Comprehensive in vitro and in vivo risk assessments of chitosan microparticles using human epithelial cells and Caenorhabditis elegans

Ma, Zhengxin; Garrido‐Maestu, Alejandro; Lee, Choonghee; Chon, Jung‐Whan; Jeong, Daehee; Yue, Yiren; Sung, Kidon; Park, Yeonhwa; Jeong, Kwangcheol C.

doi:10.1016/j.jhazmat.2017.07.071

Cited by 25 publications

(24 citation statements)

References 34 publications

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“…[51][52][53] In the present study, the histological analysis showed an increase in ileal and colonic submucosal infiltration 5 days after mice were treated with ETEC K88. [58][59][60][61] Our results are consistent with previous studies showing that ETEC can colonize epithelial cells to disrupt the intestinal absorption system and cause chronic malnutrition. Consistent with the present study, previous studies have found that other AMPs supplemented by diet as well as MccJ25 and sublancin significantly improved the nutrient digestibility of weaning pigs and the villus morphology of broilers, respectively.…”

Section: Discussionsupporting

confidence: 92%

Therapeutic administration of the recombinant antimicrobial peptide microcin J25 effectively enhances host defenses against gut inflammation and epithelial barrier injury induced by enterotoxigenic Escherichia coli infection

Wang

Zeng

et al. 2019

The FASEB Journal

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Recombinant antimicrobial peptide microcin J25 (MccJ25) causes potent antimicrobial activity against enterotoxigenic Escherichia coli (ETEC) in vitro; however, independently of this activity, its role in suppressing intestinal inflammation and epithelial barrier injury in vivo remains unclear. We investigated the therapeutic effects of MccJ25 on intestinal inflammation and epithelial barrier dysfunction and the underlying mechanism, using gentamicin for comparison. In a mouse model of intestinal inflammation, therapeutic administration of either MccJ25 or gentamicin after ETEC K88 infection attenuated clinical symptoms, reduced intestinal pathogen colonization, improved intestinal morphology, and decreased inflammatory pathologies and intestinal permeability, ultimately improving the hosts' health. MccJ25 also attenuated ETEC-induced mouse intestinal barrier dysfunction by enhancing tight junction proteins (TJPs). Using the human epithelial cell line Caco-2, we verified the epithelial barrier-strengthening and mucosal injury-alleviating effects of MccJ25 on ETEC infection: increased expression of TJPs by activating the p38/MAPK pathway, balancing the microbiota, and improving short-chain fatty acid concentrations in the cecum of ETEC-infected mice. Although gentamicin and MccJ25 had similar effects in the inflamed gut, MccJ25 was superior to gentamicin with regard to defending the host from ETEC infection. Overall, MccJ25 may be a promising therapeutic drug for treating enteric pathogen-induced intestinal inflammation diseases. K E Y W O R D S gut microbiota, inflamed gut, inflammation diseases, intestinal barrier injury, mice, pathogens infection | 1019 YU et al.

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Section: Discussionsupporting

confidence: 92%

Therapeutic administration of the recombinant antimicrobial peptide microcin J25 effectively enhances host defenses against gut inflammation and epithelial barrier injury induced by enterotoxigenic Escherichia coli infection

Wang

Zeng

et al. 2019

The FASEB Journal

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“…In our study, we found that biogenic MccJ25 exert strong antimicrobial activity without raising IPEC-J2 cells cytotoxicity that did not cause cellular membrane damage and reduction in cell activity even at high concentrations. Consistent with the previous studies which found that AMPs sublancin, porcine lactoferrin peptide LF-6 or chitosan microparticles also did not cause cytotoxicity in intestinal cells (Jiang et al, 2016 ; Ma et al, 2017 ; Wang et al, 2017 ). On the basis of the cytotoxicity findings, we choose the lowest doses (2 μg/mL) biogenic MccJ25 to investigate the impacts on following experiments.…”

Section: Discussionsupporting

confidence: 91%

“…Consistent with the previous studies, biogenic MccJ25 had been shown to extremely strong bactericidal activity in the 5–500 nanomolar range against E. coli, Salmonella , and Shigella strains (Blond et al, 1999 ; Sable et al, 2000 ). Compared to animal experiments, in vitro studies of cell culture are always the first step in studying how drugs respond because they are relatively cost-effective and simple, easy to handle, and ethically unclear (Ma et al, 2017 ). In this study, we selected highly similar IPEC-J2 cells between pigs and humans, and because it is a better model for normal intestinal epithelial cells to study pathogen-host interaction and gut barrier function (Skjolaas et al, 2006 ; Schmidt et al, 2008 ; Wu et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

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Protective Ability of Biogenic Antimicrobial Peptide Microcin J25 Against Enterotoxigenic Escherichia Coli-Induced Intestinal Epithelial Dysfunction and Inflammatory Responses IPEC-J2 Cells

Ding

Shang

et al. 2018

Front. Cell. Infect. Microbiol.

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Poison of intestinal induce severe health problems in human infants and young animals due to contaminating foods and feedstuffs. With the emergence of public health concerns and high-speed diffuse of drug-opposition of bacteria, the adoption of antimicrobial peptides as potential candidates in treating pathogen infections raised up. Nature Microcin J25 (MccJ25), a class of lasso peptides separated from a fecal strain of E. coli, has been replied to display powerful antimicrobial behavior. Herein, the study was to assess the usefulness of biogenic MccJ25 in the prophylaxis of ETEC K88 infection in IPEC-J2 cells. In vitro antimicrobial activity against ETEC K88 and cytotoxicity of biogenic MccJ25 were determined first. To further understand how biogenic MccJ25 mediates its impact, ETEC K88 adhesion in cells, membrane permeability [as indicated by reduced release of lactate dehydrogenase (LDH)], transepithelial electrical resistance (TEER), barrier function, and proinflammatory cytokines levels were determined in IPEC-J2 cells after treatment with biogenic MccJ25 and challenge with ETEC K88. Biogenic MccJ25 had a minimum inhibitory concentration of 0.25 μg/mL against ETEC K88, decreased ETEC K88 adhesion in cells and did not cause cytotoxicity toward cells. Furthermore, biogenic MccJ25 protects against ETEC-induced barrier dysfunction by increasing the TEER, decreasing the LDH and promoting tight junction proteins (TJPs) by promoting the assembly of occludin and claudin-1 in the tight junction complex. Biogenic MccJ25 was further found to relieve inflammation responses through modulation of interleukine-6, IL-8 and tumor necrosis factor-α levels via inhibition of mitogen-activated protein kinase (MAPK) and nuclear factor κB activation. In summary, biogenic MccJ25 can protects against ETEC K88-induced intestinal damage and inflammatory response, recommend the hidden adoption of biogenic MccJ25 as a novel prophylactic agent to reduce pathogen infection in animals, food or humans.

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“…3 Although, nano-based agents are presently being extensively utilized in biological and medicinal approaches, there is a momentous concern regarding human 4 and environmental risk 5 upon implications of fabricated nanomaterials. Recent in vivo 6 and in vitro 6,7 investigations have suggested that utilization of some nanoparticles (NPs) may induce serious toxic health impacts and the application of nanomaterials-based medical agents may result in chronic or acute health problems. 8 Thus, along with the development of unique NPs, simultaneous investigation of the impacts of NPs on the biological systems should be carried out.…”

Section: Introductionmentioning

confidence: 99%

<p>Amorphous aggregation of tau in the presence of titanium dioxide nanoparticles: biophysical, computational, and cellular studies</p>

Fardanesh¹,

Zibaie²,

Shariati³

et al. 2019

IJN

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BackgroundNanoparticles (NPs) when injected into the body can reach target tissues like nervous system and interact with tau proteins and neurons. This can trigger conformational changes of tau and may affect NP toxicity.MethodsIn this study, we used several biophysical techniques (extrinsic and intrinsic fluorescence spectroscopy, circular dichroism (CD) spectroscopy, ultraviolet (UV)-visible spectroscopy), transmission electron microscopy (TEM) investigations, molecular docking and molecular dynamics studies, and cellular assays [3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) and flow cytometry) to reveal how structural changes of tau protein can change the cytotoxicity of titanium dioxide (TiO2) NPs against neuron-like cells (SH-SY5Y) cells.ResultsIt was shown that TiO2 NPs result in hydrophilic interactions, secondary and tertiary structural changes, and the formation of amorphous tau aggregates. Conformational changes of tau increased the induced cytotoxicity by TiO2 NPs. These data revealed that the denatured adsorbed protein on the NP surface may enhance NP cytotoxicity.ConclusionTherefore, this study provides useful insights on the NP–protein interactions and discusses how the protein corona can increase cytotoxicity to determine the efficacy of targeted delivery of nanosystems.

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Comprehensive in vitro and in vivo risk assessments of chitosan microparticles using human epithelial cells and Caenorhabditis elegans

Cited by 25 publications

References 34 publications

Therapeutic administration of the recombinant antimicrobial peptide microcin J25 effectively enhances host defenses against gut inflammation and epithelial barrier injury induced by enterotoxigenic Escherichia coli infection

Therapeutic administration of the recombinant antimicrobial peptide microcin J25 effectively enhances host defenses against gut inflammation and epithelial barrier injury induced by enterotoxigenic Escherichia coli infection

Protective Ability of Biogenic Antimicrobial Peptide Microcin J25 Against Enterotoxigenic Escherichia Coli-Induced Intestinal Epithelial Dysfunction and Inflammatory Responses IPEC-J2 Cells

<p>Amorphous aggregation of tau in the presence of titanium dioxide nanoparticles: biophysical, computational, and cellular studies</p>

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