Lactobacillus acidophilus alleviates the inflammatory response to enterotoxigenic Escherichia coli K88 via inhibition of the NF-κB and p38 mitogen-activated protein kinase signaling pathways in piglets.
BACKGROUND
A newly isolated L. acidophilus strain has been reported to have potential anti-inflammatory activities against lipopolysaccharide (LPS) challenge in piglet, while the details of the related inflammatory responses are limited. Here we aimed to analysis the ability of L. acidophilus to regulate inflammatory responses and to elucidate the mechanisms involved in its anti-inflammatory activity.


RESULTS
The ETEC (enterotoxigenic Escherichia coli) K88-induced up-regulations of IL-1β, IL-8 and TNF-α were obviously inhibited by L. acidophilus while IL-10 was significantly increased. Moreover, L. acidophilus down-regulated pattern recognition receptors TLR (Toll-like receptor) 2 and TLR4 expression in both spleen and mesenteric lymph nodes of ETEC-challenged piglets, in accompanied with the reduced phosphorylation levels of nuclear factor kappa B (NF-κB) p65 and mitogen-activated protein kinase (MAPK) p38 as well in spleen of ETEC-infected piglets. Furthermore, L.acidophilus significantly increased the expression of the negative regulators of TLRs signaling, including Tollip, IRAK-M, A20 and Bcl-3 in spleen of ETEC-challenged piglets.


CONCLUSIONS
Our findings suggested that L. acidophilus regulated inflammatory response to ETEC via impairing both NF-κB and MAPK signaling pathways in piglets.
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
Haihua
H
Li
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
Lei
L
Zhang
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
Longbin
L
Chen
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
Qi
Q
Zhu
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
Wenjie
W
Wang
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China. qiaojy1979@126.com.
Jiayun
J
Qiao
D000818:Animals; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D004195:Disease Models, Animal; D054307:Enterotoxigenic Escherichia coli / Q000502:physiology*; D004927:Escherichia coli Infections / Q000517:prevention & control; D005260:Female; D007249:Inflammation / Q000382:microbiology*; D018836:Inflammation Mediators / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology; D007779:Lactobacillus acidophilus / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D019936:Probiotics; D015398:Signal Transduction; D013552:Swine; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis / Q000378:metabolism; D051996:Transcription Factor RelA / Q000037:antagonists & inhibitors* / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D051195:Toll-Like Receptor 2; D051996:Transcription Factor RelA; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases
ETEC; Inflammatory response; Innate immunity; L. acidophilus; Mitogen-activated protein kinase; Nuclear factor kappa B; Toll-like receptor