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Since the level of antimicrobial resistance in Bacteroides fragilis has increased, monitoring the antimicrobial susceptibility could be necessary. The objectives of this study were to (i) investigate the prevalence of species, the occurrence of reduced antimicrobial susceptibility (E‐test method), and antibiotic resistance genes in the B. fragilis group and (ii) evaluate the prevalence of enterotoxigenic B. fragilis and the distribution of bft gene subtypes in hospitalized patients. As many as 475 isolates out of 250 stool samples were detected to be B. fragilis group by using conventional biochemical tests (API‐32A system) and multiplex‐PCR. In addition, 48.2%, 13.9%, 76.6%, and 1.2% of B. fragilis group isolates were resistant (according to EUCAST breakpoint) to piperacillin‐tazobactam, meropenem, clindamycin, and metronidazole, respectively. Six metronidazole‐resistant strains were isolated; B. fragilis (n: 3), B. thetaiotaomicron, B. vulgates, and B. ovatus. The presence of the cfiA, cepA, ermF, and nim genes was observed in 3.8%, 15.9%, 34.1%, and 0.7% of the B. fragilis isolates, respectively. One hundred thirty‐two B. fragilis isolates (27.8%)and 21 B  fragilis isolates (15.9%) turned out to be bft gene positive by multiplex‐PCR; eleven isolates (52.4%) harbored bft‐1, eight isolates (38%) harbored bft‐2 isotypes, and two isolates (9.5%) harbored bft‐3 isotype (16.66%). These bacteria harbor antimicrobial resistance genes that could be transferred to other susceptible intestinal strains. Further investigations on lineage analysis are needed for a better understanding of these bacteria in Iran.

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The antineoplastic effects of 5‐hydroxytryptamine (5‐HT) receptor antagonists have been shown in previous studies. However, the exact underlying mechanisms mediating these antineoplastic effects are unclear. In the present study, we assessed the antineoplastic effects of tropisetron, a 5‐HT receptor antagonist, in an experimental model of lung cancer in BALB/c mouse. Lewis lung carcinoma cell line was used to induce lung cancer. Mice were divided into four groups (n = 6) as follows: tumor‐bearing mice + tropisetron (5 mg/kg intraperitoneally [IP]), tumor‐bearing mice + tropisetron (10 mg/kg IP), tumor‐bearing mice + saline, healthy mice + tropisetron (10 mg/kg). Tumor burden, interferon‐γ (IFN‐γ), interleukin (IL)‐4, pathological response, Ki‐67, and E‐cadherin were assessed using enzyme‐linked immunosorbent assay, and real‐time polymerase chain reaction. Comet assay was used to assess DNA toxicity. Tropisetrone‐treated animals (either 5 or 10 mg/kg) showed significantly lower tumor sizes at the day 24th after tumor induction. Tropisetron received animals also showed significantly higher levels of IFN‐γ, E‐cadherin, pathologic response, and necrotic cells compared to the saline‐treated counterparts. In addition, the levels of IL‐4, and Ki‐67 were significantly lower in tropisetrone treated mice in comparison with control. Furthermore, tropisteron coadministration signifcantly reduced H2O2‐induced DNA toxicity while treatment with tropisteron alone showed no adverse effect on DNA. Tropisetrone can be used as a potential antineoplastic drug in lung cancer. This agent can promote its antineoplastic effects in part through modulating inflammatory and proliferating markers.