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Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
Rasa, S, Nora-Krukle, Z, Henning, N, Eliassen, E, Shikova, E, Harrer, T, Scheibenbogen, C, Murovska, M, Prusty, BK
Journal of translational medicine. 2018;16(1):268
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The causes of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are currently unknown, however viruses have been implicated. The absence of well-designed studies has hindered the understanding of this disease and the aim of this review was to discuss the literature regarding viruses and ME/CFS. Several viruses were discussed including the herpes virus, which is responsible for illnesses such as chicken pox and cold sores. This virus has not always been associated with the onset of ME/CFS, however it may be in certain individuals. The enteroviruses, which are responsible for illnesses such as hand, foot and mouth and polio, were also reviewed and it was concluded that it is unlikely that these have a role in ME/CFS. Several other viruses were also discussed. The authors then went on to describe how these viruses can affect human cells, potentially causing ME/CFS. It was concluded that the data available is controversial and only certain individuals may be affected, better studies are required. This study could be used by healthcare professionals to identify individuals at risk of ME/CFS following viral infection and understanding how ME/CFS may develop.
Abstract
BACKGROUND AND MAIN TEXT Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and controversial clinical condition without having established causative factors. Increasing numbers of cases during past decade have created awareness among patients as well as healthcare professionals. Chronic viral infection as a cause of ME/CFS has long been debated. However, lack of large studies involving well-designed patient groups and validated experimental set ups have hindered our knowledge about this disease. Moreover, recent developments regarding molecular mechanism of pathogenesis of various infectious agents cast doubts over validity of several of the past studies. CONCLUSIONS This review aims to compile all the studies done so far to investigate various viral agents that could be associated with ME/CFS. Furthermore, we suggest strategies to better design future studies on the role of viral infections in ME/CFS.
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Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
Ferrucci, L, Fabbri, E
Nature reviews. Cardiology. 2018;15(9):505-522
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Inflammageing is a term used to describe elevated blood inflammatory markers that leads to frailty and increases an individual’s risk for heart disease, kidney disease and other physical and mental illnesses. Whether inflammageing is causal in heart disease is still uncertain. This large review of 310 papers aimed to understand the causes and role of inflammageing in heart disease and other illnesses associated with ageing. Causes of inflammageing were discussed and mechanisms are not fully understood. Genetic susceptibility, obesity, gut microbiota, gut permeability, when cells can no longer divide, and chronic infections were all implicated. The role of inflammageing in heart disease was a focus and the authors deduced that it was likely to be both causal and a result of heart disease. However, the administration of anti-inflammatories in heart disease has not always proved a successful treatment. Possible causes of inflammageing are likely to be linked and cumulative and although inflammation may cause age related diseases, its role in protecting the body means that its benefits outweigh its consequences. It was concluded that controlling inflammageing may prevent heart disease and other diseases associated with ageing. This study could be used by healthcare professionals to help understand what inflammageing is and its role in age related diseases.
Abstract
Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty - which affect clinical manifestations, prognosis, and response to treatment - and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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Synbiotics modulate gut microbiota and reduce enteritis and ventilator-associated pneumonia in patients with sepsis: a randomized controlled trial.
Shimizu, K, Yamada, T, Ogura, H, Mohri, T, Kiguchi, T, Fujimi, S, Asahara, T, Yamada, T, Ojima, M, Ikeda, M, et al
Critical care (London, England). 2018;22(1):239
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The gut microbiota is disrupted in critically ill patients. Synbiotics are combinations of probiotics and prebiotics (nondigestible food ingredients that selectively stimulate the growth and/or activity of specific beneficial bacteria in the colon). The aim of this single-blind study was to evaluate whether synbiotics maintain the microbiota and reduce infectious complications in mechanically ventilated patients with sepsis. 72 such patients were randomly assigned to either receiving a synbiotic within three days of admission or not receiving a synbiotic. The synbiotic contained Lactobacillus casei strain Shirota, Bifidobacterium breve strain Yakult and galactooligosaccharides. Patients receiving the synbiotic had an increase in total bacteria, in particular Bifidobateria, Lactobacilli and Atopobium species, as well as higher organic acids (the fermentation products of bacteria) than the no-synbiotic group. There were significantly less infectious complications in the synbiotic group, including less enteritis (an inflammation of the small intestine) and less ventilation associated pneumonia. There were no differences in bacteraemia (the presence of bacteria in the bloodstream) or mortality between the two groups.
Abstract
BACKGROUND Commensal microbiota deteriorate in critically ill patients. The preventive effects of probiotic/synbiotic therapy on microbiota and septic complications have not been thoroughly clarified in patients with sepsis. The objective of this study was to evaluate whether synbiotics have effects on gut microbiota and reduce complications in mechanically ventilated patients with sepsis. METHODS Sepsis patients who were mechanically ventilated in the intensive care unit (ICU) were included in this randomized controlled study. Patients receiving daily synbiotics (Bifidobacterium breve strain Yakult, Lactobacillus casei strain Shirota, and galactooligosaccharides) initiated within 3 days after admission (the Synbiotics group) were compared with patients who did not receive synbiotics (the No-Synbiotics group). The primary outcome was infectious complications including enteritis, ventilator-associated pneumonia (VAP), and bacteremia within 4 weeks from admission. The secondary outcomes included mortality within 4 weeks, fecal bacterial counts, and organic acid concentration. Enteritis was defined as the acute onset of continuous liquid stools for more than 12 h. RESULTS Seventy-two patients completed this trial; 35 patients received synbiotics and 37 patients did not receive synbiotics. The incidence of enteritis was significantly lower in the Synbiotics than the No-Synbiotics group (6.3% vs. 27.0%; p < 0.05). The incidence of VAP was also significantly lower in the Synbiotics than the No-Synbiotics group (14.3% vs. 48.6%; p < 0.05). The incidence of bacteremia and mortality did not differ significantly between the two groups. In the analysis of fecal bacteria, the number of Bifidobacterium and Lactobacillus in the Synbiotics group was significantly higher than that in the No-Synbiotics group. In the analysis of fecal organic acids, total organic acid concentration, especially the amounts of acetate, were significantly greater in the Synbiotics group than in the No-Synbiotics group at the first week (p < 0.05). CONCLUSIONS Prophylactic synbiotics could modulate the gut microbiota and environment and may have preventive effects on the incidence of enteritis and VAP in patients with sepsis. TRIAL REGISTRATION UMIN, R000007633 . Registered on 29 September 2011.
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Longitudinal Study of the Psoriasis-Associated Skin Microbiome during Therapy with Ustekinumab in a Randomized Phase 3b Clinical Trial.
Loesche, MA, Farahi, K, Capone, K, Fakharzadeh, S, Blauvelt, A, Duffin, KC, DePrimo, SE, Muñoz-Elías, EJ, Brodmerkel, C, Dasgupta, B, et al
The Journal of investigative dermatology. 2018;138(9):1973-1981
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Chronic plaque psoriasis is an immune-mediated disease of the skin and joints. A growing appreciation of the role of the innate immune system in psoriasis pathogenesis stems from the prominent role of inflammatory cytokines and cells associated with innate immunity in the disease and associations observed between psoriasis and genetic variations involved in innate immunity. The aim of this study was to assess changes of the skin microbiome in the setting of a longitudinal phase 3b study of patients receiving up to 2 years of ustekinumab therapy. Results show that prior to treatment, there were minor, body-site specific differences in microbial diversity and composition when comparing lesional with non-lesional skin. Microbial heterogeneity was greater in lesional skin than non-lesional skin. During ustekinumab treatment, the composition of microbiota diverged further between lesional and non-lesional skin across body sites. The divergence observed between lesional and non-lesional skin during ustekinumab treatment varied by body site. Authors conclude that their findings may help inform future study design and it may also have medically relevant implications for diagnostics and therapeutics involving the skin microbiome.
Abstract
Plaque psoriasis, a chronic inflammatory disease primarily affecting the skin, is thought to have a multifactorial etiology, including innate immune system dysregulation, environmental triggers, and genetic susceptibility. We sought to further understand the role of skin microbiota in psoriasis pathogenesis, as well as their response to therapy. We systematically analyzed dynamic microbiota colonizing psoriasis lesions and adjacent nonlesional skin in 114 patients prior to and during ustekinumab treatment in a phase 3b clinical trial. By sequencing the bacterial 16S ribosomal RNA gene from skin swab samples obtained at six anatomical sites, we identified minor, site-specific differences in microbial diversity and composition between pretreatment lesional and nonlesional skin. During therapy, microbial communities within lesional and nonlesional skin diverged, and body-site dispersion increased, reflecting microbial skin site-specificity. Microbiota demonstrated greater pretreatment heterogeneity in psoriatic lesions than in nonlesional skin, and variance increased as treatment progressed. Microbiota colonizing recurrent lesions did not overlap with pretreatment lesional microbiota, suggesting colonization patterns varied between initial and recurrent psoriatic lesions. While plaque psoriasis does not appear to be associated with specific microbes and/or microbial diversity, this large dataset provides insight into microbial variation associated with (i) disease in different body locations, (ii) initial versus recurrent lesions, and (iii) anti-IL12/23 therapy.
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Long-term outcome of patients with steroid-refractory acute severe UC treated with ciclosporin or infliximab.
Laharie, D, Bourreille, A, Branche, J, Allez, M, Bouhnik, Y, Filippi, J, Zerbib, F, Savoye, G, Vuitton, L, Moreau, J, et al
Gut. 2018;67(2):237-243
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Intravenous steroids are the first-line therapy for ulcerative colitis (UC) patients who are hospitalised during a severe UC flare-up. In the 40% of patients who don’t respond to steroids, the drugs ciclosporin and infliximab have been found to be efficient in preventing surgery to remove part or all of the colon, but there is a lack of data on the long-term outcomes of using these medications in UC patients. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. Between 2007 and 2010, 115 patients with UC that did not respond to steroids were randomised to receive ciclosporin or infliximab in association with azathioprine. Patients were followed to January 2015 or death. After a median follow-up of 5.4 years, colectomy-free survival rates at 1 and 5 years were, respectively, 70.9% and 61.5% in patients who received ciclosporin and 69.1% and 65.1% in those who received infliximab. Long-term colectomy-free survival was independent from initial treatment. However, a higher proportion of patients initially treated with ciclosporin needed a new treatment compared with those who received infliximab first. The researchers concluded that these results further confirm a similar efficacy and good safety profiles of both drugs.
Abstract
OBJECTIVE Ciclosporin and infliximab have demonstrated short-term similar efficacy as second-line therapies in patients with acute severe UC (ASUC) refractory to intravenous steroids. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. DESIGN Between 2007 and 2010, 115 patients with steroid-refractory ASUC were randomised in 29 European centres to receive ciclosporin or infliximab in association with azathioprine. Patients were followed until death or last news up to January 2015. Colectomy-free survival rates at 1 and 5 years and changes in therapy were estimated through Kaplan-Meier method and compared between initial treatment groups through log-rank test. RESULTS After a median follow-up of 5.4 years, colectomy-free survival rates (95% CI) at 1 and 5 years were, respectively, 70.9% (59.2% to 82.6%) and 61.5% (48.7% to 74.2%) in patients who received ciclosporin and 69.1% (56.9% to 81.3%) and 65.1% (52.4% to 77.8%) in those who received infliximab (p=0.97). Cumulative incidence of first infliximab use at 1 and 5 years in patients initially treated with ciclosporin was, respectively, 45.7% (32.6% to 57.9%) and 57.1% (43.0% to 69.0%). Only four patients from the infliximab group were subsequently switched to ciclosporin. Three patients died during the follow-up, none directly related to UC or its treatment. CONCLUSIONS In this cohort of patients with steroid-refractory ASUC initially treated by ciclosporin or infliximab, long-term colectomy-free survival was independent from initial treatment. These long-term results further confirm a similar efficacy and good safety profiles of both drugs and do not favour one drug over the other. TRIAL REGISTRATION NUMBER EudraCT: 2006-005299-42; ClinicalTrials.gouv number: NCT00542152; post-results.
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Dietary Cholesterol and the Lack of Evidence in Cardiovascular Disease.
Soliman, GA
Nutrients. 2018;10(6)
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For years, dietary cholesterol was implicated in increasing blood cholesterol levels, therefore contributing to the development of cardiovascular disease (CVD). While it is known that saturated fatty acids and trans-fatty acids increase CVD risk, the evidence of dietary cholesterol increasing this risk remains inconclusive. This review summarises the current evidence regarding dietary cholesterol, blood cholesterol, saturated fatty acids and the risk of CVD. This review found that the current literature does not support the notion that dietary cholesterol increases the risk of heart disease in healthy individuals. The fact that dietary cholesterol is common in foods that are high in saturated fats may have contributed to the hypothesis that dietary cholesterol increases the risk of CVD. Based on these results, the author suggests individuals incorporate nutrient-dense, calorie controlled, balanced meals in eating patterns.
Abstract
Cardiovascular disease (CVD) is the leading cause of death in the United States. For years, dietary cholesterol was implicated in increasing blood cholesterol levels leading to the elevated risk of CVD. To date, extensive research did not show evidence to support a role of dietary cholesterol in the development of CVD. As a result, the 2015⁻2020 Dietary Guidelines for Americans removed the recommendations of restricting dietary cholesterol to 300 mg/day. This review summarizes the current literature regarding dietary cholesterol intake and CVD. It is worth noting that most foods that are rich in cholesterol are also high in saturated fatty acids and thus may increase the risk of CVD due to the saturated fatty acid content. The exceptions are eggs and shrimp. Considering that eggs are affordable and nutrient-dense food items, containing high-quality protein with minimal saturated fatty acids (1.56 gm/egg) and are rich in several micronutrients including vitamins and minerals, it would be worthwhile to include eggs in moderation as a part of a healthy eating pattern. This recommendation is particularly relevant when individual’s intakes of nutrients are suboptimal, or with limited income and food access, and to help ensure dietary intake of sufficient nutrients in growing children and older adults.
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Association between plasma fatty acids and inflammatory markers in patients with and without insulin resistance and in secondary prevention of cardiovascular disease, a cross-sectional study.
Bersch-Ferreira, ÂC, Sampaio, GR, Gehringer, MO, Torres, EAFDS, Ross-Fernandes, MB, da Silva, JT, Torreglosa, CR, Kovacs, C, Alves, R, Magnoni, CD, et al
Nutrition journal. 2018;17(1):26
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It is known that people with cardiovascular disease (CVD) have increased inflammation and raised levels of circulating inflammatory molecules. The presence of insulin resistance is thought to increase these levels, as are certain fatty acids coming from dietary fats. The aims of this cross-sectional study were to compare the levels of inflammatory biomarkers in patients with CVD with and without insulin resistance, and to evaluate the possible link between the blood levels of fatty acids and inflammatory biomarkers among these patients. The authors concluded that the CVD patients with insulin resistance had a higher concentration of some inflammatory molecules in the blood than those without insulin resistance. They also observed that saturated fatty acids were linked to higher levels of inflammatory molecules in the blood, while unsaturated fatty acids correlated with lower levels.
Abstract
BACKGROUND Proinflammatory biomarkers levels are increased among patients with cardiovascular disease, and it is known that both the presence of insulin resistance and diet may influence those levels. However, these associations are not well studied among patients with established cardiovascular disease. Our objective is to compare inflammatory biomarker levels among cardiovascular disease secondary prevention patients with and without insulin resistance, and to evaluate if there is any association between plasma fatty acid levels and inflammatory biomarker levels among them. METHODS In this cross-sectional sub-study from the BALANCE Program Trial, we collected data from 359 patients with established cardiovascular disease. Plasma fatty acids and inflammatory biomarkers (interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12, high sensitive C-reactive protein (hs-CRP), adiponectin, and tumor necrosis factor (TNF)-alpha) were measured. Biomarkers and plasma fatty acid levels of subjects across insulin resistant and not insulin resistant groups were compared, and general linear models were used to examine the association between plasma fatty acids and inflammatory biomarkers. RESULTS Subjects with insulin resistance had a higher concentration of hs-CRP (p = 0.002) and IL-6 (p = 0.002) than subjects without insulin resistance. Among subjects without insulin resistance there was a positive association between stearic fatty acid and IL-6 (p = 0.032), and a negative association between alpha-linolenic fatty acid and pro-inflammatory biomarkers (p < 0.05). Among those with insulin resistance there was a positive association between monounsaturated fatty acids and arachidonic fatty acid and adiponectin (p < 0.05), and a negative association between monounsaturated and polyunsaturated fatty acids and pro-inflammatory biomarkers (p < 0.05), as well as a negative association between polyunsaturated fatty acids and adiponectin (p < 0.05). Our study has not found any association between hs-CRP and plasma fatty acids. CONCLUSIONS Subjects in secondary prevention for cardiovascular disease with insulin resistance have a higher concentration of hs-CRP and IL-6 than individuals without insulin resistance, and these inflammatory biomarkers are positively associated with saturated fatty acids and negatively associated with unsaturated fatty acids.
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Crying Time and RORγ/FOXP3 Expression in Lactobacillus reuteri DSM17938-Treated Infants with Colic: A Randomized Trial.
Savino, F, Garro, M, Montanari, P, Galliano, I, Bergallo, M
The Journal of pediatrics. 2018;192:171-177.e1
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The causes of infant colic are unknown, but growing evidence shows a possible link with the gut microbiome. Increased inflammation has also been found in infants with colic, and this could be linked to dysbiosis. This double-blind, placebo-controlled clinical trial investigated whether supplementation with the probiotic Lactobacillus reuteri (L reuteri) DSM 17938 could reduce the crying time and modify inflammation in a group of infants with colic. Infants enrolled in the trial were less than 12 weeks old, with a healthy birth weight and predominantly breastfed. Infants with colic were given either 5 million colony-forming units (CFU) of L reuteri DSM 17938 or a placebo daily for 1 month. Crying times were significantly shortened among infants with colic given the probiotic, whilst the concentration of transcription factors for cells that help to regulate the immune system increased significantly. Infants treated with the probiotic showed an increase in the percentage of Lactobacillus and a decrease in the inflammatory marker faecal calprotectin. The authors concluded that their findings support the hypothesis that dysbiosis and inflammation may contribute to the onset of infant colic.
Abstract
OBJECTIVES To evaluate crying time, retinoid-related orphan receptor-γ (RORγ) and forkhead box P3 (FOXP3) messenger RNA levels (transcription factors that can modulate T cell responses to gut microbes), and to investigate gut microbiota and fecal calprotectin in infants treated with Lactobacillus reuteri for infantile colic. STUDY DESIGN A double-blind, placebo-controlled randomized trial was conducted in primary care in Torino from August 1, 2015 to September 30, 2016. Patients suffering from infantile colic were randomly assigned to receive daily oral L reuteri (1 × 108 colony forming unit) or placebo for 1 month. Daily crying times were recorded in a structured diary. FOXP3 and RORγ messenger RNA in the peripheral blood was assessed with real-time TaqMan reverse transcription polymerase chain reaction. Gut microbiota and fecal calprotectin were evaluated. RESULTS After infants with colic were supplemented with L reuteri DSM 17938 for 30 days, crying times were significantly shorter among infants with colic in the probiotic group compared with infants in the placebo group (74.67 ± 25.04 [IQR = 79] minutes /day vs 147.85 [IQR = 135] minutes /day [P = .001]). The FOXP3 concentration increased significantly (P = .009), resulting in decreased RORγ/FOXP3 ratios: 0.61 (IQR = 0.60) at day 0 and 0.48 (IQR = 0.28) at day 30 (P = .028). Furthermore, the probiotic increased the percentage of Lactobacillus (P = .049) and decreased fecal calprotectin (P = .0001). CONCLUSIONS Infants with colic treated with L reuteri for 30 days had a significantly decreased crying time and an increased FOXP3 concentration, resulting in a decreased RORγ/FOXP3 ratio. The treatment reduced fecal calprotectin. TRIAL REGISTRATION ClinicalTrials.gov: NCT00893711.
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Long-term Lactobacillus rhamnosus BMX 54 application to restore a balanced vaginal ecosystem: a promising solution against HPV-infection.
Palma, E, Recine, N, Domenici, L, Giorgini, M, Pierangeli, A, Panici, PB
BMC infectious diseases. 2018;18(1):13
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There is increasing interest in the role that the vaginal microbiome (the bacterial profile) plays in women’s health. Lactobacilli are the most dominant vaginal bacteria present in healthy women and it is known that when the bacteria get out of balance (a state called dysbiosis), disorders such as vaginosis and sexually transmitted diseases such as the Human Papilloma Virus (HPV) increase. This randomised pilot study aimed to investigate whether long-term use of Lactobacillus rhamnosus in women with dysbiosis and HPV-infection had an impact on treatment outcomes. 117 women with diagnosed vaginosis or vaginitis and HPV-infection were treated with standard antibiotic therapy and then randomly assigned to receive either 2-months or 6 months of vaginal Lactobacillus. At the median follow-up of 14 months post treatment, more than double the number of women in the 6-month probiotic treatment group received a negative HPV-pap smear, when compared to the 2-month treatment group. Randomised controlled trials are required to further this research, however Nutrition Practitioners working with women with vaginosis/vaginitis may want to consider the possible use of probiotics to support a healthy vaginal microbiome.
Abstract
BACKGROUND Over recent years, a growing interest has developed in microbiota and in the concept of maintaining a special balance between Lactobacillus and other bacteria species in order to promote women's well-being. The aim of our study was to confirm that vaginal Lactobacilli long-lasting implementation in women with HPV-infections and concomitant bacterial vaginosis or vaginitis might be able to help in solving the viral infection, by re-establishing the original eubiosis. METHODS A total of 117 women affected by bacterial vaginosis or vaginitis with concomitant HPV-infections were enrolled at Department of Gynecological Obstetrics and Urological Sciences, La Sapienza University, Rome, Italy between February 2015 and March 2016. Women were randomized in two groups, standard treatment (metronidazole 500 mg twice a day for 7 days or fluconazole 150 mg orally once a day for 2 consecutive days) plus short-term (3 months) vaginal Lactobacillus implementation (group 1, short probiotics treatment protocol group, n = 60) versus the same standard treatment plus long-lasting (6 months) vaginal Lactobacillus rhamnosus BMX 54 administration (group 2, treatment group, n = 57). RESULTS After a median follow up of 14 months (range 9-30 months) the chance to solve HPV-related cytological anomalies was twice higher in probiotic long-term users (group 2) versus short probiotics implementation group (group 1) (79.4% vs 37.5%, p = 0.041). Moreover, a total HPV-clearance was shown in 11.6% of short schedule probiotics implementation patients compared to a percentage of 31.2% in vaginal Lactobacilli long term users (p = 0.044), assessed as negative HPV-DNA test documented at the end of the study period. CONCLUSIONS The consistent percentage of clearance of PAP-smear abnormalities and HPV-clearance obtained in long-term treatment group has been interestingly high and encouraging. Obviously, larger and randomized studies are warranted to confirm these encouraging results, but we believe that eubiosis re-establishment is the key to tackle effectively even HPV-infection. TRIAL REGISTRATION Retrospectively registered on PRS NCT03372395 (12/12/2017).
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Profiling of lung microbiota in the patients with obstructive sleep apnea.
Lu, D, Yao, X, Abulimiti, A, Cai, L, Zhou, L, Hong, J, Li, N
Medicine. 2018;97(26):e11175
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Obstructive sleep apnoea is a disease of lower airways of the lungs. Numerous studies have reported that various commensal bacteria such as Streptococcus, Veillonella, Prevotella, and Actinomyces are predominant in healthy human lungs. Therefore the current study was designed to analyse and assess the lower airway microbiota in patients with Obstructive sleep apnoea (OSA) and compared it to that of control group (who did not have OSA but had other lung disease). Sleep apnoea was examined with a sleep diagnostic device and data were analysed with Profusion PSG software. The study was conducted in China and total number of subjects who took part in the study was 19. On comparison between the two groups revealed that, Fusobacteria species of bacteria was higher in OSA patients whilst firmicutes species was significantly less. The result from the study indicated that lung microbiota in OSA patients were different from those of control group(non OSA )patients and maybe manipulation of the microbiota could be considered as an intervention to increase airway immunity and decrease susceptibility to airway infections. Though the authors concluded that more studies are needed before these findings and interventions can be confirmed.
Abstract
Lung microbiota may affect innate immunity and treatment consequence in the obstructive sleep apnea (OSA) patients. Bronchoalveolar lavage fluid (BALF) was obtained from 11 OSA patients and 8 patients with other lung diseases as control, and used for lung microbiota profiling by PCR amplification and sequencing of the microbial samples. It was demonstrated that phyla of Firmicutes, Fusobacteria, and Bacteriodetes were relatively abundant in the lung microbiota. Alpha-diversity comparison between OSA and control group revealed that Proteobacteria and Fusobacteria were significantly higher in OSA patients (0.3863 ± 0.0631 and 0.0682 ± 0.0159, respectively) than that in control group (0.119 ± 0.074 and 0.0006 ± 0.0187, respectively, P < .05 for both phyla). In contrast, Firmicutes was significantly less in OSA patients (0.1371 ± 0.0394) compared with that in the control group (0.384 ± 0.046, P < .05). Comparison within a group (ß-diversity) indicated that the top 5 phyla in the OSA lung were Proteobacteria, Bacteroidetes, Firmicutes, Fusobacteria, and Acidobacteria, while the top 5 phyla in the control group were Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Acidobacteria. These findings indicated that lung microbiota in OSA is distinct from that of non-OSA patients. Manipulation of the microbiota may be an alternative strategy to augment airway immunity and to reduce susceptibility to airway infection.