Thymol kills bacteria, reduces biofilm formation, and protects mice against a fatal infection of Actinobacillus pleuropneumoniae strain L20

Cheng

et al. 2018

Appl Environ Microbiol

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Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we observed the ability of the phage lysin LysGH15 to eliminate staphylococcal planktonic cells and biofilms formed by ,, , and All these strains were sensitive to LysGH15, showing reductions in bacterial counts of approximately 4 log units within 30 min after treatment with 20 μg/ml of LysGH15, and the MICs ranged from 8 μg/ml to 32 μg/ml. LysGH15 efficiently prevented biofilm formation by the four staphylococcal species at a dose of 50 μg/ml. At a higher dose (100 μg/ml), LysGH15 also showed notable disrupting activity against 24-h and 72-h biofilms formed by and coagulase-negative species. In the experiments, a single intraperitoneal injection of LysGH15 (20 μg/mouse) administered 1 h after the injection of at double the minimum lethal dose was sufficient to protect the mice. The cell counts were 4 log units lower in the blood and 3 log units lower in the organs of mice 24 h after treatment with LysGH15 than in the untreated control mice. LysGH15 reduced cytokine levels in the blood and improved pathological changes in the organs. The broad antistaphylococcal activity exerted by LysGH15 on planktonic cells and biofilms makes LysGH15 a valuable treatment option for biofilm-related or non-biofilm-related staphylococcal infections. Most staphylococcal species are major causes of health care- and community-associated infections. In particular, is a common and dangerous pathogen, and is a ubiquitous skin commensal and opportunistic pathogen. Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we found that all tested ,, , and strains were sensitive to the phage lysin LysGH15 (MICs ranging from 8 to 32 μg/ml). More importantly, LysGH15 not only prevented biofilm formation by these staphylococci but also disrupted 24-h and 72-h biofilms. Furthermore, the efficacy of LysGH15 was demonstrated in a mouse model of bacteremia. Thus, LysGH15 exhibits therapeutic potential for treating biofilm-related or non-biofilm-related infections caused by diverse staphylococci.

Section: Methodsmentioning

confidence: 99%

Antibacterial Effects of Phage Lysin LysGH15 on Planktonic Cells and Biofilms of Diverse Staphylococci

Cheng

et al. 2018

Appl Environ Microbiol

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“…Thymol is a naturally occurring phenolic compound and one of the primary active constituents present in the essential oil of Thymus vulgaris ( Villanueva Bermejo et al., 2015 ). Reports have demonstrated that thymol has shown anti-oxidant, anti-microbial ( Tsai et al., 2011 ; Wang et al., 2017 ), and hepatoprotective effects ( Alam et al., 1999 ). Moreover, it has been demonstrated that thymol markedly inhibits the production of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in inflammation ( Liang et al., 2014 ; Luna et al., 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of thymol against adrenaline-induced myocardial injury in rats

El-Marasy

Awdan

Hassan

et al. 2020

Heliyon

Cardiovascular disease represents a vital global disease burden. This study aims to assess the possible cardioprotective effect of thymol against adrenaline-induced myocardial injury (MI) in rats. Furthermore the effect of thymol on cardiac function biomarkers, electrocardiogram (ECG) alterations, oxidative stress, inflammation, apoptosis and histopathological changes was assessed. MI was induced by adrenaline (2 mg/kg, s.c.) injected as a single dose for 2 consecutive days (24 h apart). Normal and control groups received the vehicle for 21 consecutive days. The other 3 groups were orally administered thymol (15, 30, 60 mg/kg) for 21 consecutive days and on day 22, adrenaline was injected as a single dose for 2 consecutive days. Then ECG examination, biochemical, histopathological, immunohistochemical analyses were carried out. Thymol reversed adrenaline-induced reduction of heart rate, prolongation of RR interval and elevation of ST interval. Thymol pretreatment significantly reduced serum aspartate dehydrogenase (AST), lactate dehydrogenase (LDH), and creatine kinase (CK) levels in MI rats. Oral pretreatment with thymol increased reduced glutathione (GSH), reduced malondialdehyde (MDA), nuclear factor-kappa B (NF-κB), and interleukin-1β (IL-1β) cardiac contents in MI rats. Additionally, thymol administration significantly decreased protein expression of caspase-3, increased Bcl-2 protein expression in cardiac tissue and ameliorated histopathological changes. This study reveals that thymol exerted cardioprotective effect against adrenaline-induced MI in rats evidenced by improving cardiac function, attenuating ECG and histopathological changes which may be partly mediated through its anti-oxidant, anti-inflammatory and anti-apoptotic effect.

“…Images were obtained using a DM3000 microscope (PHASE CONTRAST, Japan). Image-Pro software (Media Cybernetics, USA) was used to measure the villous height and crypt depth, and then, the ratio of villous height to crypt depth was calculated [15].…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

Antimicrobial Peptide MPX Against Escherichia Coli O157:H7 Infection and Inhibiting inﬂammation, Enhancing Epithelial Barrier and Promoting Nutrient Absorption in the Intestine

Zhao

Wang

Zhu

et al. 2020

Preprint

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Background: Escherichia coli can cause intestinal diseases in humans and livestock, destroy the intestinal barrier, exacerbate systemic inflammation, and seriously threaten human health and animal husbandry development. The antimicrobial peptide MPX is extracted from venom and possesses good antibacterial activity against gram-negative bacteria. The aim of this study was to investigate whether MPX could be effective against E. coli infection. Results: In this study, the CCK-8 and lactic dehydrogenase results showed that MPX exhibited no toxicity in IPEC-J2 cells even at a concentration of 128 µg/mL. Furthermore, MPX notably suppressed the levels of IL-2, IL-6, TNF-α, myeloperoxidase and LDH induced by E. coli and reduced inflammation by inhibiting the p-p38-, TLR4- and p-p65-dependent pathways. In addition, MPX improved the expression of ZO-1, occludin, and claudin and enhanced the wound healing ability of IPEC-J2 cells. The therapeutic effect of MPX was evaluated in a murine model, and the results showed that MPX could protect mice against lethal infection with E. coli, improve the survival rate of the mice, and reduce the colonization of E. coli in organs and feces. H&E staining showed that MPX increased the length of villi and reduced the infiltration of inflammatory cells into the jejunum, and the effect of MPX was better than that of enrofloxacin. The SEM and TEM results showed that MPX effectively ameliorated the damage caused by E. coli to the jejunum and increased the number and length of microvilli. In addition, real-time PCR revealed that MPX decreased the expression of IL-2, IL-6, and TNF-α in the jejunum and colon. Furthermore, immunohistochemistry and immunofluorescence studies revealed that MPX could reduce the expression of p-p38 and p-p65 in the jejunum, thereby reducing the secretion of inflammatory factors. Moreover, MPX increased the mRNA and protein expression of ZO-1, occludin and MUC2 in the jejunum and colon, improved the function of the intestinal barrier and promoted the absorption of nutrients. Conclusion: This study suggests that MPX may be an effective therapeutic agent against E. coli infection and other intestinal diseases, laying the foundation for the development of new drugs for bacterial infections.