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.

Authors

Giovanna Pinheiro Martins, João Pedro S Cândido, Rubens da Silva Araújo, Jannerson Cesar Xavier de Pontes, Rachel Passos Rezende, Carla Cristina Romano, Adailson de Souza Assunção, Daniele Idalino Janebro, Janeusa Trindade de Souto, Wallace Felipe Blohem Pessoa, Adriano Francisco Alves

Published in

International microbiology : the official journal of the Spanish Society for Microbiology. Jun 19, 2026. Epub Jun 19, 2026.

Abstract

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.
This study investigated the anti-inflammatory potential of Lactiplantibacillus plantarum 6.2 (Lp62), administered orally in a murine ALI model.
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).
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.
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.

PMID:
42319604
Bibliographic data and abstract were imported from PubMed on 19 Jun 2026.

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