title: Suppressive effects of oral administration of heat-killed Lactobacillus acidophilus on T helper-17 immune responses in a bovine β-lactoglobulin-sensitized mice model.
abstract: The present study was planned to explore the effect of Lactobacillus (L.) acidophilus on the T helper-17 (Th17) immune response in a mouse model of β-lactoglobulin (β-lg) allergy. Bovine β-lg sensitised BALB/c mice were orally administered with different doses of heat-killed L. acidophilus (low, 5×10(7) colony forming unit (CFU); medium, 5×10(8) CFU; high, 5×10(9) CFU) in 200 µL of phosphate buffered saline (PBS) three times a week, starting from 1 week before β-lg sensitisation for 4 weeks. After the allergen challenge, the numbers of blood eosinophils and neutrophils were examined by light microscope; the levels of cytokine (interleukin (IL)-12, IL-4, tumor growth factor (TGF)-β, IL-10, IL-6 and IL-17A), total immunoglobulin E (IgE) and β-lg-specific IgE contents in the serum were measured with enzyme-linked immunosorbent assay (ELISA); The mRNA expression levels of TGF-β, IL-17A,CD25, Foxp3, retinoic acid-related orphan receptor γt (RORγt) and IL-10 were analyzed using real-time polymerase chain reaction (PCR). The results showed that oral administration of L. acidophilus suppressed hypersensitivity responses, attenuated the numbers of inﬂammatory cells and inhibited IgE production. We found up-regulation of TGF-β and down-regulation of IL-17A in the serum of L. acidophilus-treated group, along with IL-6 levels was significantly decreased than that of the allergy group (p<0.05). Moreover, the mRNA expression levels of CD25, forkhead box P3 and TGF-β were significantly higher in the spleen of L. acidophilus-treated group, while the mRNA expression levels of IL-17A, RORγt and IL-10 were significantly lower than that in the allergy group (p<0.05). In conclusion, the suppression of major allergic symptoms by oral administration of L.acidophilus was probably due to improve the regulatory T (Treg)/Th17 balance and inhibit the IL-6 production.
authors.affiliation: Key Laboratory of Dairy Science, Ministry of Education, College of Food Science, Northeast Agriculture University, 59 Mucai Street, Xiangfang District, Harbin, Heilongjiang 150030, China.
authors.forename: Ai-Li
authors.initials: AL
authors.lastname: Li
authors.forename: Xiang-Chen
authors.initials: XC
authors.lastname: Meng
authors.forename: Cui-Cui
authors.initials: CC
authors.lastname: Duan
authors.forename: Gui-Cheng
authors.initials: GC
authors.lastname: Huo
authors.forename: Quan-Ling
authors.initials: QL
authors.lastname: Zheng
authors.forename: Dan
authors.initials: D
authors.lastname: Li
mesh_terms: D000284:Administration, Oral; D000485:Allergens / Q000009:adverse effects*; D000818:Animals; D018926:Anti-Allergic Agents / Q000008:administration & dosage*; D002417:Cattle; D016207:Cytokines / Q000097:blood / Q000235:genetics; D005260:Female; D015870:Gene Expression; D006358:Hot Temperature; D007073:Immunoglobulin E / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000235:genetics; D007779:Lactobacillus acidophilus; D007782:Lactoglobulins / Q000009:adverse effects*; D007958:Leukocyte Count; D051379:Mice; D008807:Mice, Inbred BALB C; D016269:Milk Hypersensitivity / Q000209:etiology / Q000276:immunology / Q000628:therapy*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D058504:Th17 Cells / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D000485:Allergens; D018926:Anti-Allergic Agents; D016207:Cytokines; D053645:Interleukin-2 Receptor alpha Subunit; D007782:Lactoglobulins; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; C539901:Rorc protein, mouse; D016212:Transforming Growth Factor beta; D007073:Immunoglobulin E