From the emerging studies, the more diverse the microbial population in the gut, the healthier the gut. Health benefits are associated with the functional characteristics of these diverse microbial genes. Extrinsic factors causing dysbiosis are extensively studied however, linking the varying degree of consequences to the respective factors and therapeutic possibilities are not explored at length. This review aims to examine from previous studies and put forward the types of dysbiosis, the immediate consequences and the scientific approaches to restore disrupted microbiota. Dietary supplements are found to be one of the factors contributing profoundly to the alteration of gut microbiota. While diet rich in fibre and fermented food established a diverse microbiome and produce vital metabolites, high fat, animal proteins and high caloric carbohydrate are as well relative to dysbiosis among infants, adult or diseases individuals. The intermittent fasting, feeding methods, the pH and water quality are among the factors associated with dysbiosis. Prebiotics and Probiotics maintain and restore gut homeostasis. Antibiotic-induced dysbiosis are relatively on the spectrum of activity, the pharmacokinetics properties, the dose taken during the treatment route of administration and the duration of drug therapy. The higher the altitude, the lesser the diversity. Extreme temperatures as well are related to reduced microbial activity and metabolism. Delivery through caserium-section deprived the newborn from restoring valuable vaginal bacterial species and the baby will instead assumed intestinal microbiota-like. While exercise and oxidative stress contribute even though moderately, fecal microbial transfer (FMT) also influence gut microbiota.

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Background/Aims: The previous study in our lab showed that Nodal molecule on bronchial epithelial cells (BECs) was modulated by all kinds of lung microbes. The present study was designed to determine the effects of Nodal on proliferation of BECs and BECs-induced differentiation of T-helper (Th) cells. The epigenetic mechanisms of Nodal expression following treatments of different lung microbes were also identified. Methods: Real-time polymerization chain reaction (PCR) and western blot were used to determine the expression of Nodal. Flow cytometry was used to observe the effects of proliferation of BECs and subsequent BECs-induced differentiation of Th cells. Methylation levels of CpG islands in Nodal promoters were also analyzed by time of flight mass spectrometry. Results: The results showed that Nodal promoted proliferation of BECs and BECs-induced differentiation of Th cell from Th1 to Th2 and Th17. Nodal promoter showed a hyper-methylation in normal BECs. Through methylation modification in the promoter, P. aeruginosa or A.baumanni inhibited the expression of Nodal while RSV promoted the expression of Nodal. Conclusions: Our data showed that Nodal promoted Th2 and Th17 differentiation and inhibited Th1 differentiation which may cause imbalance of airway microenvironment. P. aeruginosa or A.baumanni may be hopeful for the treatment of airway hyperresponsveness by inhibition Nodal expression through DNA methylation modification in the promoter.

Antibiotics are lifesaving therapeutic drugs that have been used by human for decades. They are used both in the fight against bacterial pathogens for both human and for animal feeding. However, of recent, their effects on the gut microbial compositions and diversities have attracted much attention. Existing literature have established the dysbiosis (reduced diversity) in the gut microbiota in association with antibiotic and antibiotic drug doses. In the light of spelling out the varying effects of antibiotic use on gut microbiota, this review aimed at given an account on the degree of gut microbial alteration caused by common antibiotics. While some common antibiotics are found to destroy the common phyla, other debilitating effects were observed. The effects can be attributed to the mode of mechanism, the class of antibiotic, the degree of resistance of the antibiotic used, the dosage used during the treatment, the route of administration, the pharmacokinetic and pharmacodynamics properties and the spectrum of the antibiotic agent. Health status, stress or the type of diet an individual feeds on could be a great proportion as confounding factors. While it is understood that only the bacterial communities are explored in the quest to establishing the role of gut in health, other gut microbial species are somehow contributing to the dysbiosis status of the gut microbiota. Until now, long term natural fluctuations like diseases outbreaks and mutations of the strain might as well rendered alteration to the gut independent of antibiotic treatments.

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This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Background Respiratory viral infections (RSV) can induce acute asthma attacks, thereby destroying lung function and accelerating the progression of the disease. However, medications in the stable phase of asthma are often not effective for acute attacks induced by viral infections. We aimed to clarify the possible mechanism of viral infection–induced asthma through fatty acid metabolism. Methods and Results The airway resistances, inflammatory injuries, and oxidative stress in the RSV‐induced animal models were significantly higher than those in the control group at acute phase (7 days) and chronic phase (28 days). Moreover, the concentrations of the medium‐ and long‐chain fatty acids in lung tissue at (28 days) were significantly increased, including 14:0 (myristic acid), 16:0 (palmitic acid, PA), 18:1 (oleic acid, OA), and 18:2 (linoleic acid, LA) using non‐targeted metabonomics. Airway epithelial cells treated with RSV showed the reduced expression of FSP27, RAB8A, and PLIN5, which caused the fusion and growth of lipid droplet (LD), and increased expression of the LD dispersion gene perilipin 2. There was also a decrease in PPARγ expression and an increase in the fatty acid catabolism gene PPARα, causing lipid oxidation, free fatty acid releases, and an upsurge in IL‐1, IL‐2, IL‐4, and IL‐6 expression, which could be abrogated by GPR40 inhibitor. Treated mice or epithelial cells with C18 fatty acid exhibited inhibition of epithelial proliferation, increases of inflammation, and oxidative damage. Conclusions RSV promoted lipid dispersion and utilization, causing enlarged oxidative injuries and an upsurge in the pro‐inflammatory cytokines, leading to the progression of airway hyperresponsiveness (AHR).

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