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Metals are widely used in animal feed for their growth-stimulating and antimicrobial effects, yet their use may potentially promote the proliferation of antibiotic resistance through co-selection. We studied the prevalence and associations of metal, antibiotic, and disinfectant resistances of 300 Salmonella Typhimurium isolates from pig meat, pig manure, chicken meat, poultry manure, and human stool from Sichuan, China. Seventy four percent of the 300 Salmonella Typhimurium isolates were considered resistant to Cu, almost 50% to Zn and Cr, over 25% to Mn and Cd, and almost 10% to Co. Most of the isolates carried at least one heavy metal resistance gene (HMRG). The Cr-Zn-Cd-resistance gene czcD was carried by 254 isolates and the Cu-resistance genes pcoR and pcoC by 196 and 179 isolates, respectively. Most of the isolates were resistant to at least one antibiotic and almost 80% were multidrug-resistant. The prevalence of resistance to six antibiotics was higher among the pig meat and manure isolates than among other isolates, and that of streptomycin and ampicillin were highest among the pig meat isolates and that of ciprofloxacin and ofloxacin among the pig manure isolates. From 55 to 79% of the isolates were considered resistant to disinfectants triclosan, trichloroisocyanuric acid, or benzalkonium chloride. The metal resistances and HMRGs were associated with resistance to antibiotics and disinfectants. Especially, Cu-resistance genes were associated with resistance to several antibiotics and disinfectants. The transfer of the Cr-Zn-Cd-resistance gene czcD , Cu-resistance gene pcoC , and Co-Ni-resistance gene cnrA into Escherichia coli and the increased Cu-resistance of the transconjugants implied that the resistance genes were located on conjugative plasmids. Thus, the excessive use of metals and disinfectants as feed additives and in animal care may have the potential to promote antibiotic resistance through co-selection and maintain and promote antibiotic resistance even in the absence of antibiotics., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Mustafa, Zhao, He, Chen, Liu, Mustafa, He, Yang, Yu, Penttinen, Ao, Liu, Shabbir, Xu and Zou.)

Purpose: The purpose of this study was to compare the efficacy and safety of thoracoscopic-laparoscopic Ivor-Lewis surgery and McKeown surgery in the treatment of thoracic middle-lower segment esophageal cancer., Methods: The clinical data of 136 patients with thoracic middle-lower segment esophageal cancer were divided into Ivor-Lewis group (n=68) and McKeown group (n=68). The perioperative indexes and the levels of tumor markers were observed. The patients' long-term survival condition was recorded via follow-up. Finally, the long-term quality of life of patients with a survival time >3 years was compared between the two groups after operation using EORTC QLQ-C30 and EORTC QLQ-OES18., Results: The operation time was significantly shorter in Ivor-Lewis group than that in McKeown group. The hospitalization expenses were obviously higher in Ivor-Lewis group than those in McKeown group. The incidence rate of anastomotic fistula, anastomotic stenosis and pulmonary infection was evidently lower in Ivor-Lewis group than that in McKeown group. Moreover, the levels of serum CYFRA21-1, CA125 and CEA evidently declined in both groups after treatment compared with those before treatment. The follow-up results revealed that the 3-year survival rate was 72.1% and 64.7%, respectively. The analysis results of postoperative 3-year quality of life manifested that no statistically significant difference was observed in each index in QLQ-C30 between the two groups, but the dysphagia and reflux scores in QLQ-EOS18 were remarkably superior in Ivor-Lewis group to those in McKeown group., Conclusions: In the treatment of thoracic middle-lower segment esophageal cancer, minimally-invasive Ivor-Lewis surgery has shorter operation time, better life quality, and fewer postoperative complications (pulmonary infection, anastomotic fistula and anastomotic stenosis) than minimally-invasive McKeown surgery, while the treatment expenses are higher.

Objectives: With the wide use of heavy metals as feed additives in animal production, little attention has been paid to heavy metal resistance in pathogenic bacteria. This study was performed to investigate the presence of heavy metal resistance genes (HMRGs) in Escherichia coli and Salmonella isolates and its correlation with disinfectant resistance genes (DRGs) and antibiotic resistance genes (ARGs)., Methods: HMRGs of 178 E. coli and 294 Salmonella isolated from chicken broiler farms and retail meat were detected by PCR. Minimum inhibitory concentrations (MICs) of heavy metals were determined by the broth microdilution method. The complete genome of E. coli E308, which had indications of multidrug resistance, was recovered and assembled using third-generation sequencing., Results: The frequency of different HMRGs in E. coli and Salmonella ranged from 0.60-77.0% and 0.30-87.1%, respectively. MICs of heavy metals for E. coli and Salmonella ranged widely from ≤12.5 mg/L to 1600 mg/L. Moreover, HMRGs (zntA, arsB, merA, pcoR, pcoA, pcoC and chrA) were found to be significantly associated with one or more DRGs [sugE(c), emrE, mdfA, ydgE/ydgF, qacF, sugE(p) and qacEΔ1] and ARGs (sul1, sul2, sul3, tetA, tetB, tetC, bla TEM , bla SHV and bla CTX ) (P < 0.05)., Conclusion: This study demonstrated that HMRGs are widely present in E. coli and Salmonella isolated from chicken farms and retail meat. The association between HMRGs with DRGs and ARGs may lead to co-resistance to heavy metals and other antimicrobial agents., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Pesticides introduced inadvertently or deliberately into environment by anthropogenic activity have caused growing global public concern, therefore the search of approaches for elimination of such xenobiotics should be encouraged. A cypermethrin-degrading bacterial strain Bacillus licheniformis B-1 was found to efficiently degrade carbaryl in LB medium at concentrations of 50-300 mg L -1 within 48 h, during which temperature and pH played important roles as reflected by increase in pollutant depletion. A stimulatory effect of Fe 3+ and Mn 2+ on microbial growth was observed, whereas Cu 2+ caused inhibition of degradation. Results showed that 1-naphthol was a major transformation product of carbaryl which was further metabolised. An approximately 29 kDa carbaryl-degrading enzyme was purified from B-1 with 15.93-fold purification and an overall yield of 6.02% was achieved using ammonium sulphate precipitation, DEAE-Sepharose CL-6B anion-exchange chromatography and Sephadex G-100 gel filtration. The enzyme was identified through nano reversed-phase liquid chromatography coupled with hybrid triple quadrupole time-of-flight mass spectrometry as a phosphodiesterase (PDE). This is the first report on the characterization of carbaryl-degrading by Bacillus spp. and the role of a PDE in carbaryl-detoxifying. Also, strain B-1 showed versatile in carbosulfan, isoprocarb and chlorpyrifos degradation, demonstrating as ideal candidate for environment bioremediation.

Numerous studies suggest a long duration of anesthesia during the late gestation period and infancy is associated with an increased risk of neuronal damage and neurocognitive impairment. The noble gas xenon is an anesthetic that is reported to have neuroprotective effects in some circumstances at certain concentrations. Currently, the effects of xenon on the brain and its potential neuroprotective properties, and/or the effects of xenon used in combination with other anesthetics, are not clearly understood and some reported data appear contradictory. In the present study, human neural stem cells were employed as a human-relevant model to evaluate the effects of xenon when it was co-administered with propofol, a frequently used anesthetic in pediatric anesthesia, and to understand the mechanism(s). The expression of polysialic acid (PSA) neural cell adhesion molecule (NCAM) on human neural stem cell-differentiated neurons was investigated as a key target molecule. PSA is a specific marker of developing neurons. It is essential for neuronal viability and plasticity. Human neural stem cells were maintained in neural differentiation medium and directed to differentiate into neuronal and glial lineages, and were exposed to propofol (50 μM) for 16 h in the presence or absence of xenon (33%). The neural stem cell-derived neurons were characterized by labelling cells with PSA-NCAM, after 5 days of differentiation. Propofol- and/or xenon-induced neurotoxicities were determined by measuring PSA immunoreactivity. A time course study showed that neuronal cell surface PSA was clearly cleaved off from NCAM by endoneuraminidase N (Endo-N), and eliminated PSA immunostaining was not re-expressed 4, 8, or 16 h after Endo-N washout. However, in the presence of 33% xenon, intense PSA staining on neuronal cell surface and processes was evident 16 h after Endo-N washout. In addition, prolonged (16 h) propofol exposure significantly decreased the positive rate of PSA-labeled neurons. When combined with xenon, propofol's adverse effects on neurons were attenuated. This work, conducted on the human neural stem cell-derived models, has provided evidence of the beneficiary effects of xenon on neurons and helps develop xenon-based anesthesia regimens in the pediatric population.

Early life exposure to general anesthetics can have neurotoxic consequences. Evidence indicates that xenon, a rare noble gas with anesthetic properties, may lessen neuronal damage under certain conditions. However, its potential neuroprotective properties, when used alone or in combination with other anesthetics, remain largely unknown. While it is difficult to verify the adverse effects of long duration anesthetic exposure in infants and children, the utilization of relevant non-clinical models (i.e., human-derived neural stem cells) may serve as a "bridging" model for evaluating the vulnerability of the nervous system. Neural stem cells, purchased from PhoenixSongs Biologicals, Inc., were guided to differentiate into neurons, astrocytes, and oligodendrocytes, which were then exposed to propofol (50 μM) for 16 h in the presence or absence of xenon (33%). Differentiation into cells of the neural lineage was confirmed by labelling with cell-specific markers, β-tubulin for neurons, glial fibrillary acidic protein (GFAP) for astrocytes, and galactocerebroside (GALC) for oligodendrocytes after 5 days of differentiation. The presence and severity of neural damage induced by anesthetic exposures were assessed by several methods, including the TUNEL assay, and immuno-histochemical measurements. Our data demonstrate that prolonged exposure to propofol results in a significant increase in the number of TUNEL-positive cells, indicating increased neural apoptosis. No significant changes were detected in the number of GFAP-positive astrocytes or GALC-positive oligodendrocytes. However, the number of β-tubulin-positive neurons was substantially reduced in the propofol-exposed cultures. Co-administration of xenon effectively blocked the propofol-induced neuronal damage/loss. No significant effects were observed when xenon was administered alone. The data indicate that prolonged exposure to propofol during development produces elevated levels of neuronal apoptosis in a human neural stem cell-derived model. However, sub-clinical, non-anesthetic concentrations of xenon, when used in combination with propofol, can prevent or ameliorate the toxic effects associated with prolonged anesthetic exposure. This is important as a more complete understanding of the neurotoxic mechanisms associated with a variety of clinically relevant anesthetic combinations becomes available. Protective approaches are critical for developing sound guidance on best practices for the use of these agents in the pediatric setting.

The authors have synthesized a phosphorescent probe of type SiO 2 -QD-MIP, where QD stands for Mn:ZnS quantum dots and MIP is a polymer coating that was molecularly imprinted with cephalexin. The nanoprobe with high specificity was prepared via sol-gel polymerization using thioglycolic acid (TGA)-modified QDs as luminescent materials, cephalexin as the template, 3-aminopropyltriethoxysilane as the functional monomer, and tetraethoxysilane as the crosslinking agent. The SiO 2 -QD-MIPs were characterized by X-ray powder diffraction, transmission electron microscopy, scanning electron microscopy, and Fourier transform infrared spectrometry. The orange emission of the probe, with excitation/emission maxima at 295/590 nm, decreases linearly in the 2.5-50 μg·L -1 cephalexin concentration range with a limit of detection (LOD) of 0.81 μg·L -1 . The nanoprobe was successfully applied to the determination of cephalexin in (spiked) raw milk and milk powder. The recoveries ranged from 91.7 to 103.7%.

LncRNAs are played crucial roles in athogenesis of NSCLC. LOXL1-AS1 involved in development of several tumors. So far, there is no study about expression and function pattern of the LOXL1-AS1 in NSCLC. In this reference, we firstly proved that LOXL1-AS1 was overexpressed in NSCLC cell lines (H23, A549, H1299 and SPC-A1) compared to 16HBE cell. The expression of LOXL1-AS1 was overexpressed in NSCLC specimens than adjacent control specimens. We found that 29 of 40 cases showed higher LOXL1-AS1 expression in NSCLC samples as compared to adjacent control specimens. Ectopic expression of LOXL1-AS1 promoted H1299 cell and H23 cell proliferation. LOXL1-AS1 overexpression promoted ki-67 and cyclin D1 expression in the NSCLC cell. Overexpression of LOXL1-AS1 promoted cell invasion and induced N-cadherin and Vimentin expression and suppressed E-cadherin expression in the NSCLC cell. LOXL1-AS1 acts as one sponge for miR-324-3p in NSCLC cell. Moreover, the expression of miR-324-3p was lower in NSCLC specimens than adjacent control specimens. We found that 24 of 40 cases showed lower miR-324-3p expression in NSCLC samples as compared to adjacent control specimens. Further correlation assay indicated a negative association between miR-324-3p and LOXL1-AS1 expression. miR-324-3p restoration attenuates the function of LOXL1-AS1 overexpression on NSCLC cell. These results indicated that LOXL1-AS1 enhanced NSCLC cell proliferation and invasion via sponging miR-324-3p in NSCLC cell., Competing Interests: None., (AJTR Copyright © 2019.)

Beta-cypermethrin (β-CY) and its major metabolite 3-phenoxybenzoic acid (3-PBA) spread extensively in the environment because of utilization in agricultural and home formulations, exerting negative impact on environment as well as human health. Several golden flower fungi were isolated from fu brick tea, by which the biodegradation of β-CY and 3-PBA was evaluated, turning out strain Eurotium cristatum ET1 had the highest capacity. Furthermore, β-CY and 3-PBA degradation rates were positively correlated with biomass of E. cristatum ET1, and the processes of degradation fitted well with a first-order kinetic equation. The half-lives of β-CY and 3-PBA ranged from 3.382 to 11.517 days and 1.749 to 3.194 days, respectively, under different substrate concentrations, incubation temperatures, and pH values. The degraded products were analyzed using gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry, and results showed that E. cristatum ET1 degrades β-CY by transforming it into 3-PBA, which is then gradually metabolized into phenol and catechol. Moreover, E. cristatum ET1 showed efficiency in degrading these metabolites. Our results suggest that this strain is a potential microorganism for bioremediation of pesticide-contaminated environments and fermented foods., (© 2018 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.)

Background: Salmonella is recognized as a common bacterial cause of foodborne diarrheal illness worldwide, and animal or its food products have been the most common vehicles of the Salmonella infections. This study aimed to investigate the distribution of Salmonella in two commercial layer farms and to determine the genetic relatedness between these strains. The Salmonella isolates were serotyped by slide agglutination using commercial antisera and analyzed for genetic relatedness using pulsed-field gel electrophoresis (PFGE)., Results: The internal environment had the highest prevalence of Salmonella (14/15, 93.3%), followed by external environment (60/96, 62.5%) and egg samples (23/84, 27.3%). The prevalence of Salmonella in the environment was significantly higher than that in egg samples ( p  < 0.05). The occurrence of Salmonella in the internal environment (93.3%) was relatively higher than in the external environment (55.6-77.2%). The 111 isolates were distributed among 15 PFGE types, and the PFGE results suggested that there existed cross-contamination between these strains not only from eggs, but also from the environments., Conclusions: The findings indicated ongoing Salmonella cross-contamination inside or outside of the layer farms, and that Salmonella could also spread along the egg production line.

Background: Animals exposed to sevoflurane during development sustain neuronal cell death in their developing brains. In vivo micro-positron emission tomography (PET)/computed tomography imaging has been utilized as a minimally invasive method to detect anesthetic-induced neuronal adverse effects in animal studies., Methods: Neonatal rhesus monkeys (postnatal day 5 or 6, 3 to 6 per group) were exposed for 8 h to 2.5% sevoflurane with or without acetyl-L-carnitine (ALC). Control monkeys were exposed to room air with or without ALC. Physiologic status was monitored throughout exposures. Depth of anesthesia was monitored using quantitative electroencephalography. After the exposure, microPET/computed tomography scans using F-labeled fluoroethoxybenzyl-N-(4-phenoxypyridin-3-yl) acetamide (FEPPA) were performed repeatedly on day 1, 1 and 3 weeks, and 2 and 6 months after exposure., Results: Critical physiologic metrics in neonatal monkeys remained within the normal range during anesthetic exposures. The uptake of [F]-FEPPA in the frontal and temporal lobes was increased significantly 1 day or 1 week after exposure, respectively. Analyses of microPET images recorded 1 day after exposure showed that sevoflurane exposure increased [F]-FEPPA uptake in the frontal lobe from 0.927 ± 0.04 to 1.146 ± 0.04, and in the temporal lobe from 0.859 ± 0.05 to 1.046 ± 0.04 (mean ± SE, P < 0.05). Coadministration of ALC effectively blocked the increase in FEPPA uptake. Sevoflurane-induced adverse effects were confirmed by histopathologic evidence as well., Conclusions: Sevoflurane-induced general anesthesia during development increases glial activation, which may serve as a surrogate for neurotoxicity in the nonhuman primate brain. ALC is a potential protective agent against some of the adverse effects associated with such exposures.

To demonstrate the resistance of antibiotics and disinfectants to Escherichia coli isolates, 255 E. coli strains were isolated from 328 retail meat samples in this study. Susceptibility testing results showed that 85.5% isolates were resistant to at least one antibiotic drug. The E. coli isolates showed the highest resistance to sulfamethoxazole (61.6%), followed by tetracycline (61.2%), ampicillin (48.2%), cefalotin (29.8%), and kanamycin (22.4%). The minimum inhibitory concentrations of the disinfectants cetyltrimethylammonium bromide, N,N-didecyl-N,N-dimethylammonium chloride, cetyltrimethylammonium bromide, and cetylpyridinium chloride for E. coli were 16-1,024, 4-1,024, 16-512, and 8-512 mg/L, respectively. The emrE, ydgE/ydgF, mdfA, and sugE(c) genes were commonly present (53.7-83.1%), but the qac and sugE(p) genes were less prevalent (0.0-14.9%). The qac genes were highly associated with antimicrobial resistance. Conjugative transfer experiment indicated that the disinfectant resistance genes, qacF, sugE(p), and qacEΔ1, were located on conjugative plasmids. Pulsed-field gel electrophoresis revealed that the antimicrobial-resistant isolates were associated with the sampling supermarkets or groceries. This study indicated that using quaternary ammonium compounds to decontaminate food processing environments may be ineffective and even provide a selective pressure for strains with acquired resistance to other antimicrobials.

3-phenoxybenzoic acid (3-PBA) with estrogen toxicity is one of the intermediate products of most pyrethroid pesticides. 3-PBA is difficult to degrade in the natural environment, and threatens food safety and human health. Microbial degradation of pyrethroids and their intermediate product (3-PBA) has become a hot topic in recent years. Here, we reviewed microbial species, degrading enzymes and degradation genes, degradation pathways of 3-PBA degrading and the application of 3-PBA degradation strains. This article provides references for the study of 3-PBA degradation by microorganisms.

Objective: To investigate the antimicrobial resistance and resistance profiles of Salmonella isolates, from the pork production chain in several districts of Sichuan province and to determine the correlation between serotype and the pulse field gel electrophoresis (PFGE) patterns., Methods: From 2010 to 2011, a total of 112 Salmonella isolates from pork production chain were examined for their antimicrobial susceptibility, using the micro-dilution method against 10 antimicrobial agents., Results: were assessed by the standard by the Clinical and Laboratory Standards Institute (CLSI, 2010). In addition, PFGE patterns were investigated among the Salmonella strains from different sources, under different serovars and antimicrobial profiles., Results: For Salmonella isolated from the pork production chain, resistance to tetracycline (89.29%) was frequently observed. Many isolates were resistant to spectinomycin (36.61%), trimethoprim/sulfamethoxazole (35.71%), nalidixic acid (33.93%) and ampicillin (24.11%), but all of the isolates were susceptible to ceftiofur. 33.93% of the isolates were multi-drug resistant. Salmonella isolates from the pork production chain had 19 antibiotic resistance profiles. Totally, 34 PFGE patterns were detected among 74 Salmonella isolates from the pork production chain, with the PFGE patterns of the 74 Salmonella isolates sharing 40% to 100% similarities., Conclusion: The antimicrobial resistances of the Salmonella isolates were commonly detected from the pork production chain in Sichuan province suggesting that Salmonella might horizontally spread from food animals to retail meat products.

Objective: To analyze the antimicrobial susceptibility of lactic acid bacteria (LAB) from yogurt, and to provide references for evaluating the safety of LAB and screening safe strains., Methods: The sensitivity of 43 LAB strains, including 14 strains of Streptococcus thermophilus, 12 strains of Lactobacillus acidophilus, 9 strains of Lactobacillus bulgaricus and 8 strains of Bifidobacterium, to 22 antibiotics were tested by agar plate dilution method., Results: All 43 LAB strains were resistant to trimethoprim, nalidixic acid, ciprofloxacin, lomefloxacin, danofloxacin and polymyxin E. Their resistances to kanamycin, tetracycline, clindamycin, doxycycline and cephalothin were varied. The sensitivity to other antibiotics were sensitive or moderate. All isolates were multidrug-resistant., Conclusion: The antimicrobial resistance of tested LAB strains was comparatively serious, and continuously monitoring their antimicrobial resistance and evaluating their safety should be strengthened.

Two strains of Enterobacteriaceae producing prodigiosin were isolated from meat in the Sichuan province of China in 2010. The strains were identified by Vitek system, 16S rDNA, rpoB, pfs and luxS genes. Minimum inhibitory concentrations were determined using the broth microdilution method. The two strains were screened for the presence of β-lactamase genes (blaTEM, blaSHV, blaOKP, and blaCTX-M genes). Based on PCR amplification and 16S rDNA sequencing the analysed strains were identified as Serratia marcescens. In addition, morphological and biochemical identification showed that the two stains were definitely S. marcesens. Antimicrobial susceptibility test showed that both strains were resistant to ampicillin and first-generation cephalosporins while being susceptible to cefotaxime, ceftiofur, ceftriaxone, imipenem and aztreonam. It was found that blaOKP had been identified first from the two S. marcescens strains, ch1 and ch2. The isolates were closely related as shown by pulsed-field gel electrophoresis (PFGE). The narrow-spectrum OKP-A β-lactamase gene blaOKP-A-13 was found to be chromosomally located in S. marcescens. The isolates produced a β-lactamase with a pI of approximately 8.2, which corresponds to the OKPA family. Findings indicate that OKP enzymes are not Klebsiella pneumoniae-specific chromosomal ?-lactamases, and the first isolation of S. marcescens producing OKP-A ?-lactamase suggests that the blaOKP gene may be disseminated between different species.

Brain abscesses result from a pyogenic parenchymal infection commonly initiated by Gram-positive bacteria such as Staphylococcus aureus. Although the host immune response elicited following infection is essential for effective bacterial containment, this response also contributes to the significant loss of brain parenchyma by necrosis that may be reduced by modulating the inflammatory response. Ciglitazone, a PPAR-gamma agonist with anti-inflammatory properties, was evaluated for its ability to influence the course of brain abscess development when treatment was initiated 3 days following infection. Interestingly, abscess-associated bacterial burdens were significantly lower following ciglitazone administration, which could be explained, in part, by the finding that ciglitazone enhanced S. aureus phagocytosis by microglia. In addition, ciglitazone attenuated the expression of select inflammatory mediators during brain abscess development including inducible NO synthase, TNF-alpha, IL-1beta, CXCL2, and CCL3. Unexpectedly, ciglitazone also accelerated brain abscess encapsulation, which was typified by the heightened expression of fibronectin and alpha-smooth muscle actin-positive myofibroblasts. Collectively, through its ability to attenuate excessive inflammation and accelerate abscess encapsulation, ciglitazone may effectively sequester brain abscesses and limit bacterial dissemination.

Microglia and astrocytes express numerous members of the Toll-like receptor (TLR) family that are pivotal for recognizing conserved microbial motifs expressed by a wide array of pathogens. Despite the critical role for TLRs in pathogen recognition, when dysregulated these pathways can also exacerbate CNS tissue destruction. Therefore, a critical balance must be achieved to elicit sufficient immunity to combat CNS infectious insults and downregulate these responses to avoid pathological tissue damage. We performed a comprehensive survey on the efficacy of various PPAR-gamma agonists to modulate proinflammatory mediator release from primary microglia and astrocytes in response to numerous TLR ligands relevant to CNS infectious diseases. The results demonstrated differential abilities of select PPAR-gamma agonists to modulate glial activation. For example, 15d-PGJ(2) and pioglitazone were both effective at reducing IL-12 p40 release by TLR ligand-activated glia, whereas CXCL2 expression was either augmented or inhibited by 15d-PGJ(2), effects that were dependent on the TLR ligand examined. Pioglitazone and troglitazone demonstrated opposing actions on microglial CCL2 production that were TLR ligand-dependent. Collectively, this information may be exploited to modulate the host immune response during CNS infections to maximize host immunity while minimizing inappropriate bystander tissue damage that is often characteristic of such diseases.