An Italian team studied the gut microbiota of 52 patients who experienced at least two symptomatic episodes of kidney stones made of over 80% of calcium oxalate crystals (group C+), and compared it to that of 48 healthy controls. This type of stones is present in 70% of renal colic cases, usually with no identified primary cause. Diet (too high intakes of calcium and oxalate) is the only factor currently identified in the genesis of this idiopathic lithiasis, which is often recurrent. The involvement of the gut microbiota had already been suggested in a study that brought to light the ability of a gut bacterium (Oxalobacter formigenes) to degrade oxalate, thus reducing its absorption and urinary excretion.

Bacterial genera involved in hyperoxaluria

New studies support this hypothesis: samples from group C+ contained a lower diversity and, taxonomically, a significantly lower representation of three genera: Faecalibacterium, Enterobacter, Dorea. Nevertheless, the content of Oxalobacter formigenes detected in each sample was very low, and with no difference between groups. Scientists then researched a potential difference in oxalate-degrading activity. Five samples from each group were analyzed through a specific sequencing method targeting the genes involved in oxalate degradation. Samples from group C+ contained a reduced proportion of these genes that was inversely correlated to hyperoxaluria after 24 hours and fecal excretion. This genetic approach also identified for the first time bacteria and Archaea carrying genes involved in the degradation of oxalate (Escherichia coli among others) whose content was higher in the healthy control group.

Modulation of the microbiota: a promising avenue?

Previous studies were not able to demonstrate the efficacy of pre- and probiotics targeting Oxalobacter formigenes to prevent the recurrence of kidney stones. According to the researchers, this failure could come from the involvement of other species in the calcium oxalate balance. That is why these works provide new lines of research on the gut-liver axis and on the physiopathology of nephrolithiasis. They should make it possible to assess new therapeutic strategies related to the modulation of the gut microbiota.

Although poor diet and insufficient physical activity are unquestionable risk factors for excess weight and obesity, the gut microbiota could also play a major role: according to different studies, its composition during the first two years of life is related to the weight progression during that same time period. In a new study, researchers analyzed the gut microbiota of 165 Norwegian children as well as their mother’s BMI during pregnancy at 6 different timepoints between birth and the age of two. They then tried to correlate these results with the body mass index (BMI) (sidenote: Body Mass Index.  Ratio of weight in kg to square of height in sq.m ) of these same children ten years later.

An “obesogenic” microbiota despite a “normal” BMI

In children of normal weight, the BMI remains the same during their entire childhood; while in obese children, BMI constantly increases between 2 and 12 years old. However, the authors point out that only an extremely small minority of these children have a BMI at the age of 2 that heralds a future obesity. On the contrary, they observed a strong association between the composition of the microbiota at the age of 2 and the BMI at the age of 12. According to their calculations, the impact of the intestinal ecosystem on the BMI largely exceeds that of other known factors such as mode of delivery, duration of exclusive breastfeeding, exposure to antibiotics, or various maternal factors such as smoking, pre-pregnancy BMI, education level.

Early identification for a better prevention

According to the authors, having an “obesogenic” gut microbiota precedes weight gain by several years and seems to be mainly the result of direct mother-to-child transmission (mother excess weight or obesity, excessive weight gain during pregnancy…). They suggest that these findings are a step towards new and more targeted strategies to prevent childhood obesity that are based on the identification of high-risk children before the age of two, when their weight is still within the normal range.

Chronic obstructive pulmonary disease (COPD) affected 3.5 million people in France in 2010. It is responsible for over 100,000 hospitalizations per year for acute exacerbations (AE) (sidenote: Data from the French Haute Autorité de Santé (HAS) ) . These episodes are associated with an increase of short- and medium-term mortality rates. Studies have shown that patients with COPD have a decreased lung microbiota diversity, and this dysbiosis has been cited as a potential cause of airway inflammation and decreased local immunity.

Diversity ensures a better prognosis

A new international study recently found a possible severity marker of COPD, that could identify patients at high risk of death. 102 patients hospitalized for AE were included in the study and their sputum was collected on Day 1. The microbiome was analyzed through 16S rRNA sequencing, but unfortunately it could not be compared to standard sputum cultures (cytobacteriological examination). Patients were then monitored to determine the survival rate one year after this hospitalization. According to different indices, there is an inverse linear correlation between microbiota diversity and one-year mortality: the more diverse the microbiota, the lower one-year mortality.

A dangerous bacterial combination

<>In this study, two genera (sidenote: The technique used did not allow to identity relevant species from these two genera )  were discovered as having a strong prognostic potential. The first–Veillonella–is a bacterium from the oral commensal flora found in the lungs of adults. Its absence in the sputum of patients is associated to a 13-fold higher risk of death at one year, and Veillonella-positive (V+) patients have, in average, a shorter length of hospital stay than Veillonella-negative (V-) patients. Additionally, the presence of species from the Staphylococcus (S+) genus in the sputum is associated to a 7-fold higher risk of death at one year, and to longer hospital stays. A higher comorbidity in V‑/S+ patients was not detected: the combination of these two criteria is extremely unfavorable since V-/S+ patients are 85 times more likely to die within the first year than V+/S- patients. If these results are confirmed by other studies, screening for these two bacterial genera could thus become a “standard” test to identify high-risk patients.

The first four years of life are a key period for the development of the gut microbiota, based on the largest study ever carried out in children. This study was conducted in 903 American and European children and demonstrated that our “second brain” is built according to three very distinct phases. Between 3 and 14 months of age, bacteria colonize the gastrointestinal tract, settle and proliferate during the “developmental phase”. In the following 15 months, the flora experiences a “transitional phase”: some bacteria that were present until then disappear in favor of other species. Finally, starting on the 31^st month, children’s flora “stabilizes” to reach its final state.

Breastfeeding seems to be a key factor…

According to the authors, breastfeeding, either exclusive or partial, is “the main factor impacting the composition of the microbiota during the developmental phase”. It is associated to the presence of beneficial intestinal bacteria (even if the children have also received formula or solid food), and to a lesser diversity. However, we know that the microbiota’s diversity is a sign of maturity. At the age of 14 months, the flora of breastfed children should thus be less mature than that of other children. But when their diet does not contain breast milk anymore, their microbiota gets richer and diversifies. The researchers wrote that “these results seem to confirm the idea that maturation of the intestinal flora is induced by weaning, and not by dietary diversification”. The earlier breastfeeding is stopped, the quicker the microbiota matures, but it is unknown whether the impact on children’s health is positive or not.

…as well as environment

Other result: vaginal delivery promotes the development of the intestinal flora of newborns. Similarly, growing with siblings and/or having pets impact the composition of the microbiota and seems to accelerate its maturation. These different results will be useful to future research: they will allow scientists to more precisely analyze the link between the microbiota and the onset of some diseases and provide the opportunity to assess new therapeutic strategies.

Stunted growth affects one quarter of children under 5 years old in the world. One possible cause is pediatric environmental enteropathy (PEE), a syndrome responsible for malnutrition that associates repeated bacterial gut infections (caused by poor hygiene) and chronic inflammation attributable to SIBO (sidenote: SIBO Small Intestine Bacterial Overgrowth ) . According to a French study on children with stunted growth (from Madagascar and Central African Republic), this syndrome is not the only factor.

Translocation of the oral microbiota

Despite genetic, environmental and nutritional differences between the two countries, researchers discovered that affected children from either community have a gut microbiota colonization by bacteria from the oropharyngeal microbiota. Species belonging to Haemophilus, Neisseria, Moraxella or even Porphyromonas genera (that usually colonize the oral flora) were observed in the 57 gastric samples and 46 duodenal samples collected. However, according to the scientific literature, some of these bacteria are associated with inflammatory diseases (including gastrointestinal cancers, type 2 diabetes, cardiovascular diseases).

A fecal marker with diagnostic value

These oropharyngeal bacteria were also found in the duodenal samples and overrepresented in the 404 perirectal samples collected from children with stunted growth, and not in children from the control group. Enteropathogenic bacteria belonging to the Escherichia coli/Shigella and Campylobacter genera were also more abundant. A decrease in Clostridiales was also found in affected children. These bacteria produce butyrate, a short-chain fatty acid (SCFA) that feeds epithelial cells and participates in the resistance of the host against opportunistic bacteria proliferation. The stool of affected children could thus contain a characteristic signature of stunted growth combining oropharyngeal bacteria, enteropathogens and low level of Clostridiales. This could pave the way to the development of non-invasive markers.

New hypothesis

The authors suggest that the presence of oropharyngeal bacteria in the fecal microbiota could be a contributing factor to PEE physiopathology. Proliferation of these oropharyngeal bacteria in the small intestine and colon could lead to inflammation. Associated to the presence of enteropathogens and decreased rates of butyrate, it could prompt chronic malnutrition in children, and thus result into stunted growth. This hypothesis could be confirmed by the cohort study of 1,000 children which is currently in progress.

International researchers reached this conclusion by studying over 510 women aged 18 to 78 belonging to the Hmong and Karen tribes, minorities from South East Asia whose migrants to the US are particularly affected by obesity. Scientific literature has previously shown that there is a link between excess weight and disruptions of microbiota. To understand the impact of migration on the gut microbiota, scientists analyzed the intestinal flora of women still living in Thailand, of women who left their country of origin, as well as of about fifty female volunteers belonging to the second generation of migrants. Nineteen Karen refugees were also monitored before their departure and after arriving in the US, as well as 36 persons born in the US or from Europe.

Some indigenous bacteria disappear

These different analyses indicated that the microbiota is much more diverse and abundant in people living in Thailand than in immigrants. Microbiotas of migrants and native-born Americans were similar. More precisely, the researchers reported the disappearance of some bacteria in favor of others, suggesting that the migrants’ flora goes through a “westernization” process, and all within a few months. Consequence: first- and second-generation migrants have lost an enzyme able to degrade complex sugars (especially vegetable fibers), which is naturally absent in native-born Americans but abundant in Thai people still living in their country of origin.

Diet cannot explain everything

Researchers consider that dietary changes alone cannot explain these variations. The scientists indicated that “although children of immigrants and native-born Americans followed a different diet, surprisingly, their microbiotas were still similar”. They also pointed out that exposure to antibiotics, stress or different drinking water could also induce these disruptions. Finally, they moderated their results by indicating that it was still too early to conclude that these changes are caused by migration, or to state that they directly contribute to the high incidence of obesity in US immigrants.

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