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首页> 外文期刊>Journal of dermatological science >Adjuvant effect of lipopolysaccharide on the induction of contact hypersensitivity to haptens in mice.
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Adjuvant effect of lipopolysaccharide on the induction of contact hypersensitivity to haptens in mice.

机译：脂多糖对小鼠半抗原接触性超敏反应的佐剂作用。

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BACKGROUND: Toll-like receptor (TLR) 4 is a critical receptor and signal transducer for lipopolysaccharide (LPS), a major component of Gram-negative bacteria. The MyD88-independent pathway downstream of TLR4 leads to functional dendritic cell (DC) maturation, although LPS-induced cytokine production from DCs is MyD88-dependent. OBJECTIVES: We investigated whether intracutaneously injected LPS alters the functions of cutaneous DCs, leading to enhanced contact hypersensitivity (CH). METHODS: The ear swelling response was measured to evaluate the magnitude of CH. Cell proliferation of allogeneic splenocytes stimulated by DC-enriched draining lymph node (LN) cells was measured by performing a [(3)H]-thymidine incorporation assay. Epidermal I-A+ cells were evaluated under an epifluorescent microscope. I-A+ FITC-bearing cells from the draining LNs 24h after FITC application were analyzed on FACScan. RESULTS: LPS augmented CH induction in C3H/HeN (HeN) and MyD88-knockout (KO) mice but not in C3H/HeJ (HeJ) andH-2S(d)-bearing strains such as BALB/c mice. LPS failed to augment the allo-stimulatory ability of DCs in the draining LNs after hapten applications. LPS altered the density and morphology of epidermal I-A+ cell in HeN and BALB/c mice but not in TLR4-deficient HeJ mice. LPS increased the proportion of I-A+ FITC-bearing cells in the LNs 24h after FITC application in HeN, but not in BALB/c and HeJ. CONCLUSIONS: LPS augments the ability of DCs to migrate to the draining LNs, leading to enhanced CH via a TLR4-dependent, MyD88-independent pathway. The different effects of LPS on CH in some strains of mice may explain individual differences in the susceptibility to establish CH to daily antigen exposures in clinical settings.
机译：背景：Toll样受体（TLR）4是脂多糖（LPS）的关键受体和信号转导子，脂多糖是革兰氏阴性细菌的主要成分。尽管LPS诱导的DC产生的细胞因子是MyD88依赖性的，但TLR4下游的MyD88依赖性途径导致功能性树突状细胞（DC）成熟。目的：我们调查了皮内注射脂多糖是否会改变皮肤DC的功能，从而导致接触性超敏反应（CH）增强。方法：测量耳肿胀反应以评估CH的大小。通过执行[（3）H]-胸苷掺入试验，测量了富含DC的引流淋巴结（LN）细胞刺激的同种异体脾细胞的细胞增殖。表皮的I-A +细胞在荧光显微镜下进行评估。在FACScan上分析应用FITC后24小时内引流的LN中带有I-A + FITC的细胞。结果：LPS增强了C3H / HeN（HeN）和MyD88基因敲除（KO）小鼠的CH诱导，但不增强C3H / HeJ（HeJ）和带有H-2S（d）的品系如BALB / c小鼠的CH诱导。在半抗原施用后，LPS无法增强排水LN中DC的同种异体刺激能力。 LPS改变了HeN和BALB / c小鼠的表皮I-A +细胞的密度和形态，但没有改变TLR4缺陷的HeJ小鼠。在HeN中应用FITC后24小时，LPS会增加LN中I-A + FITC携带细胞的比例，但在BALB / c和HeJ中却没有。结论：LPS增强了DC迁移至引流LN的能力，从而通过TLR4依赖性，MyD88依赖性途径增强了CH。 LPS对某些小鼠品系中CH的不同作用可能解释了在临床环境中建立CH对日常抗原暴露的敏感性的个体差异。

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