Inducible nitric oxide synthase response and associated cytokine gene expression in the spleen of mice infected with Clonorchis sinensis

Shen, Ji-Qing; Yang, Qingli; Xue, Yan; Cheng, Xiaobing; Jiang, Zhihua; Yang, Yue; Chen, Ying-Dan; Zhou, Xiao‐Nong

doi:10.1007/s00436-015-4347-9

Cited by 6 publications

(8 citation statements)

References 51 publications

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“…Among the three major isoforms of NOS, inducible NOS (iNOS) is most associated with the pathophysiology of inflammatory diseases [ 7 ]. In our recent studies, we confirmed iNOS induction and associated cytokine expression in BALB/c mice after C. sinensis infection [ 8 , 9 ].…”

Section: Introductionsupporting

confidence: 71%

“…Amplification and data acquisition were performed with an Applied Biosystems 7500 Real-Time PCR system running on V2.0.6 software (Life Technologies, Carlsbad, CA, USA) and using the following cycling parameters: predenaturation at 95 °C for 30 s, 40 cycles of amplification at 95 °C for 5 s, and annealing and extension at 60 °C for 30 s. Melt curve analysis was performed from 65 °C to 95 °C to determine the melting temperatures (Tm) (Additional file 1 : Table S1) of the identified specific DNA product populations. The mRNA transcript of iNOS was quantified with RT-PCR assay based on the slope of standard curve described previously [ 8 , 30 ]. Serial diluted cDNA samples were used as standards for the preparation of standard curves and acquisition of slopes.…”

Section: Methodsmentioning

confidence: 99%

“…Several studies reported that many strains of mice, including FVB/NJ (FVB) [ 20 – 22 ], BALB/c [ 8 , 9 , 20 – 23 ], and C3H/He [ 24 ] are susceptible to C. sinensis . By contrast, C57BL/6 mice are resistant to C. sinensis infection [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

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TLR2 signal influences the iNOS/NO responses and worm development in C57BL/6J mice infected with Clonorchis sinensis

et al. 2017

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BackgroundAlthough the responses of inducible nitric oxide synthase (iNOS) and associated cytokine after Clonorchis sinensis infection have been studied recently, their mechanisms remain incompletely understood. In this study, we investigated the effects of toll-like receptor 2 (TLR2) signals on iNOS/nitric oxide (NO) responses after C. sinensis infection. We also evaluated the correlations between iNOS responses and worm development, which are possibly regulated by TLR2 signal.MethodsTLR2 wild-type and mutant C57BL/6 J mice were infected with 60 C. sinensis metacercariae, and the samples were collected at 30, 60, 90 and 120 days post-infection (dpi). The total serum NO levels were detected using Griess reagent after nitrate was reduced to nitrite. Hepatic tissue samples from the infected mice were sliced and stained with hematoxylin and eosin (HE) to observe worm development in the intrahepatic bile ducts. The iNOS mRNA transcripts in the splenocytes were examined by real time reverse transcriptase polymerase chain reaction (qRT-PCR), and iNOS expression was detected by immunohistochemistry.ResultsDeveloping C. sinensis juvenile worms were more abundant in the intrahepatic bile ducts of TLR2 mutant mice than those of TLR2 wild-type mice. However, no eggs were found in the faeces of both mice samples. The serum levels of total NO significantly increased in TLR2 mutant mice infected with C. sinensis at 30 (t (5) = 2.595, P = 0.049), 60 (t (5) = 7.838, P = 0.001) and 90 dpi (t (5) = 3.032, P = 0.029). Meanwhile, no changes occurred in TLR2 wild-type mice compared with uninfected controls during the experiment. The iNOS expression in splenocytes showed unexpected higher background levels in TLR2 mutant mice than those in TLR2 wild-type mice. Furthermore, the iNOS mRNA transcripts in splenocytes were significantly increased in the TLR2 wild-type mice infected with C. sinensis at 30 (t (5) = 5.139, P = 0.004), 60 (t (5) = 6.138, P = 0.002) and 90 dpi (t (5) = 6.332, P = 0.001). However, the rising of iNOS transcripts dropped under the uninfected control level in the TLR2 mutant mice at 120 dpi (t (5) = -9.082, P < 0.0001). Both total NO and iNOS transcripts were significantly higher in the TLR2 mutant mice than those in the TLR2 wild-type mice at 30 (t (5) = 3.091/2.933, P = 0.027/0.033) and 60 dpi (t (5) = 2.667/6.331, P = 0.044/0.001), respectively. In addition, the remarkable increase of iNOS expressions was immunohistochemically detected in the splenic serial sections of TLR2 wild-type mice at 30 and 60 dpi. However, the expressions of iNOS were remarkably decreased in the splenocytes of both TLR2 wild-type and mutant mice at 120 dpi.ConclusionsThese results demonstrate that TLR2 signal plays an important role in the regulation of iNOS expression after C. sinensis infection. TLR2 signal is also beneficial to limiting worm growth and development and contributing to the susceptibility to C. sinensis in which the iNOS/NO reactions possibly participate.Electronic supplementary materialThe online version of this articl...

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Section: Introductionsupporting

confidence: 71%

Section: Methodsmentioning

confidence: 99%

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TLR2 signal influences the iNOS/NO responses and worm development in C57BL/6J mice infected with Clonorchis sinensis

et al. 2017

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“…NO from iNOS-expressing cells suppresses mouse T cell proliferation. Also, in case of deficient iNOS, NO did not produced and this may attributed to increase the infiltration and expansion of CD4 cells (Aheng et al,2011).The spleen was approved to be important organ for iNOS/NO responses and highly expressed iNOS in the splenocytes may regulate Th response negatively (Qing Shen et al,2015).…”

Section: Introductionmentioning

confidence: 99%

The immunotoxic effects of short term chronic exposure to Titanium Dioxide Nanoparticles on spleen of adult albino rats and the role of after toxic effect follow up

El-Sheikh

Ameen

Ibrahim

et al. 2016

Ain Shams Journal of Forensic Medicine and Clinical Toxicology

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The usage of Titanium Dioxide NanoParticles (TiO2NPs) on a large scale of applications was a reason of a variety of many health problems. The aim of the current study was to evaluate the immune toxic effects of short term administration of TiO2NPs on spleen. Material and Methods: Forty Adult male Rats were equally divided into four groups as follows: Group I: negative control, Group II: positive control, Group III: received TiO2NPs (1200 mg/kg) orally daily for 12 weeks. Group IV: follow up group received TiO2NPs by the same dose, route and for the same duration as TiO2NPs group and then they were left untreated for another 8 weeks. Total leukocytes, differential leukocytic counts, Interleukins IL-2 and IL-10 levels were measured, the spleen sections were examined immunohistochemically for the detection of CD4+ and iNOS expressing cells. Histopathological alterations in the spleen were also evaluated. Moreover, DNA damage was evaluated by comet assay. The results: TiO2NPs exposure for 12 weeks resulted in significant decreased in the total and deferential leukocytic counts, serum interleukins IL-2 as well as IL-10. It caused marked decrease in CD4+T-lymphocytes and increase in iNOS expressing cells indicating oxidative stress in spleen tissues. It also caused histopathological disruption of spleen architecture and produced DNA damage in splenocytes. Discontinuation of TiO2NPs administration for 8 weeks resulted in significant improvement of leukocytes, interleukins, increase in CD4+ T-lymphocytes and decrease in iNOS expressing cells in spleen tissues. Moreover, there was moderate improvement in histopathological alterations and DNA damage. Conclusion:TiO2NPs consumption have immunotoxic effects which may resulted from genetic damage and oxidative stress in the spleen of adult male albino rats which could be improved by its discontinuation for a period of time and it was recommended to increase the period of discontinuation as complete improvement may occur

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“…In contrast to other constitutively expressed isoforms, iNOS is only expressed in response to inflammatory cytokines such as TNF-α and IL-1β and transcriptional activators, such NF-kB [48, [66][67][68][69]. In chronic inflammation models and inflammation-related tumorigenesis, iNOS may be persistently stimulated by cytokines and NF-kB activation in the tumor microenvironment.…”

Section: Introductionmentioning

confidence: 99%

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

Baydoun¹,

Ratner²

2015

J Leuk

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The Human T-cell Leukemia Virus type 1 (HTLV-1), is the first retrovirus associated with a human cancer. HTLV-1 is the causative agent of an aggressive and fatal malignancy of CD4+ T lymphocytes known as Adult T-cell Leukemia lymphoma (ATLL). Since the discovery of the virus in 1980, intensive investigations have been undertaken to determine how HTLV-1 drives the transformation process in infected cells. This is because the oncogenic features of HTLV-1 make it an excellent tool to dissect the molecular pathways involved in cancer development. More important, HTLV-1 induced leukemia is a typical inflammation-mediated malignancy with constitutive activation of the NF-kB pathway, which is also a critical determinant in many other cancers. How NF-kB contributes to the leukemogenic process is not completely defined. We recently demonstrated that the NF-kB pathway induces the expression of inducible nitric oxide synthase (iNOS) in HTLV-1 induced leukemia. iNOS enzymatically generates nitric oxide, which is an oxidative and nitrosative agent of DNA and proteins. Nitric oxide was found to be associated with a large number of DNA Double Strand Breaks (DSBs) in HTLV-1 transformed cells. Here, we will review the major effects of nitric oxide on HTLV-1 induced leukemia.

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Inducible nitric oxide synthase response and associated cytokine gene expression in the spleen of mice infected with Clonorchis sinensis

Cited by 6 publications

References 51 publications

TLR2 signal influences the iNOS/NO responses and worm development in C57BL/6J mice infected with Clonorchis sinensis

TLR2 signal influences the iNOS/NO responses and worm development in C57BL/6J mice infected with Clonorchis sinensis

The immunotoxic effects of short term chronic exposure to Titanium Dioxide Nanoparticles on spleen of adult albino rats and the role of after toxic effect follow up

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

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