Abstract
BackgroundThymus is the crucial site for T cell development and once believed to be immune privileged. Recently, thymus has gained special attention as it is commonly targeted by infectious agents which may cause pathogenic tolerance and subsequent immunosuppression.ResultsWe analyzed thymic responses to the challenge with Salmonella typhimurium (STm) or lipopolysaccharide (LPS) derived from STm in chicks. Newly hatched chicks were injected intraperitoneally with 5 × 104 CFU/mL STm or 50 mg/kg LPS. After LPS treatment, maximum thymocyte death (3 ~ 5-fold change) compared to controls was found at 12 h, and maximum loss of thymic weight (35 %) and reduced thymic index (20 %) were found at 36 h. After STm infection, maximum thymocyte death and thymic atrophy occurred at 36 and 72 h, respectively. No significant changes of thymic structure, chT1+ and CD4+/CD8+ T cell ratio were observed in thymus or spleen tissues after LPS treatment. Furthermore, transcriptome analysis revealed important roles for the TLR4-FOS/JUN signaling pathway in thymic injury. Thus, the major process of thymic atrophy in this study first involved activation of transcriptional factors FOS/JUN upon LPS binding to TLR4 that caused release of inflammatory factors, thereby inducing inflammatory responses and DNA damage and ultimately cell cycle arrest and thymic injury.ConclusionsSTm and Salmonella LPS could induce acute chick thymic injury. LPS treatment acted faster than STm. TLR4-FOS/JUN pathway may play an important role in LPS induced chick thymic injury.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2674-6) contains supplementary material, which is available to authorized users.
Highlights
Thymus is the crucial site for T cell development and once believed to be immune privileged
Treatment with LPS derived from Salmonella typhimurium (STm) resulted in the maximum 35 % loss of thymus weight (P < 0.01, 0.18 ± 0.04 g vs. 0.27 ± 0.05 g) and 20 % decrease of thymus index (P < 0.05, 2.66 ± 0.37 vs. 3.34 ± 0.40) at 36 hpt; it caused 17 % loss of thymus weight (P < 0.05, 0.30 ± 0.05 g vs. 0.36 ± 0.03 g) and 17 % loss of thymus index (P < 0.05, 2.81 ± 0.23 vs. 3.37 ± 0.38) at 72 hpt (Fig. 1a and b)
STm infection resulted in the maximum 43 % loss of thymus weight (P < 0.01, 0.13 ± 0.02 g vs. 0.22 ± 0.05 g) and 26 % decrease of thymus index (P < 0.05, 1.86 ± 0.25 vs. 2.52 ± 0.55) at 72 hpt compared with controls, and these effects were attenuated at 120 hpt (Additional file 1: Figure S1)
Summary
Thymus is the crucial site for T cell development and once believed to be immune privileged. Thymus has gained special attention as it is commonly targeted by infectious agents which may cause pathogenic tolerance and subsequent immunosuppression. The thymus is the primary immune organ providing naïve T cells for peripheral immune tissues [1]. Thymic injury can cause serious consequences, which are related to local tissue homeostasis and immune development, especially in young individuals with an immature immune system. In mammals, multiple pathogens can target the thymus and cause. Salmonella typhimurium (STm) is one of the most deleterious food-borne pathogens that can induce typhoid fever and enteritis through infected chicken eggs and meat [10]. STm infection could cause the death of newly hatched chicks [11].
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