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Meccanismi di virulenza del Clostridium botulinum A3 nell’intestino umano

Meccanismi di virulenza del Clostridium botulinum A3 nell’intestino umano

Chellapandi P. / Roja B.

104,14 €
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Editorial:
KS OmniScriptum Publishing
Año de edición:
2025
Materia
Biologia, ciencias de la vida
ISBN:
9786209246012
104,14 €
IVA incluido
Disponible

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Il genoma del Clostridium botulinum A3 Loch Maree (4.259.691 bp) produce neurotossine di tipo A3 e altri fattori di virulenza, con il gene bont/A sul plasmide pCLK_A0076. Questo ceppo mostra un alto tasso evolutivo, adattandosi agli ospiti e agli ambienti, e possiede 43 geni unici di virulenza e di difesa dell’ospite. Elementi extracromosomici ne potenziano la virulenza, tra cui la tossina botulinica A3. Su 521 proteine ipotetiche, molte sono coinvolte nel metabolismo degli aminoacidi e abbiamo previsto 13 nuove proteine di virulenza. Un modello di rete di regolazione globale ha rivelato 12 regolatori trascrizionali omologhi a Bacillus subtilis, che controllano i fattori di virulenza. Sono stati sviluppati un vaccino ricombinante a subunità e un vaccino multi-epitopo, mirati a proteine come l’idrolasi del peptidoglicano e la proteina extracellulare SCP-like, che mostrano interazioni stabili con i recettori immunitari. Questi vaccini, con allergenicità minima, sono candidati promettenti contro la virulenza del ceppo A3. La modellazione della rete ha rivelato interazioni ospite-microbo-farmaco, identificando l’acido linoleico come metabolita chiave. La clorochina è risultata efficace per il trattamento delle infezioni di origine alimentare, sostenendo la riproposizione degli antibiotici senza danneggiare i microbi intestinali benefici.

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