مکانیسمهای جدید مولکولی مقاومت به آنتی‌بیوتیک‌ها در باکتری‌ها

نوع مقاله : مقاله مروری

نویسندگان

1 دانشجوی دکتری، گروه زیست‌شناسی، دانشکده‌ی علوم، دانشگاه اصفهان، اصفهان، ایران

2 دانشیار، گروه زیست‌شناسی، دانشکده‌ی علوم، دانشگاه اصفهان، اصفهان، ایران

چکیده

فقط زمان کوتاهی بعد از کشف آنتی‌بیوتیک‌ها توسط الکساندر فلمینگ، باکتری‌های مقاوم به آنتی‌بیوتیک‌ها گزارش شدند. در کنار مکانیسم‌های قدیمی مقاومت در باکتری‌ها، مکانیسم‌های جدیدی توسط محققین مختلف توصیف پیشنهاد شده است. برای مثال، به تازگی، یک اپرون جدید D-آلانین-D-سرین به نام VanL، که باعث مقاومت به آنتی‌بیوتیک ونکومایسین می‌شود، گزارش شد. محققین نشان داده‌اند که از دست رفتن پورین Ompk36 در یک سویه‌ی کلبسیلا پنومونیه، که نقش مهمی در نفوذ آنتی‌بیوتیک‌ها به داخل سلول دارد، باعث مقاومت بالا به کارباپنم‌ها می‌شود. در سال 2011، برای اولین بار مقاومت کامل به آنتی‌بیوتیک تیگسیکلین گزارش شد که در آن آنزیم منواکسیژناز وابسته به فلاوین TetX باعث هیدروکسیله شدن آنتی‌بیوتیک و در نتیجه، غیرفعال شدن آن شده بود. در سال 2012، یک مقاومت بالا به آنتی‌بیوتیک موپریسین توصیف شد که توسط یک لوکوس جدید به نام mupB واسطه‌گری می‌شد. همچنین، در سال 2013 نشان داده شد که سویه‌هایی از باکتری انتروکوک فکالیس می‌توانند آنتی‌بیوتیک داپتومایسین را از محل هدف اصلی‌اش، یعنی محل تقسیم دیواره‌ی سلولی، به مکان‌های دیگر منتقل کرده، اثر آن را مهار کنند. یک مکانیسم جدید دیگر در باکتری بولخوردریا پسودومالئی گزارش شد که در آن، ژن هدف آنتی‌بیوتیک سفتازیدیم (PBP3) به طور کامل حذف شده بود. از طرف دیگر، نقش جدید ریبوسویچ‌ها در مقاومت به آنتی‌بیوتیک‌های آمینوگلیکوزیدی در سال 2013 گزارش شد. همچنین، مطالعات اخیر نشان‌دهنده‌ی ارتباط پاسخ SOS و حد نصاب احساس (Quorum sensing) با مقاومت آنتی‌بیوتیکی می‌باشد؛ مکانیسم‌های جدید مقاومت در بیوفیلم‌ها و سلول‌های Persister نیز شناخته شده است. در این مقاله‌ی مروری، به انواع این مکانیسم‌های جدید پرداخته شده است.

کلیدواژه‌ها


عنوان مقاله [English]

New Molecular Resistance Mechanisms against Antibiotics in Bacteria

نویسندگان [English]

  • Dariush Shokri 1
  • Mohammad Rabbani-Khorasgani 2
1 PhD Candidate, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran
2 Associate Professor, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran
چکیده [English]

Only a short time after the discovery of antibiotics by Alexander Fleming, antibiotic-resistant bacteria were reported. Besides the traditional mechanisms of resistance in bacteria, new mechanisms have been described by different researchers. For example, recently a new gene operon of D-alanine-D-serine called VanL that cuased resistant to the antibiotic vancomycin was reported. Other researchers have shown that Klebsiella pneumoniae strains lost purine Ompk36 that have a major role in the antibiotic diffusion into cells, are resistant to carbapenem. In 2011, the first full resistance to tigecycline was reported that the enzyme-linked monooxygenase flavin hydroxyl TetX cause deactivation of antibiotics. In 2012, high resistance to mupricin antibiotic was described that intermediated by a new locus named mupB. In addition, in 2013, it was showed that some strains of Enterococcus faecalis can move daptomycin antibiotic from its target to other places and so inhibit its activity. Removal of whole target gene (PBP3) of ceftazidime in Burkholderia pseudomallei was reported in 2012. In other hand, new role of riboswitch for resistance to aminoglycoside antibiotics reported in 2013. In addition, recent studies have indicated a relationship between SOS response and quorum sensing with antibiotic resistance and new antibiotic resistance mechanisms in bacterial biofilm and persister cells are known. In this review, recent studies have been conducted to identify these new mechanisms.

کلیدواژه‌ها [English]

  • Antibiotic
  • Antibiotic Resistance
  • Riboswitch
  • SOS response
  • Quorum sensing
  • Persister cells
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