MicroRNA‐98 and<i>let‐7</i>Regulate Expression of Suppressor of Cytokine Signaling 4 in Biliary Epithelial Cells in Response to<i>Cryptosporidium parvum</i>Infection

Hu, Guoku; Zhou, Rui; Li, Jun; Gong, Ai Yu; Chen, Xian Ming

doi:10.1086/653212

Cited by 70 publications

(52 citation statements)

References 41 publications

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“…In contrast, as a positive control, a significant increase of IL-8 mRNA was found in cells following exposure to C. parvum (Fig. 1C), which is consistent with results from previous studies [23]. …”

Section: Resultssupporting

confidence: 92%

Cryptosporidium parvum induces SIRT1 expression in host epithelial cells through downregulating let-7i

et al. 2014

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Epithelial cells along human gastrointestinal mucosal surface express pathogen-recognizing receptors and actively participate in the regulation of inflammatory reactions in response to microbial infection. The NAD-dependent deacetylase sirtuin-1 (SIRT1), one member of the sirtuin family of proteins and an NAD-dependent deacetylase has been implicated in the regulation of multiple cellular processes, including inflammation, longevity, and metabolism. In this study, we demonstrated that infection of cultured human biliary epithelial cells (H69 cholangiocytes) with a parasitic protozoan, Cryptosporidium parvum, induced SIRT1 expression at the protein level without a change in SIRT1 mRNA content. Using real-time PCR and Northern blot analyses, we found that C. parvum infection decreased the expression of let-7i in infected H69 cells. Down-regulation of let-7i caused relief of miRNA-mediated translational suppression of SIRT1 and consequently, resulted in an increased SIRT1 protein level in infected H69 cell cultures. Moreover, gain- and loss-of-function studies revealed that let-7i could modulate NF-κB activation through modification of SIRT1 protein expression. Thus, our data suggest that let-7i regulates SIRT1 expression in human biliary epithelial cells in response to microbial challenge, suggesting a new role of let-7i in the regulation of NF-κB-mediated epithelial innate immune response.

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Section: Resultssupporting

confidence: 92%

Cryptosporidium parvum induces SIRT1 expression in host epithelial cells through downregulating let-7i

et al. 2014

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“…MiRNAs are potentially ideal tools for parasites to modulate gene expression in host cells, since miRNAs are non-immunogenic, can be transported and transferred in exosomes from the pathogen to the host cells, and can evolve rapidly to target new transcripts [43]. The involvement of parasite's miRNAs in the manipulation of host cells has already been postulated [44]. Nevertheless, the implication and roles of parasite-derived miRNAs delivered at the host-parasite interface in the parasite's evasion mechanisms have not been evidenced and characterized to date.…”

Section: Role Of Micrornas In the Regulation Of The Host-parasite Intmentioning

confidence: 99%

MicroRNAs in parasitic diseases: Potential for diagnosis and targeting

Manzano-Román

Siles-Lucas

2012

Molecular and Biochemical Parasitology

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“…An increase in miR27b is required for expression if inducible nitric oxide synthase (iNOS) during infection of epithelial cells by Crytosporidium parvum : miR27b decreases expression of a negative regulator [61], [62]. In contrast, mir27b decreased in HAT patient peripheral blood.…”

Section: Discussionmentioning

confidence: 99%

The miRNA and mRNA Signatures of Peripheral Blood Cells in Humans Infected with Trypanosoma brucei gambiense

et al. 2013

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Simple, reliable tools for diagnosis of human African Trypanosomiases could ease field surveillance and enhance patient care. In particular, current methods to distinguish patients with (stage II) and without (stage I) brain involvement require samples of cerebrospinal fluid. We describe here an exploratory study to find out whether miRNAs from peripheral blood leukocytes might be useful in diagnosis of human trypanosomiasis, or for determining the stage of the disease. Using microarrays, we measured miRNAs in samples from Trypanosoma brucei gambiense-infected patients (9 stage I, 10 stage II), 8 seronegative parasite-negative controls and 12 seropositive, but parasite-negative subjects. 8 miRNAs (out of 1205 tested) showed significantly lower expression in patients than in seronegative, parasite-negative controls, and 1 showed increased expression. There were no clear differences in miRNAs between patients in different disease stages. The miRNA profiles could not distinguish seropositive, but parasitologically negative samples from controls and results within this group did not correlate with those from the trypanolysis test. Some of the regulated miRNAs, or their predicted mRNA targets, were previously reported changed during other infectious diseases or cancer. We conclude that the changes in miRNA profiles of peripheral blood lymphocytes in human African trypanosomiasis are related to immune activation or inflammation, are probably disease-non-specific, and cannot be used to determine the disease stage. The approach has little promise for diagnostics but might yield information about disease pathology.

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MicroRNA‐98 andlet‐7Regulate Expression of Suppressor of Cytokine Signaling 4 in Biliary Epithelial Cells in Response toCryptosporidium parvumInfection

Cited by 70 publications

References 41 publications

Cryptosporidium parvum induces SIRT1 expression in host epithelial cells through downregulating let-7i

Cryptosporidium parvum induces SIRT1 expression in host epithelial cells through downregulating let-7i

MicroRNAs in parasitic diseases: Potential for diagnosis and targeting

The miRNA and mRNA Signatures of Peripheral Blood Cells in Humans Infected with Trypanosoma brucei gambiense

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