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Urethritis is a sexually transmitted infection (STI) caused mainly by Neisseria gonorrhoeae, but also by Chlamydia trachomatis or Mycoplasma genitalium, and less commonly by a virus, such as herpes simplex. But up to 50% of non-gonococcal urethritis is considered to be idiopathic. In rare cases it is non-infectious and of undetermined etiology, which poses a diagnostic and therapeutic challenge for clinicians. Probabilistic antibiotic therapy is used widely in such cases, but can result in inadequate or excessive treatment with a risk of antibiotic resistance. Recent studies also suggest that the infectious agents responsible for non-gonococcal urethritis in men who have sex with women (MSW) are not the same as in those who have sex with men (MSM).

Exploration of urinary and urethral microbiota in relation to sexual orientation

Some Australian researchers sought to determine which infectious agents, apart from those already known, might contribute to non-gonococcal urethritis in men, taking into account their sexual practices and the biological sex of their partner. For this, they conducted a case study including 199 men, 96 of whom had symptoms of idiopathic urethritis and 103 of whom did not, who served as controls. The median age of participants was 31 years, 73 had had a sexual relationship with a man in the month prior to inclusion (classified as MSM), and the remainder were classified as MSW. For all of them, the researchers had samples of urinary and urethral microbiota available for sequencing analysis.

Urethritis not always “idiopathic”: hope for more targeted treatments 

Their results revealed that Haemophilus influenzae, which naturally colonizes nasopharyngeal microbiota, was more abundant in MSM participants with idiopathic urethritis. In addition, H. influenzae was clearly associated with clinical features such as urethral burning, dysuria and purulent discharge. The researchers believe having oral sex without a condom could be the main mode of contamination by this bacterium. They observed more of the genus Corynebacterium in affected MSW, which they found surprising since it is considered commensal in male genital microbiota. The scientists conclude that some specific species of Corynebacterium may become pathogenic when present in abundance. There were also more Ureaplasma, Staphylococcus haemolyticus, Streptococcus pyogenes, Escherichia and Streptococcus pneumoniae in the urinary and urethral microbiota of symptomatic subjects, so they may all promote urethritis. 

Possible infectious causes of non-gonococcal urethritis, previously described as idiopathic, have thus been discovered. If these results are confirmed by other studies, doctors may eventually be able to offer their patients more targeted treatments.

It’s hard to sleep like a baby when you’ve already celebrated your 65th birthday. At this age, one person in two suffers from chronic insomnia (sidenote: Insomnia Difficulty falling asleep or maintaining sleep, waking up early or feeling unrefreshed on waking. Severity is measured in terms of frequency of occurrence and daytime impact on everyday activities and on social and cognitive performance. Insomnia can be acute if it lasts less than a month, or chronic if it lasts more than 6 months.  Amatéis, C., Büla, C., Insomnies chez les personnes âgées : quelle approche ?, Rev Med Suisse, 2007/132 (Vol.-7), p. 2537–2541. ) , which aggravates age-related cognitive (sidenote: Cognition All the mental processes related to knowledge that involve attention, learning, intelligence, language, memory, perception, decision-making, problem-solving, reasoning, etc. Cognition_National Cancer Institute ) disorders. But rest assured: researchers are working hard to decipher the underlying mechanisms, about which we still know little.  One team decided to study gut microbiota, revealed several years ago as being capable of influencing brain function¹.

_{Sources (sidenote: https://www.revmed.ch/revue-medicale-suisse/2007/revue-medicale-suisse-132/insomnies-chez-les-personnes-agees-quelle-approche )}

As we get older, our dentition, salivary function, digestion and intestinal transit come under strain, affecting gut microbiota and causing an imbalance (dysbiosis): the composition and diversity of this mixed flora of bacteria, fungi, viruses and other small microorganisms (sidenote: Microorganisms Living organisms that are too small to be seen with the naked eye. They include bacteria, viruses, fungi, archaea and protozoa, and are commonly referred to as “microbes”. What is microbiology? Microbiology Society. ) evolve over the years, to the point where the elderly progressively develop a microbiota that is very different to that of younger adults.

Changes in gut microbiota linked to insomnia 

In elderly people suffering from insomnia, the researchers found that one bacterial phylum (Bacteroidetes) occupies the lion’s share, while there are fewer Firmicutes and Proteobacteria compared with healthy patients. More importantly, they discovered that in elderly people with insomnia, sleep and cognition alone explain 7.5 to 7.9% of the variation in gut microbiota composition, which has a significant impact, comparable according to a previous study² to that exerted by medication, blood parameters, digestive transit, diet, health status, weight and height!

Typical bacteria in insomniacs

They also found that elderly people with insomnia having high levels of Lachnoclostridium bacteria in their guts have high-quality sleep and better cognitive performance. Conversely, lower cognitive performance is associated with more Blautia.
There is no point attempting to deduce causal relationships; it would be impossible at this stage. On the other hand, gut microbiota may one day help in the diagnosis of elderly people with insomnia and cognitive decline. If a causal relationship is ever proven, it could also become a new therapeutic target in the field of aging... and sleep. But by then the sandman will have come and gone multiple times...

What is your opinion regarding the fact that nonalcoholic & alcoholic beer increased gut microbiota diversity, which has been associated with positive health outcomes?

Does that mean you could recommend your patients to drink 330 mL of beer every day? A recent randomized clinical trial investigated the effect of one daily beer (330 mL) with alcohol (5.2%) or without alcohol (0.0%) during a 4-week period [1]. Twenty-two healthy men were enrolled and the fecal microbiota was assessed. Bacterial diversity increased when baseline stool was compared with samples collected 4 weeks after the intervention in each group. However, diversity was not different between subjects consuming alcoholic or non-alcoholic beer. As the only difference between the two groups was alcohol, other substances present in both beverages might explain these differences. Bioactive compounds such as polyphenols and phenolic acids, which are present in alcoholic and non-alcoholic beer, might have a positive health effect possibly mediated via an increase in bacterial diversity. Some of these bioactive compounds develop during the brewing process and can originate from hops or malt. Bacteria in our gut are known to metabolize dietary compounds and might utilize them for their own metabolism. More experimental evidence is required to determine the effects of these bioactive compounds on gut bacteria. Ideally, such a trial should be done in a larger cohort of subjects who do not consume alcohol at baseline.

More studies are required before a recommendation for daily consumption of one beer can be made. This should be preferably non-alcoholic beer as alcohol, even in small amounts, has been associated with worse health outcomes.

How do you explain that drinking nonalcoholic or alcoholic beer daily during 4 weeks did not increase body weight and body fat mass and did not significantly change serum cardiometabolic biomarkers?

Comparison of the nine subjects in the non-alcoholic beer group versus ten subjects in the alcohol containing beer group finishing the aforementioned study showed largely no differences on liver function, inflammatory or metabolic markers. There are several possibilities why increased bacterial diversity did not translate into improvement of these markers. The study duration might have been too short and the number of participants in each group might have been too small. Although subjects in both groups were overweight, most other markers were within normal range. It would therefore be interesting to assess the effects in patients with metabolic syndrome, whether there is an improvement in intestinal dysbiosis, increase in bacterial diversity and a concomitant improvement in metabolic parameters.

ATOPIC DERMATITIS: SKIN MYCOBIOTA UNDER THE MICROSCOPE

^{Schmid B, Künstner A, Fähnrich A et al. Dysbiosis of skin microbiota with increased fungal diversity is associated with severity of disease in atopic dermatitis. J Eur Acad Dermatol Venereol. 2022 Jun 21.}

Atopic dermatitis (AD) is a complex and multifactorial inflammatory skin disease in which genetics, the immune system, and microbes play a role. For example, the skin of AD patients generally has an increased abundance of Staphylococcus aureus. But what about fungal communities? A recent study has shed some light on this little-known area. Skin swabs were taken from 16 AD patients and 16 healthy individuals at four skin sites (antecubital crease, dorsal neck, glabella, and vertex). To observe the course of the disease, the AD patients were sampled at three time points (weeks 0, 2, and 4) and the controls at two time points (weeks 0 and 4). An analysis of the 320 swabs showed that the Malassezia fungus predominated in all subjects, whether healthy or ill. However, in patients suffering from severe AD, this dominance was reduced in favor of fungi such as Candida or Debaryomyces, resulting in greater fungal diversity. As for bacteria, AD was characterized by lower levels of Cutibacterium and a greater relative abundance of Staphylococcus, particularly S. aureus and S. epidermidis. A higher presence of S. aureus may favor the proliferation of Candida, a synergistic activity between the two microorganisms having previously been shown. The study also showed a link between skin dysbiosis and the severity of AD: the bacterial and fungal communities of patients with severe AD differed significantly from those of controls and patients with mild-to-moderate forms of the disease. The skin communities of the latter two groups (mild-to-moderate AD and controls) were similar overall, with some distinctions in the bacterial communities (more staphylococci and less cutibacteria in mild-to-moderate AD versus no AD). Thus, a pronounced dysbiosis of the microbiota is characteristic of severe forms of AD, but not of less severe forms.

LINKING GASTROINTESTINAL MICROBIOTA AND METABOLOME DYNAMICS TO CLINICAL OUTCOMES IN PAEDIATRIC HAEMATOPOIETIC STEM CELL TRANSPLANTATION

^{Vaitkute G, Panic G, Alber DG, et al. Linking gastrointestinal microbiota and metabolome dynamics to clinical outcomes in paediatric haematopoietic stem cell transplantation. Microbiome 2022; 10: 89.}

Haematopoietic stem cell transplantation (HSCT) is used to treat many pathological conditions. At post-HSCT graft-versushost disease and infections can develop, being major causes of mortality. The current understanding of the role of the gut microbiota (GM) on adverse outcomes in paediatric patients post-HSCT is scarce. In a longitudinal study, Vaitkute et al. determined whether the GM and fecal metabolome associates with the clinical outcomes in 64 paediatric HSCT patients during ~ 66-days inpatient stay. Following HSCT, the GM alpha-diversity decreased. There were compositional shifts in the GM, and most of the patients did not return to their initial GM composition. The GM was clustered into community state types [CST(s)]. CST1 was common before HSCT, and included abundant Clostridium XIVa, Bacteroides and Lachnospiraceae. The lack of total parenteral nutrition contributed to CST1. CST2 was common at post-HSCT and was characterized by abundant Streptococcus and Staphylococcus as well as the use of vancomycin and metronidazole. CST3 was also common at post-HSCT and included abundant Enterococcus, Enterobacteriaceae and Escherichia. CST3 associated with a higher risk of viraemia, total parenteral nutrition and various antimicrobials. The metabolomic analyses revealed that fecal butyrate at baseline associated with a lower risk of viraemia. Longitudinally, acetate and butyrate decreased, and glucose increased after HSCT. The identified GM taxa and metabolites may be useful biomarkers for predicting the risk of complications post-HSCT. However, larger longitudinal studies are warranted.

A PROSPECTIVE STUDY OF THE INFANT GUT MICROBIOME IN RELATION TO VACCINE RESPONSE

^{Moroishi Y, Gui J, Nadeau KC, et al. A prospective study of the infant gut microbiome in relation to vaccine response. Pediatr Res 2022 [Epub ahead of print].}

The establishment of infant gut microbiota (GM) early in life is essential for the developing immune system. In addition, GM contributes to immune responses to vaccination, such as polio vaccine. However, research in this field is still scarce. Moroishi et al. enrolled 83 infants and studied the composition and functions of the early-life (6-weeks of age) GM in relation to infant antibody response to pneumococcal capsular polysaccharide (PCP) and tetanus toxoid (TT) at 1-year of age. PERMANOVA analyses of pair-wise GM community composition showed a weak association with PCP and TT antibody responses. In metagenome analyses, the authors found a negative association between TT response and Aeriscardovia aeriphila, whereas the association was positive with Staphylococcus aureus, Escherichia coli, Streptococcus thermophilus, and Anaerococcus vaginalis. However, only A. aeriphila remained significant after FDR correction. Lower PCP vaccine response associated with nine pathways, such as phenylalanine biosynthesis and pyrimidine deoxyribonucleotides de novo biosynthesis. In contrast, pantothenate and coenzyme A biosynthesis III, pyrimidine ribonucleosides degradation, methylphosphonate degradation II, and pyrimidine ribonucleotides de novo biosynthesis pathways were associated with higher PCP response. Five pathways associated positively with TT response, including especially CDP-diacylglycerol biosynthesis I and CDP-diacylglycerol. As a conclusion of this study, A. aeriphila could be used as a biomarker of TT response. Further, the early-life GM functions may influence an infant’s vaccine response.

META-ANALYSIS OF MUCOSAL MICROBIOTA REVEALS UNIVERSAL MICROBIAL SIGNATURES AND DYSBIOSIS IN GASTRIC CARCINOGENESIS

^{Liu C, Ng SK, Ding Y, et al. Meta-analysis of mucosal microbiota reveals universal microbial signatures and dysbiosis in gastric carcinogenesis. Oncogene 2022; 41: 3599-10.}

Gastric cancer (GC) is the 4th leading cause of cancer death. The developmental stages of GC are superficial gastritis (SG), atrophic gastritis (AG), intestinal metaplasia (IM), dysplasia and gastric carcinoma. Helicobacter pylori infection is a common player in GC that reduces secretion of stomach acid, allowing overgrowth of non-H. pylori microbes. Studies on the associations between gastric microbiota and GC have been inconsistent. Liu et al. did a meta-analysis of gastric microbiota from six independent studies to identify microbial signatures in GC. Alpha-diversity was lower in GC than in SG, AG and IM. Veillonella, Dialister, Granulicatella, Herbaspirillum, Comamonas, Chryseobacterium, Shewanella and Helicobacter were newly identified in this study as universal biomarkers discriminating GC from SG. In addition, opportunistic pathobionts Fusobacterium, Parvimonas, Veillonella, Prevotella and Peptostreptococcus were more abundant in GC than in SG. Contrarily, the abundance of Bifidobacterium, Bacillus and Blautia were lower. The microbial functions were inferred using PICRUSt2. Compared to SG, the most enriched pathway in GC was peptidoglycan maturation of peptidoglycan biosynthesis. The most depleted pathway in GC was Helicobacter specific tricarboxylic acid cycle, which agrees with the very low abundance of Helicobacter in GC patients. The authors further found that Helicobacter seems to affect gastric microbiota as H. pylori-negative patients had higher microbial diversity than the H. pylori-positive. To conclude, gastric microbiome can be a biomarker capable of distinguishing patients across disease stages.

A GLIMPSE AT THE HEALTHY MICROBIOME

Despite the timing on the last day, the high attendance of the popular session on “The microbiome as modulators of gut function” is easily explained by the selection of experts. Chaired by Pr. Harry Sokol (Paris, France) and Prof. Tim Vanuytsel (Leuven, Belgium), the first lecture by Pr. Jeroen Raes from the VIB Center for Microbiology (Leuven, Belgium) focused on the healthy gut microbiome. He stated that a definition of normal microbiota variation is essential to allow robust diagnostics, but that we do not even know what a healthy flora means. Indeed, only <10% of microbiota variation could be explained by host and environmental factors in the population- level analysis of the Flemish Gut Flora Project [1]. He showed that many of these variables replicated in the Dutch Microbiome Project, which recently confirmed the important effects of the environment and cohabitation [2].

In addition to the high between-individual variability, Pr. Raes showed evidence for substantial within-individual variation in the quantitative presence of microbial genera [3]. He explained that gut transit time was not only the primary confounder for microbiota composition but also the driver of temporal variation in healthy individuals. While the enterotypes (preferred community compositions) remained relatively stable, he richly illustrated the dysbiotic nature of the novel high-Bacteroides and low microbial load or B2-enterotype. Besides the diagnostic value of this marker across different diseases, he presented surprising findings of statins as a modulator of the microbiome. Finally, he stressed the need for more in vitro ecology work, as identification and isolation of species and their interactions is crucial to refine probiotic treatments and fecal microbiota transplantation (FMT).

FOCUS ON MICROBIAL STRAINS AND METABOLITES

As an alternative to in vitro work, Italian researchers presented improved strain-level metagenomics or the identification of subtypes of species in relation to FMT. As the first of many strong abstracts in the session on “Gut microbiome as pathogenic and therapeutic player”, the engraftment or strain sharing events within donors and recipients of FMT were nicely illustrated for different diseases. Interestingly, clinical success of FMT was associated with higher donor strain engraftment, which further improved with multiple routes of delivery and after antibiotics for infectious diseases [4]. Based on these findings, future donor-selection may not only optimize the microbiota composition but also the response after FMT, with specific protocols for different diseases.

During the main microbiome session, Pr. Nicolas Cenac (Toulouse, France) elaborated on the role of bacterial lipopeptides in irritable bowel syndrome (IBS), one of the most common gastrointestinal disorders. Following evidence of analgesic properties of these metabolites, his group explored the link between stress-induced dysbiosis during pregnancy and the development of colonic visceral hyper- sensitivity (VHS), a hallmark of IBS. He nicely illustrated that prenatal stress induced IBS-like symptoms in mice, with a decrease in Ligilactobacillus murinus, which was associated with VHS. This also led to a lower production of lipopeptides containing γ-aminobutyric acid (GABA), with reversal of VHS after colonic administration in mice. Pr. Cenac explained how translation in humans was needed and confirmed by lower GABA-lipopeptides in feces of IBS-patients. The microbial metabolites are exciting new players in IBS and were fully published after the congress.[5]

MICROBIOME, MEDITERRANEAN DIET AND IMMUNOTHERAPY

Important abstracts of UEG Week covered the potential factors related to the success of immuno-therapy in melanoma, a type of skin cancer. Dr. Johannes R. Björk (Groningen, The Netherlands) presented changes in the gut microbiome in response to immunotherapy. As one of the Top Abstract awardees, he kicked off the second part of the opening session by showing evidence of baseline gut microbial biomarkers predictive of response. However, he explained that microbiota dynamics over the treatment course are still unexplored. Based on a multi-center cohort study, his longitudinal analysis of repeated stool sampling showed that species from the family Lachnospiraceae increased in responders, while species from the family Bacteroides increased in non-responders. Besides these novel potential targets (e.g., for FMT), the microbiota changes in those affected by immunotherapy-induced colitis may also provide diagnostic markers for the future. Interestingly, the increased butyrate producers in responders suggested a role of fiber degradation. Therefore, the same groups of researchers from the Netherlands and UK focused on the role of dietary intake in a separate analysis. They showed that patients who responded to immunotherapy were more likely to adhere to a Mediterranean diet, which is high in mono-unsaturated fatty acids, polyphenols, and fiber. In addition, immunerelated side effects were less likely with intake of whole grains or legumes and more likely with high red and processed meat. Future clinical trials will show whether this translates to treatment benefits for various tumor types, including gastrointestinal cancers.

In conclusion, important and novel findings on microbial strains, metabolites and the role of diet have advanced our understanding of the gut microbiome in disease, while taking important confounders (even in the healthy microbiome) into account.

WHAT DO WE ALREADY KNOW ABOUT THE SUBJECT?

Food intake is essential to the survival of animals, and the inappropriate regulation of feeding behavior leads to serious metabolic and psychiatric consequences, such as obesity and anorexia [2]. Food intake involves complex processes from nutrient processing and uptake in the gut and its periphery to the central nervous system that regulates appetite and drives feeding. Much focus in the field of appetite biology has centered on the characterization of neural circuits involved in feeding, such as the agouti-related peptide (AgRP)-expressing neurons in the arcuate hypothalamus that are necessary for homeostatic feeding [3]. More recently, the gut and its resident microbes have been shown to regulate metabolism [4] and aspects of feeding behavior [5]. Whether compounds produced by microbes are influencing appetite remains less well-established. Short chain fatty acids as a byproduct of microbial fermentation reduce food intake in mice [6].

However, a gut-brain pathway that links microbial compounds to neuronal processes that regulate appetite and feeding behavior has not been previously shown. The microbial pattern recognition receptor Nod2 is suggested to mediate feeding, as Nod2 knockout mice shows enhanced weight gain when fed a high fat diet [7]. Furthermore, the downstream signaling component of Nod2, nuclear factor kB (NFkB), is expressed in neurons of the hypothalamus, and its hypothalamic activation regulates energy balance [8]. This suggests that the hypothalamus may present a unique integration point for signals derived from the microbiome and feeding behaviors.

WHAT ARE THE MAIN INSIGHTS FROM THIS STUDY?

The authors demonstrated that activation of Nod2 signaling in the hypothalamus affected feeding and thermoregulatory behavior in mice (Figure 1). Nod2 was found to be expressed in neurons in multiple regions of the mouse brain, including the striatum, thalamus, and hypothalamus. The authors then investigated whether radiolabeled muropeptides could reach the brain, when introduced through the gastrointestinal tract directly or via radiolabeled bacteria. Both methods of delivery resulted in the accumulation of muropeptides in the brain.

To investigate the functional role of Nod2 in neurons, conditional knockout mouse models that targeted Nod2 for deletion were utilized to show that older female mice with Nod2 deleted in inhibitory neurons expressing the vesicular GABA transporter (Vgat/ Slc32a1) display increased weight gain and dysregulated temperature control. Measurement of Fos expression in the brain revealed that older female mice have higher neuronal activity in the arcuate and dorsomedial regions of the hypothalamus. Next, the authors injected Cre-expressing adeno-associated viruses (AAVs) into Nod2^flox mice to knockout Nod2 expression locally in inhibitory neurons of the arcuate hypothalamus, demonstrating that Nod2 deficiency in hypothalamic neurons was sufficient to cause weight changes and temperature dysregulation (Figure 2).

Finally, to examine the role of the microbiota in the Nod2-dependent changes in appetite and temperature regulation, the authors treated hypothalamic neuron-specific Nod2 knockout mice with broad-spectrum antibiotics. Hypothalamic Nod2-deficent mice that underwent antibiotic treatment display normal appetite and weight gain until the antibiotics are removed, at which point they exhibit increased appetite and weight gain compared to Nod2-sufficient control mice. This data suggests that microbiota- derived products can modulate appetite in female mice via a Nod2-dependent mechanism.

WHAT ARE THE CONSEQUENCES IN PRACTICE?

In this interesting new work, Gabanyi et al. identified a functional role for Nod2 expression in neurons of the hypothalamus in regulating appetite and temperature in aging female mice, but not in male mice. The cellular and molecular mechanisms that determine this effect remain to be elucidated. Sex differences in microbiome composition may play a role in the dissimilarities in response to neuronal Nod2 deficiency; however, microbial composition was not investigated by the authors. Moreover, in addition to muropeptides, other microbe-derived products and endogenous stimuli can regulate the expression or activation of Nod2 [9], though are not addressed in this study. Additional data is needed to distinguish the activity and contribution of these alternative stimuli from muropeptides. Other possible contributors to the outcomes reported in the paper may include the increased gut and blood-brain barrier permeability that occurs with age, which may allow more microbe-derived molecules to enter the circulation from the gut and accumulate in the brain [10]. Further investigation is required to clarify the roles of sex and age in the observed phenotypes.

Schizophrenia is a psychiatric illness counted among the psychotic disorders and is often unjustly reduced to the aggressive behavior of affected patients. What causes this propensity to aggressiveness? According to a team of Chinese researchers¹, the gut microbiota may be involved.

From inflammation to dysbiosis

The starting point for their hypothesis is that the bodies of schizophrenic patients with aggressive tendencies are rich in inflammatory molecules. According to the authors, this state of generalized inflammation may impact patients’ gut microbiota (although this causal relationship has yet to be confirmed). They note that the gut flora of schizophrenic patients with aggressive tendencies varies significantly from that of schizophrenic patients with no such tendencies: it is less diverse, with some species dominating, while others have been depleted. The gut bacteria are involved in the production of certain molecules, notably short-chain fatty acids (sidenote: Short chain fatty acids (SCFA) Short chain fatty acids (SCFA) are a source of energy (fuel) for an individual’s cells. They interact with the immune system and are involved in communication between the intestine and the brain. Silva YP, Bernardi A, Frozza RL. The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication. Front Endocrinol (Lausanne). 2020;11:25. ) (SCFAs) and neurotransmitters (sidenote: Neurotransmitters Specific molecules that enable communication between the neurons (the nerve cells in the brain), as well as with the bacteria in the microbiota. They are produced by the individual’s cells and by the bacteria in the microbiota.    Baj A, Moro E, Bistoletti M, Orlandi V, Crema F, Giaroni C. Glutamatergic Signaling Along The Microbiota-Gut-Brain Axis. Int J Mol Sci. 2019;20(6):1482. ) . In the schizophrenic patients with aggressive tendencies, six SCFAs and six neurotransmitters were significantly depleted.

From dysbiosis to oxidation and aggressiveness?

According to the researchers’ theory, a direct consequence of this imbalance (or dysbiosis) is that the gut is more permeable. Usually the gut wall, made up of a layer of tightly joined cells, acts as a barrier between the contents of the digestive tract and the bloodstream. When the gut microbiota is unbalanced (as with schizophrenic patients with aggressive tendencies), the gut barrier becomes permeable and porous, allowing gut bacteria to reach the bloodstream. The researchers suspect that this mechanism generates a specific reaction known as oxidative stress (sidenote: Oxidative stress Oxidative stress is where the cell no longer controls the excessive presence of toxic molecules (free radicals) that can damage cells and DNA. Pizzino G, Irrera N, Cucinotta M, et al. Oxidative Stress: Harms and Benefits for Human Health. Oxid Med Cell Longev. 2017;2017:8416763.  ) , where molecules harmful to the body (pro-oxidant molecules called free radicals) and known to damage cells are produced in excess. They also showed that the level of oxidative stress in patients is associated with the severity of aggressiveness. The circuit is thus completed: hyper-inflammation leads, via the gut microbiota, to hyper-oxidation, and ultimately to aggressiveness.

Breaking the vicious circle

The study also suggests a possible solution: using probiotics to rebalance the gut flora of schizophrenia patients, or anti-inflammatories to block the harmful mechanism referred to above, thus reducing patients’ aggressiveness. The gut microbiota thus presents a promising line of research.