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• Conference paper
  Monaghan T, Russell L, Rosati E, Mullish BH, Roach B, Wong K, Wong GK-S, Polytarchou C, Franke A, Marchesi J, Kao Det al., 2021,
  , BSG Campus, Publisher: BMJ Publishing Group, Pages: A199-A200, ISSN: 0017-5749
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• Journal article
  Michael DR, Davies TS, Jack AA, Masetti G, Marchesi JR, Wang D, Mullish BH, Plummer SFet al., 2020,
  , Scientific Reports, Vol: 11

  <jats:title>Abstract</jats:title><jats:p>This 9-month randomised, parallel, double-blind, single-centre, placebo-controlled study (PROBE, ISRCTN18030882) assessed the impact of probiotic supplementation on bodyweight. Seventy overweight Bulgarian participants aged 45–65 years with BMI 25–29.9 kg/m<jats:sup>2</jats:sup> received a daily dose of the Lab4P probiotic comprising lactobacilli and bifidobacteria (50 billion cfu/day). Participants maintained their normal diet and lifestyle over the duration of the study. The primary outcome was change from baseline in body weight and secondary outcomes included changes in waist circumference, hip circumference and blood pressure. A significant between group decrease in body weight (3.16 kg, 95% CI 3.94, 2.38, <jats:italic>p</jats:italic> &lt; 0.0001) was detected favouring the probiotic group. Supplementation also resulted in significant between group decreases in waist circumference (2.58 cm, 95% CI 3.23, 1.94, <jats:italic>p</jats:italic> &lt; 0.0001) and hip circumference (2.66 cm, 95% CI 3.28, 2.05, <jats:italic>p</jats:italic> &lt; 0.0001) but no changes in blood pressure were observed. These findings support the outcomes of a previous shorter-term Lab4P intervention study in overweight and obese participants (PROMAGEN, ISRCTN12562026). We conclude that Lab4P has consistent weight modulation capability in free-living overweight adults.</jats:p>

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• Journal article
  Mullish BH, Allegretti JR, 2021,
  , Therapeutic Advances in Gastroenterology, Vol: 14, ISSN: 1756-2848

  <jats:p> Clostridioides difficile infection (CDI) remains a major global cause of gastrointestinal infection, with significant associated morbidity, mortality and impact upon healthcare system resources. Recent antibiotic use is a key risk factor for the condition, with the marked antibiotic-mediated perturbations in gut microbiome diversity and composition that underpin the pathogenesis of CDI being well-recognised. However, only relatively recently has further insight been gained into the specific mechanistic links between these gut microbiome changes and CDI, with alteration of gut microbial metabolites – in particular, bile acid metabolism – being a particular area of focus. A variety of in vitro, ex vivo, animal model and human studies have now demonstrated that loss of gut microbiome members with bile-metabolising capacity (including bile salt hydrolases, and 7-α-dehydroxylase) – with a resulting alteration of the gut bile acid milieu – contributes significantly to the disease process in CDI. More specifically, this microbiome disruption results in the enrichment of primary conjugated bile acids (including taurocholic acid, which promotes the germination of C. difficile spores) and loss of secondary bile acids (which inhibit the growth of C. difficile, and may bind to and limit activity of toxins produced by C. difficile). These bile acid changes are also associated with reduced activity of the farnesoid X receptor pathway, which may exacerbate C. difficile colitis throughout its impact upon gut barrier function and host immune/inflammatory response. Furthermore, a key mechanism of efficacy of faecal microbiota transplant (FMT) in treating recurrent CDI has been shown to be restoration of gut microbiome bile metabolising functionality; ensuring the presence of this functionality among defined microbial communities (and other ‘next generation’ FMT products) designed to treat CDI may be critical to their success. &

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• Journal article
  Huus KE, Frankowski M, Pučić-Baković M, Vučković F, Lauc G, Mullish BH, Marchesi JR, Monaghan TM, Kao D, Finlay BBet al., 2021,
  , Gut Microbes, Vol: 13, ISSN: 1949-0976
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• Journal article
  Mullish BH, Michael DR, McDonald JA, Masetti G, Plummer SF, Marchesi JRet al., 2021,
  , Gut, Vol: 70, Pages: 225-226
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• Conference paper
  Innes AJ, Ghani R, Mullish BH, Szydlo R, Palanicawandar R, Olavarria E, Apperley JF, Thursz MR, Williams HR, Marchesi JR, Davies F, Pavlu Jet al., 2020,
  , The 46th Annual Meeting of the European Society for Blood and Marrow Transplantation, Publisher: Springer Nature [academic journals on nature.com], Pages: 122-122, ISSN: 0268-3369
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• Journal article
  Baunwall SMD, Lee MM, Eriksen MK, Mullish BH, Marchesi JR, Dahlerup JF, Hvas CLet al., 2020,
  , EClinicalMedicine, Vol: 29-30, Pages: 100642-100642, ISSN: 2589-5370
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• Journal article
  Molinaro A, Bel Lassen P, Henricsson M, Wu H, Adriouch S, Belda E, Chakaroun R, Nielsen T, Bergh P-O, Rouault C, Andre S, Marquet F, Andreelli F, Salem J-E, Assmann K, Bastard J-P, Forslund S, Le Chatelier E, Falony G, Pons N, Prifti E, Quinquis B, Roume H, Vieira-Silva S, Hansen TH, Pedersen HK, Lewinter C, Sonderskov NB, Kober L, Vestergaard H, Hansen T, Zucker J-D, Galan P, Dumas M-E, Raes J, Oppert J-M, Letunic I, Nielsen J, Bork P, Ehrlich SD, Stumvoll M, Pedersen O, Aron-Wisneswky J, Clement K, Backhed Fet al., 2020,
  , Nature Communications, Vol: 11, ISSN: 2041-1723

  Microbiota-host-diet interactions contribute to the development of metabolic diseases. Imidazole propionate is a novel microbially produced metabolite from histidine, which impairs glucose metabolism. Here, we show that subjects with prediabetes and diabetes in the MetaCardis cohort from three European countries have elevated serum imidazole propionate levels. Furthermore, imidazole propionate levels were increased in subjects with low bacterial gene richness and Bacteroides 2 enterotype, which have previously been associated with obesity. The Bacteroides 2 enterotype was also associated with increased abundance of the genes involved in imidazole propionate biosynthesis from dietary histidine. Since patients and controls did not differ in their histidine dietary intake, the elevated levels of imidazole propionate in type 2 diabetes likely reflects altered microbial metabolism of histidine, rather than histidine intake per se. Thus the microbiota may contribute to type 2 diabetes by generating imidazole propionate that can modulate host inflammation and metabolism.

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• Journal article
  Martinez-Gili L, McDonald JAK, Liu Z, Kao D, Allegretti JR, Monaghan TM, Barker GF, Miguéns Blanco J, Williams HRT, Holmes E, Thursz MR, Marchesi JR, Mullish BHet al., 2020,
  , Gut Microbes, Vol: 12, Pages: 1810531-1810531, ISSN: 1949-0976
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• Conference paper
  Miguens Blanco J, Selvarajah U, Liu Z, Mullish BH, Alexander J, McDonald J, Abraham S, Marchesi Jet al., 2020,
  , ACR Convergence 2020, Publisher: Wiley, ISSN: 2326-5205
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