-IL-17 antibodies. Total protein in bronchoalveolar lavage fluid (BALF) was measured by the Biuret method, and IL-1β by ELISA. Data were analyzed by one-way ANOVA with Tukey’s post hoc test (p < 0.05). Results Lp62 reduced cell migration, protein exudation, and IL-1β release in BALF, as well as macroscopic lung lesions, and attenuated histological inflammatory infiltration, increasing alveolar spaces. It also decreased TLR4, NF-κB, and IL-17 activation. Conclusion Lactiplantibacillus plantarum 6.2 is a promising therapeutic approach for ALI by inhibiting the TLR4/NF-κB pathway and reducing neutrophil recruitment via IL-17–mediated signaling in mice.

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