KABP–AB-cx13 for the alleviation of airway inflammation in a mouse model triggered by particulate matter 10(PM10) and diesel exhaust particles

Given the global burden of air pollutants, as represented by particulate matter (PM) and diesel exhaust particles (DEP) exposure, and a lack of preventive strategies, identifying safe and accessible interventions is of high public health relevance. This study investigated the protective effect of four KABP strains and their combination on airway inflammation in a PM plus DEP (PM 10 D)-induced respiratory inflammatory process model. To induce airway inflammation, BALB/c mice were intranasally exposed to PM 10 D and then orally administered for 12 days with L. plantarum KABP-033(A), −022(B), −023(C) and Pediococcus acidilactici KABP-021(D) strains alone or in various combinations. Immune cell composition, proinflammatory cytokine expression, and histopathology were evaluated in bronchoalveolar lavage fluid (BALF) and lungs. IgA and short-chain fatty acid (SCFA) levels were determined in small intestine lavage fluid. Expectorant activity was determined using phenol-red secretion. Both individual strains and various combinations protected against PM 10 D -induced lung damage, with KABP–AB-cx 13, a combination of strain A and B at a 1:3 ratio, exhibiting the most potent protective effect. KABP–AB-cx 13 inhibited the infiltration of neutrophils, the quantity of various inflammatory cells, such as CD62L − CD44 high+ , CD21/35 + B220 + , and Gr-1 + CD11b + cells, and the expression of cytokines and chemokines, including chemokine (C-X-C motif) ligand (CXCL)-1, macrophage inflammatory protein-2, tumor necrosis factor-α, interleukin (IL)-17A, IL-6, and IL-1β, in the BALF and lungs of mice with PM 10 D -triggered airway inflammation. It also decreased IL-1α and IRAK expression in alveolar macrophages along with inhibition of nuclear factor-κB (NF- κB) and JNK phosphorylation in the lungs of these mice. Furthermore, KABP–AB-cx 13 increased CD206 + F4/80 + cell numbers in mesenteric lymph nodes and IgA and SCFA levels in small intestine lavage fluid. It also exhibited better expectorant activity based on increased phenol-red secretion. KABP–AB-cx 13 suppressed the PM 10 D -induced airway inflammation and protected lung tissue from damage by inhibiting immune and inflammatory reactions in airways, activating the immune system, and increasing SCFA levels in the gut. KABP–AB-cx 13 also exhibited an expectorant effect, suggesting protective and therapeutic effects against respiratory inflammation. Overall, these findings contribute to global understanding of how probiotic interventions may help prevent or alleviate respiratory disorders induced by air pollution. • KABP–AB-cx 13 protects against PM 10 D-induced lung damage. • KABP–AB-cx 13 decreases immune responses and the expression of inflammatory cytokines in BALF and lung tissue. • KABP–AB-cx 13 inhibits NF-kB and MAPK pathways in lung. • KABP–AB-cx 13 exhibits expectoration effect.