Mo1774 Prenatal Antibiotic Treatment Increases Offspring's Susceptibility to Experimental Colitis: A Role of the Gut Microbiota

2015 ◽  
Vol 148 (4) ◽  
pp. S-708 ◽  
Author(s):  
Peris M. Munyaka ◽  
Azin Khafipour ◽  
Hongxing Wang ◽  
Nour Eissa ◽  
Ehsan Khafipour ◽  
...  
PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142536 ◽  
Author(s):  
Peris Mumbi Munyaka ◽  
N. Eissa ◽  
Charles Noah Bernstein ◽  
Ehsan Khafipour ◽  
Jean-Eric Ghia

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S173-S173
Author(s):  
L O’Connell ◽  
K Olli ◽  
C Rapp ◽  
C Collins ◽  
E McNamee ◽  
...  

Abstract Background The mucus gel layer (MGL) lining the colon is integral to exclusion of bacteria and maintaining intestinal homeostasis in health and disease. MGL defects allowing bacteria to directly contact the colonic surface are commonly observed in ulcerative colitis (UC). The major macromolecular component of the colonic MGL is the secreted gel-forming mucin, MUC2, whose expression is essential for homeostasis in health. In UC, another gel-forming mucin, MUC5AC is induced. In mice, Muc5ac is protective during intestinal helminth infection. Here, we tested the expression and functional role of MUC5AC/Muc5ac in colitis patient biopsies and murine colitis. Methods We measured MUC5AC/Muc5ac expression in UC patient biopsies and during acute dextran sulphate sodium (DSS) colitis. We performed DSS-colitis in mice deficient in Muc5ac (Muc5ac−/−) to model the potential functional role of Muc5ac in colitis. To assess MGL integrity, we quantified bacterial–epithelial interaction and translocation to mesenteric lymph nodes (MLNs). Antibiotic treatment was performed to directly investigate the role of colonic bacteria in our murine colitis studies. Results Colonic MUC5AC/Muc5ac mRNA expression increased significantly in active UC and murine colitis. Muc5ac−/− mice experienced worsened injury and inflammation in DSS-colitis compared with controls. This was associated with increased bacterial–epithelial contact and translocation to the MLN. Antibiotic treatment normalised colitis severity in Muc5ac−/− mice to that of antibiotic treated controls. Conclusion We demonstrate for the first time that MUC5AC/Muc5ac induction in acute colitis controls injury by reducing bacterial breach of the MGL. Therefore, developing strategies to induce MUC5AC expression may protect the intestinal barrier in UC.


2016 ◽  
Vol 150 (4) ◽  
pp. S583 ◽  
Author(s):  
Pedro M. Miranda ◽  
Viktoria Serkis ◽  
Giada de Palma ◽  
Marc Pigrau ◽  
Jun Lu ◽  
...  

Biology ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1013
Author(s):  
Maria Muñoz-Benavent ◽  
Amparo Latorre ◽  
Ester Alemany-Cosme ◽  
Jesús Marín-Miret ◽  
Rebeca Domínguez-Santos ◽  
...  

Blattella germanica presents a very complex symbiotic system, involving the following two kinds of symbionts: the endosymbiont Blattabacterium and the gut microbiota. Although the role of the endosymbiont has been fully elucidated, the function of the gut microbiota remains unclear. The study of the gut microbiota will benefit from the availability of insects deprived of Blattabacterium. Our goal is to determine the effect of the removal (or, at least, the reduction) of the endosymbiont population on the cockroach’s fitness, in a normal gut microbiota community. For this purpose, we treated our cockroach population, over several generations, with rifampicin, an antibiotic that only affects the endosymbiont during its extracellular phase, and decreases its amount in the following generation. As rifampicin also affects gut bacteria that are sensitive to this antibiotic, the treatment was performed during the first 12 days of the adult stage, which is the period when the endosymbiont infects the oocytes and lacks bacteriocyte protection. We found that after this antibiotic treatment, the endosymbiont population remained extremely reduced and only the microbiota was able to recover, although it could not compensate for the endosymbiont role, and the host’s fitness was drastically affected. This accomplished reduction, however, is not homogenous and requires further study to develop stable quasi-aposymbiotic cockroaches.


2018 ◽  
Vol 34 (7) ◽  
pp. 1135-1144 ◽  
Author(s):  
Jonathan M Chemouny ◽  
Patrick J Gleeson ◽  
Lilia Abbad ◽  
Gabriella Lauriero ◽  
Erwan Boedec ◽  
...  

Abstract Background Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. IgA is mainly produced by the gut-associated lymphoid tissue (GALT). Both experimental and clinical data suggest a role of the gut microbiota in this disease. We aimed to determine if an intervention targeting the gut microbiota could impact the development of disease in a humanized mouse model of IgAN, the α1KI-CD89Tg mice. Methods Four- and 12-week old mice were divided into two groups to receive either antibiotics or vehicle control. Faecal bacterial load and proteinuria were quantified both at the beginning and at the end of the experiment, when blood, kidneys and intestinal tissue were collected. Serum mouse immunoglobulin G (mIgG) and human immunoglobulin A1 (hIgA1)-containing complexes were quantified. Renal and intestinal tissue were analysed by optical microscopy after haematoxylin and eosin colouration and immunohistochemistry with anti-hIgA and anti-mouse CD11b antibodies. Results Antibiotic treatment efficiently depleted the faecal microbiota, impaired GALT architecture and impacted mouse IgA production. However, while hIgA1 and mIgG serum levels were unchanged, the antibiotic treatment markedly prevented hIgA1 mesangial deposition, glomerular inflammation and the development of proteinuria. This was associated with a significant decrease in circulating hIgA1–mIgG complexes. Notably, final faecal bacterial load strongly correlated with critical clinical and pathophysiological features of IgAN such as proteinuria and hIgA1–mIgG complexes. In addition, treatment with broad-spectrum antibiotics reverted established disease. Conclusions These data support an essential role of the gut microbiota in the generation of mucosa-derived nephrotoxic IgA1 and in IgAN development, opening new avenues for therapeutic approaches in this disease.


2001 ◽  
Vol 120 (5) ◽  
pp. A676-A676
Author(s):  
O KANAUCHI ◽  
K BREWERY ◽  
K MITSUYAMA ◽  
A ANDOH ◽  
Y ARAKI ◽  
...  

Author(s):  
Dong-Yu Kan ◽  
Su-Juan Li ◽  
Chen-Chen Liu ◽  
Ren-Rong Wu

Schizophrenia is a chronic and severe mental disorder with antipsychotics as primary medications, but the antipsychotic-induced metabolic side effects may contribute to the elevated risk of overall morbidity and mortality in patients with psych-iatric diseases. With the development in sequencing technology and bioinformatics, dysbiosis has been shown to contribute to body weight gain and metabolic dysfunction. However, the role of gut microbiota in the antipsychotic-induced metabolic alteration remains unknown. In this paper, we reviewed the recent studies of the gut microbiota with psychiatric disorders and antipsychotic-induced metabolic dysfunction. Patients with neuropsychiatric disorders may have a different composi-tion of gut microbiota compared with healthy controls. In addition, it seems that the use of antipsychotics is concurrently associated with both altered composition of gut microbiota and metabolic disturbance. Further study is needed to address the role of gut microbiota in the development of neuropsychiatric disorders and antipsychotic-induced metabolic disturbance, to develop novel therapeutics for both neuropsychiatric disorders and metabolic dysfunction.


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