| Mehrdad Gholami | 2 Articles |
<sec>
<title>Objectives</title>
<p>Genetic determinants conferring resistance to macrolide, lincosamide, and streptogramin B (MLS<sub>B</sub>) via ribosomal modification such as, <italic>erm</italic>, <italic>msrA/B</italic> and <italic>ereA/B</italic> genes are distributed in bacteria. The main goals of this work were to evaluate the dissemination of MLS<sub>B</sub> resistance phenotypes and genotypes in methicillin-resistant <italic>Staphylococcus aureus</italic> (MRSA) isolates collected from clinical samples.</p></sec>
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<title>Methods</title>
<p>A total of 106 MRSA isolates were studied. Isolates were recovered from 3 hospitals in Tehran between May 2016 to July 2017. The prevalence of MLS<sub>B</sub>-resistant strains were determined by D-test, and then M-PCR was performed to identify genes encoding resistance to macrolides, lincosamides, and streptogramins in the tested isolates.</p></sec>
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<title>Results</title>
<p>The frequency of constitutive resistance MLS<sub>B</sub>, inducible resistance MLS<sub>B</sub> and MS<sub>B</sub> resistance were 56.2%, 22.9%, and 16.6%, respectively. Of 11 isolates with the inducible resistance MLS<sub>B</sub> phenotype, <italic>ermC</italic>, <italic>ermB</italic>, <italic>ermA</italic> and <italic>ereA</italic> were positive in 81.8%, 63.6%, 54.5% and 18.2% of these isolates, respectively. In isolates with the constitutive resistance MLS<sub>B</sub> phenotype, the prevalence of <italic>ermA</italic>, <italic>ermB</italic>, <italic>ermC</italic>, <italic>msrA</italic>, <italic>msrB</italic>, <italic>ereA</italic> and <italic>ereB</italic> were 25.9%, 18.5%, 44.4%, 0.0%, 0.0%, 11.1% and 0.0%, respectively.</p></sec>
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<title>Conclusion</title>
<p>Clindamycin is commonly administered in severe MRSA infections depending upon the antimicrobial susceptibility findings. This study showed that the D-test should be used as an obligatory method in routine disk diffusion assay to detect inducible clindamycin resistance in MRSA so that effective antibiotic treatment can be provided.</p></sec>
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<sec><title>Objectives</title><p>Gastrointestinal disorders caused by <italic>Salmonella enterica</italic> serovar Enteritidis (<italic>Se</italic>sE) are a significant health problem around the globe. Probiotic bacteria have been shown to have positive effects on the immune responses. <italic>Lactobacillus acidophilus</italic> was examined for its capability to influence the innate immune response of HT29 intestinal epithelial cells towards <italic>Se</italic>sE. The purpose of this work was to assess the effect of <italic>L. acidophilus</italic> PTCC 1643 on cultured intestinal epithelial cells infected with <italic>Se</italic>sE.</p></sec><sec><title>Methods</title><p>HT29 cells were cultured in Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. The cells were treated with <italic>L. acidophilus</italic> PTCC 1643 after or before challenge with <italic>Se</italic>sE. At 2 and 4 hours post-infection, we measured changes in the expression levels of <italic>TLR2</italic> and <italic>TLR4</italic> via real-time polymerase chain reaction.</p></sec><sec><title>Results</title><p>Treatment with <italic>L. acidophilus</italic> inhibited <italic>Se</italic>sE-induced increases in <italic>TLR2</italic> and <italic>TLR4</italic> expression in the infected HT29 cells. Moreover, the expression of <italic>TLR2</italic> and <italic>TLR4</italic> in cells that were pretreated with <italic>L. acidophilus</italic> and then infected with <italic>Se</italic>sE was significantly higher than that in cells infected with <italic>Se</italic>sE without pretreatment. Taken together, the results indicated that <italic>L. acidophilus</italic> had an anti-inflammatory effect and modulated the innate immune response to <italic>Se</italic>sE by influencing <italic>TLR2</italic> and <italic>TLR4</italic> expression.</p></sec><sec><title>Conclusion</title><p>Our findings suggested that <italic>L. acidophilus</italic> PTCC 1643 was able to suppress inflammation caused by <italic>Se</italic>sE infection in HT29 cells and reduce <italic>TLR2</italic> and <italic>TLR4</italic> expression. Additional in vivo and in vitro studies are required to further elucidate the mechanisms underlying this anti-inflammatory effect.</p></sec>
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