Topical Mupirocin in the Treatment of Bacterial Skin Infections

1986 ◽  
Vol 20 (12) ◽  
pp. 943-948 ◽  
Author(s):  
Jean Rumsfield ◽  
Dennis P. West ◽  
Iris K. Aronson
Keyword(s):  
Eradication Rate ◽  
Active Drug ◽  
Response To Treatment ◽  
Clinical Use ◽  
Skin Infections ◽  
Dry Skin ◽  
Topical Antibiotic ◽  
Bacterial Skin Infections

Mupirocin is an investigational topical antibiotic used for treatment and prophylaxis of bacterial skin infections. Mupirocin differs from other antibiotics in its synthesis, structure, and mechanism of action. In vitro, mupirocin possesses antimicrobial activity against staphylococci, streptococci, Hemophilus influenzae, and Neisseria gonorrhoeae. Few studies comparing mupirocin to other topical antibiotics are available. Initial studies comparing mupirocin to inactive vehicle in the treatment of impetigo indicate an overall 92 percent pathogen eradication rate with active drug and 58 percent eradication rate with vehicle. Overall response to treatment of secondary skin infections was favorable in 91 percent of patients treated with mupirocin and 77 percent of those treated with vehicle. Although incidence is not greater than placebo, adverse effects have included pruritus, burning, dry skin, and erythema. Additional trials and clinical use should further help determine the role of mupirocin in the treatment of minor, primary, and secondary skin infections.

scholarly journals Identification of a microRNA signature in renal fibrosis: role of miR-21

2011 ◽  
Vol 301 (4) ◽  
pp. F793-F801 ◽  
Author(s):  
Abolfazl Zarjou ◽  
Shanzhong Yang ◽  
Edward Abraham ◽  
Anupam Agarwal ◽  
Gang Liu
Keyword(s):  
Epithelial Cells ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Response To Treatment ◽  
Tubular Epithelial Cells ◽  
Altered Expression ◽  
Tnf Α ◽  
Tgf Β1

Renal fibrosis is a final stage of many forms of kidney disease and leads to impairment of kidney function. The molecular pathogenesis of renal fibrosis is currently not well-understood. microRNAs (miRNAs) are important players in initiation and progression of many pathologic processes including diabetes, cancer, and cardiovascular disease. However, the role of miRNAs in kidney injury and repair is not well-characterized. In the present study, we found a unique miRNA signature associated with unilateral ureteral obstruction (UUO)-induced renal fibrosis. We found altered expression in UUO kidneys of miRNAs that have been shown to be responsive to stimulation by transforming growth factor (TGF)-β1 or TNF-α. Among these miRNAs, miR-21 demonstrated the greatest increase in UUO kidneys. The enhanced expression of miR-21 was located mainly in distal tubular epithelial cells. miR-21 expression was upregulated in response to treatment with TGF-β1 or TNF-α in human renal tubular epithelial cells in vitro. Furthermore, we found that blocking miR-21 in vivo attenuated UUO-induced renal fibrosis, presumably through diminishing the expression of profibrotic proteins and reducing infiltration of inflammatory macrophages in UUO kidneys. Our data suggest that targeting specific miRNAs could be a novel therapeutic approach to treat renal fibrosis.

scholarly journals The Antimicrobial Peptide Temporin G: Anti-Biofilm, Anti-Persister Activities, and Potentiator Effect of Tobramycin Efficacy Against Staphylococcus aureus

2020 ◽  
Vol 21 (24) ◽  
pp. 9410
Author(s):  
Bruno Casciaro ◽  
Maria Rosa Loffredo ◽  
Floriana Cappiello ◽  
Guendalina Fabiano ◽  
Luisa Torrini ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Human Keratinocytes ◽  
Skin Infections ◽  
Positive Bacterium ◽  
Persister Cells ◽  
Dividing Cells ◽  
Adverse Environmental Conditions ◽  
Bacterial Skin Infections ◽  
First Time

Bacterial biofilms are a serious threat for human health, and the Gram-positive bacterium Staphylococcus aureus is one of the microorganisms that can easily switch from a planktonic to a sessile lifestyle, providing protection from a large variety of adverse environmental conditions. Dormant non-dividing cells with low metabolic activity, named persisters, are tolerant to antibiotic treatment and are the principal cause of recalcitrant and resistant infections, including skin infections. Antimicrobial peptides (AMPs) hold promise as new anti-infective agents to treat such infections. Here for the first time, we investigated the activity of the frog-skin AMP temporin G (TG) against preformed S. aureus biofilm including persisters, as well as its efficacy in combination with tobramycin, in inhibiting S. aureus growth. TG was found to provoke ~50 to 100% reduction of biofilm viability in the concentration range from 12.5 to 100 µM vs ATCC and clinical isolates and to be active against persister cells (about 70–80% killing at 50–100 µM). Notably, sub-inhibitory concentrations of TG in combination with tobramycin were able to significantly reduce S. aureus growth, potentiating the antibiotic power. No critical cytotoxicity was detected when TG was tested in vitro up to 100 µM against human keratinocytes, confirming its safety profile for the development of a new potential anti-infective drug, especially for treatment of bacterial skin infections.

A comparison of porcine and human thyroid tissue in the assay of thyroid stimulating immunoglobulins

1986 ◽  
Vol 113 (3) ◽  
pp. 335-339
Author(s):  
S. de Rave ◽  
H. M.J. Goldschmidt ◽  
Y. T.J. Somers-Pijnenburg ◽  
B. Bravenboer ◽  
J. H. M. Lockefeer
Keyword(s):  
Medical Treatment ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Graves Disease ◽  
Clinical Use ◽  
Human Thyroid Tissue ◽  
Thyroid Stimulating Immunoglobulins ◽  
Camp Generation

Abstract. The central role of Thyroid Stimulating Immunoglobulins (TSI) in the pathogenesis of the hyperthyroidism of Graves' disease has become generally accepted and a wide variety of assays for the detection of these antibodies has been developed. The dependence on the availability of human thyroid tissue makes most of these assays unsuitable for routine clinical use, a problem circumvented by the use of nonhuman thyroid tissue in some TSI assays. We therefore compared porcine and human thyroid tissue in a TSI assay based on in vitro cAMP generation. No major differences in within and between run variation were found and, with some notable exceptions, a reasonable correlation could be demonstrated between the results in both assays (R = 0.89, P < 0.001). However, the sensitivity of the porcine TSI assay is only 60% of the estimated sensitivity of the human TSI assay. In spite of the practical advantages this porcine TSI assay, and possibly also other TSI assays using non-human thyroid tissue, cannot totally replace human TSI assays. The value of these assays in predicting the outcome of medical treatment of Graves' disease remains to be established.

Roles of Osteoclasts in Leukemic Cells

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3184-3184 ◽  
Author(s):  
Asumi Yokota ◽  
Shinya Kimura ◽  
Ruriko Tanaka ◽  
Rina Nagao ◽  
Kazuki Sakai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Resorption ◽  
Culture System ◽  
Bone Matrix ◽  
Collagen Gel ◽  
Leukemic Cells ◽  
Response To Treatment

Abstract We have previously reported that zoledoronic acid (ZOL) augmented the in vivo effect of imatinib in a murine chronic myeloid leukemia (CML) model (Blood 2003). ZOL alone induces apoptosis in leukemic cells in vitro by inhibiting prenylation of the Ras-related proteins. In addition to this direct anti-leukemic effect, we hypothesized that ZOL also has some influence in leukemic cells in vivo indirectly by destroying osteoclasts (OCs), which is the primary therapeutic activity of ZOL in osteoporosis patients. Supporting this notion is that by mediating bone resorption, OCs release a variety of cytokines such as IGF- 1, TGF-β, etc. that have accumulated in the bone matrix. It has been reported that OCs play an important role in bone metastasis of solid tumor, especially in cancer stem cells. However, little is known about the role of OCs in leukemia. Therefore, we investigated it in vitro and in vivo. For this purpose, we established an in vitro osteoblasts (OBs) and OCs co-culture system. The stable co-culture system that we developed includes collagen gel and murine primary OBs and OCs. In addition, murine femoral bone sections were sometimes added to this culture system so that the OCs could release the cytokines from the bone matrix. Thus, the collagen gel and OBs were placed in 12-well plates with and without bone sections and/or OCs. The transwell chambers over the wells then received 1×104 Ba/F3 cells that had been transfected with wild type bcr-abl (Ba/F3/bcr-abl cells). OBs markedly enhanced the growth of Ba/F3/bcr-abl cells in this indirect contact coculture system whereas the presence of both OBs and OCs slightly suppressed cell growth. Intriguingly, when bone sections were added (OBs+OCs+bone), Ba/F3/bcr-abl cell proliferation was significantly suppressed compared to the effect of OBs alone or OBs+OCs (Figure). Cell cycle analysis revealed that the G0/G1 population was increased in Ba/F3/bcr-abl cells co-cultured with OBs+OCs+bones. We also observed that the p27 protein levels of Ba/F3/bcr-abl cells increased upon co-culture with OCs or OCs+bones, similar to their response to treatment with purified TGF-β. We performed ELISAs to determine the concentrations of cytokines in the supernatants of co-cultured OBs and OCs. There were higher levels of TGF-β1 in the OBs+OCs+bones supernatant than in the OBs+OCs supernatant. Furthermore, OBs produced high levels of IGF-1. These findings suggest that OBs and OCs affect the proliferation and the cell cycle arrest of leukemic cells by releasing soluble factors, respectively. To more comprehensively elucidate the roles OCs play in leukemia cells in vivo, we used reveromycin A (RM-A) which inhibits bone resorption by specifically inducing apoptosis in OCs (Woo et al, PNAS 2006). RM-A did not have any in vitro effects on the proliferation of Ba/F3/bcr-abl cells. Thus, we could know the unalloyed role of OCs in leukemia with RM-A compared with ZOL which inhibited directly both OCs and leukemic cells. Our preliminary data show that RM-A suppresses the engraftment of inoculated Ba/F3/bcr-abl cells to nude mice. We also present data from ongoing studies showing the effect of RM-A on leukemic cells in murine models. These findings suggested that OCs may be an important constituent of leukemia stem cell niche and destruction of OCs by either ZOL or RM-A is a novel strategy for leukemia treatment. Figure Figure

scholarly journals Role of the Ceramide-CD300f Interaction in Gram-Negative Bacterial Skin Infections

2018 ◽  
Vol 138 (5) ◽  
pp. 1221-1224 ◽  
Author(s):  
Akie Maehara ◽  
Ayako Kaitani ◽  
Kumi Izawa ◽  
Emiko Shiba ◽  
Masakazu Nagamine ◽  
...  
Keyword(s):  
Skin Infections ◽  
Gram Negative ◽  
Bacterial Skin Infections

scholarly journals The role of bacterial skin infections in atopic dermatitis: expert statement and review from the International Eczema Council Skin Infection Group

2019 ◽  
Vol 182 (6) ◽  
pp. 1331-1342 ◽  
Author(s):  
H. Alexander ◽  
A.S. Paller ◽  
C. Traidl‐Hoffmann ◽  
L.A. Beck ◽  
A. De Benedetto ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Skin Infection ◽  
Skin Infections ◽  
Infection Group ◽  
Bacterial Skin Infections

Pan-caspase inhibition as a potential host-directed immunotherapy against MRSA and other bacterial skin infections

2021 ◽  
Vol 13 (601) ◽  
pp. eabe9887
Author(s):  
Martin P. Alphonse ◽  
Jessica H. Rubens ◽  
Roger V. Ortines ◽  
Nicholas A. Orlando ◽  
Aman M. Patel ◽  
...  
Keyword(s):  
Caspase 8 ◽  
Skin Infections ◽  
Caspase 9 ◽  
Potential Host ◽  
Caspase 1 ◽  
Caspase Inhibition ◽  
Mrsa Strains ◽  
Bacterial Skin Infections

Staphylococcus aureus causes most skin infections in humans, and the emergence of methicillin-resistant S. aureus (MRSA) strains is a serious public health threat. There is an urgent clinical need for nonantibiotic immunotherapies to treat MRSA infections and prevent the spread of antibiotic resistance. Here, we investigated the pan-caspase inhibitor quinoline–valine–aspartic acid–difluorophenoxymethyl ketone (Q-VD-OPH) for efficacy against MRSA skin infection in mice. A single systemic dose of Q-VD-OPH decreased skin lesion sizes and reduced bacterial burden compared with vehicle-treated or untreated mice. Although Q-VD-OPH inhibited inflammasome-dependent apoptosis-associated speck-like protein containing caspase activation and recruitment domain (ASC) speck formation and caspase-1–mediated interleukin-1β (IL-1β) production, Q-VD-OPH maintained efficacy in mice deficient in IL-1β, ASC, caspase-1, caspase-11, or gasdermin D. Thus, Q-VD-OPH efficacy was independent of inflammasome-mediated pyroptosis. Rather, Q-VD-OPH reduced apoptosis of monocytes and neutrophils. Moreover, Q-VD-OPH enhanced necroptosis of macrophages with concomitant increases in serum TNF and TNF-producing neutrophils, monocytes/macrophages, and neutrophils in the infected skin. Consistent with this, Q-VD-OPH lacked efficacy in mice deficient in TNF (with associated reduced neutrophil influx and necroptosis), in mice deficient in TNF/IL-1R and anti-TNF antibody-treated WT mice. In vitro studies revealed that combined caspase-3, caspase-8, and caspase-9 inhibition reduced apoptosis, and combined caspase-1, caspase-8, and caspase-11 inhibition increased TNF, suggesting a mechanism for Q-VD-OPH efficacy in vivo. Last, Q-VD-OPH also had a therapeutic effect against Streptococcus pyogenes and Pseudomonas aeruginosa skin infections in mice. Collectively, pan-caspase inhibition represents a potential host-directed immunotherapy against MRSA and other bacterial skin infections.

MED-12-2103-02

2021 ◽  
pp. 17-20
Author(s):  
O. Laknitskaya
Keyword(s):  
Group A Streptococcus ◽  
Interleukin 2 ◽  
Skin Infections ◽  
Traditional Treatment ◽  
Innate And Adaptive Immunity ◽  
Recombinant Interleukin 2 ◽  
Group A ◽  
Bacterial Skin Infections ◽  
Methods Of Treatment

Currently, one of the priority medical and social problems of medicine is to optimize the treatment of bacterial skin infections, in particular pyoderma associated with Streptococcus pyogenes-group A streptococcus. The traditional treatment complex, including antibacterial drugs used systemically or topically, selected taking into account individual sensitivity, the presence of pathognomonic microflora, is not always effective due to the increase in antibiotic resistance. Currently implemented methods of immunocorrection, taking into account changes in the immune status in this pathology, corresponding to the clinic of patients, are pathogenetically justified and can be effective. The use of immunomodulatory therapy requires a change in approaches to diagnosis, clarifying the role of factors of innate and adaptive immunity, intercellular mediators and the system of antioxidant protection, allowing to optimize the methods of treatment of this pathology. The use of recombinant interleukin-2 makes up for the lack of interleukin-2 in the blood serum of patients with streptoderma and contributes to the clinical recovery of patients.

Antihepcidin antibody treatment modulates iron metabolism and is effective in a mouse model of inflammation-induced anemia

Blood ◽  
2010 ◽  
Vol 115 (17) ◽  
pp. 3616-3624 ◽  
Author(s):  
Barbra J. Sasu ◽  
Keegan S. Cooke ◽  
Tara L. Arvedson ◽  
Cherylene Plewa ◽  
Aaron R. Ellison ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Response To Treatment ◽  
Antibody Testing ◽  
Antibody Treatment ◽  
Amino Acid Peptide ◽  
Iron Deficient ◽  
Anemia Treatment

Abstract Iron maldistribution has been implicated in multiple diseases, including the anemia of inflammation (AI), atherosclerosis, diabetes, and neurodegenerative disorders. Iron metabolism is controlled by hepcidin, a 25-amino acid peptide. Hepcidin is induced by inflammation, causes iron to be sequestered, and thus, potentially contributes to AI. Human hepcidin (hHepc) overexpression in mice caused an iron-deficient phenotype, including stunted growth, hair loss, and iron-deficient erythropoiesis. It also caused resistance to supraphysiologic levels of erythropoiesis-stimulating agent, supporting the hypothesis that hepcidin may influence response to treatment in AI. To explore the role of hepcidin in inflammatory anemia, a mouse AI model was developed with heat-killed Brucella abortus treatment. Suppression of hepcidin mRNA was a successful anemia treatment in this model. High-affinity antibodies specific for hHepc were generated, and hHepc knock-in mice were produced to enable antibody testing. Antibody treatment neutralized hHepc in vitro and in vivo and facilitated anemia treatment in hHepc knock-in mice with AI. These data indicate that antihepcidin antibodies may be an effective treatment for patients with inflammatory anemia. The ability to manipulate iron metabolism in vivo may also allow investigation of the role of iron in a number of other pathologic conditions.

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