Nadifloxacin, an antiacne quinolone antimicrobial, inhibits the production of proinflammatory cytokines by human peripheral blood mononuclear cells and normal human keratinocytes

Kuwahara, K.; Kitazawa, Tazuko; Kitagaki, Hideki; Tsukamoto, Teruhisa; Kikuchi, Mikio

doi:10.1016/j.jdermsci.2005.01.002

Cited by 46 publications

(48 citation statements)

References 35 publications

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“…[132][133][134][135][136]. They are also found to exert modulatory effects on the functioning of several pro-inflammatory cytokines such as TNF-α, IL-1, IL-2, IL-6, IL-8, IL-12, IL-18, etc.…”

Section: Effect Of Antibiotics On Mmps and Cytokinesmentioning

confidence: 99%

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Antibiotics-Induced Obesity: A Mitochondrial Perspective

Andrade

Jayaprakash

Bhat

et al. 2017

Public Health Genomics

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Antibiotics are the first line of treatment against infections and have contributed immensely to reduce the morbidity and mortality rates. Recently, extensive use of antibiotics has led to alterations of the gut microbiome, predisposition to various diseases and most importantly, increase in the emergence of antibiotic-resistant bacteria, which poses a major threat to global public health. Another major issue faced worldwide due to unregulated use of antibiotics in children as well as in adults is the influence of metabolism and body weight homeostasis, leading to obesity. Apart from the involvement of biosocial causes influencing diet, physical activity, and antibiotic use, pathogenesis of obesity is linked to interconnected functional alterations in cells, tissues and organs due to biochemical, epigenetic and genetic factors. Mitochondrial dysfunction is one such factor, which is becoming the primary focus of various aspects of research on multifactorial complex diseases and is providing new perspectives on etiology, biomarker-based diagnosis, and drug sensitivity. Through this review, we have made an attempt to present the interplay between use of antibiotics, obesity, and associated mitochondrial dysfunction. This may provide insights into the molecular basis, genetic predisposition and environmental triggers, which in turn may have potential clinical applications in the management of antibiotic use.

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Section: Effect Of Antibiotics On Mmps and Cytokinesmentioning

confidence: 99%

“…They are also found to exert modulatory effects on the functioning of several pro-inflammatory cytokines such as TNF-α, IL-1, IL-2, IL-6, IL-8, IL-12, IL-18, etc. [132][133][134][135], thereby impairing the mitochondrial biogenesis pathway and, hence, affecting the normal mitochondrial activity [137].…”

Section: Effect Of Antibiotics On Mmps and Cytokinesmentioning

confidence: 99%

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Andrade

Jayaprakash

Bhat

et al. 2017

Public Health Genomics

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“…Among the pro-inflammatory cytokines, IL-6 is one of the most important immune and inflammatory mediators (Santer et al, 2010). IFN-γ possesses a wide array of biological effects and is one of the major immune regulatory molecules that induce effective immune responses against bacteria and exogenous infectious agents (Kuwahara et al, 2005). TNF-α has been recognized as an important host defense cytokine that affects tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Platycodin D exerts anti-tumor efficacy in H22 tumor-bearing mice via improving immune function and inducing apoptosis

Tian

Liu

et al. 2016

J. Toxicol. Sci.

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-Platycodin D (PD), a major saponin derived and isolated from the roots of Platycodon grandiflorum, exerts potent growth inhibition and strong cytotoxicity against various cancer cell lines. However, the anti-tumor efficacy of PD on H22 hepatocellular carcinoma remains unknown. In the present study, we aimed to explore the anti-hepatoma activity in vivo and the underlying mechanism of PD in H22 tumor-bearing mice. The results revealed that PD could considerably suppress tumor growth with no significant side effects on immune organs and body weight. Further investigations showed that the levels of serum cytokines, including interferon gamma (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-2 (IL-2), were enhanced by PD administration. On the other hand, PD inhibited the production of vascular endothelial growth factor (VEGF) in serum of H22 tumor mice. Additionally, the observations from H&E and Hoechst 33258 staining results demonstrated that PD noticeably induced apoptosis in H22 hepatocellular carcinoma cells. Importantly, immunohistochemical analysis showed that PD treatment increased Bax expression and decreased Bcl-2 and VEGF expression of H22 tumor tissues in a dose-dependent manner. Taken together, the findings in the present investigation clearly demonstrated that the PD markedly suppressed the tumor growth of H22 transplanted tumor in vivo at least partly via improving the immune functions, inducing apoptosis, and inhibiting angiogenesis.

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“…As sebum passes through the follicular duct, lipases produced by P. acnes hydrolyze triglycerides into pro-inflammatory free fatty acids [12][13][14]. P. acnes also binds TLR2 and TLR4 on sebaceous glands to stimulate sebocyte production of antimicrobial peptides (HbD1 and HbD2) and inflammatory cytokines (TNFa, IL-1a, and IL-8) [22,[49][50][51]. These observations suggest a role of sebaceous glands in pathogen recognition and stimulation of the innate immune system.…”

Section: Sebum Abnormalities In Acnementioning

confidence: 94%

Recent Advances in Acne Pathogenesis: Implications for Therapy

2014

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Acne pathogenesis is a multifactorial process that occurs at the level of the pilosebaceous unit. While acne was previously perceived as an infectious disease, recent data have clarified it as an inflammatory process in which Propionibacterium acnes and innate immunity play critical roles in propagating abnormal hyperkeratinization and inflammation. Alterations in sebum composition, and increased sensitivity to androgens, also play roles in the inflammatory process. A stepwise approach to acne management utilizes topical agents for mild to moderate acne (topical retinoid as mainstay ± topical antibiotics) and escalation to oral agents for more resistant cases (oral antibiotics or hormonal agents in conjunction with a topical retinoid or oral isotretinoin alone for severe acne). Concerns over antibiotic resistance and the safety issues associated with isotretinoin have prompted further research into alternative medications and devices for the treatment of acne. Radiofrequency, laser, and light treatments have demonstrated modest improvement for inflammatory acne (with blue-light photodynamic therapy being the only US FDA-approved treatment). However, limitations in study design and patient follow-up render these modalities as adjuncts rather than standalone options. This review will update readers on the latest advancements in our understanding of acne pathogenesis and treatment, with emphasis on emerging treatment options that can help improve patient outcomes.

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Nadifloxacin, an antiacne quinolone antimicrobial, inhibits the production of proinflammatory cytokines by human peripheral blood mononuclear cells and normal human keratinocytes

Cited by 46 publications

References 35 publications

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Antibiotics-Induced Obesity: A Mitochondrial Perspective

Platycodin D exerts anti-tumor efficacy in H22 tumor-bearing mice via improving immune function and inducing apoptosis

Recent Advances in Acne Pathogenesis: Implications for Therapy

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