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Antibiotics are frequently employed to control bacterial diseases in honeybees, but their broad-spectrum action can disrupt the delicate balance of the gut microbiome, leading to dysbiosis. This imbalance in the gut microbiota of honeybees adversely affects their physiological health and weakens their resistance to pathogens, including viruses that significantly threaten honeybee health. In this study, we investigated whether tetracycline-induced gut microbiome dysbiosis promotes the replication of Israeli acute paralysis virus (IAPV), a key virus associated with colony losses and whether IAPV infection exacerbates gut microbiome dysbiosis. Our results demonstrated that tetracycline-induced gut microbiome dysbiosis increases the susceptibility of honeybees to IAPV infection. The viral titer in worker bees with antibiotic-induced gut microbiome dysbiosis prior to IAPV inoculation was significantly higher than in those merely inoculated with IAPV. Furthermore, we observed a synergistic effect between tetracycline and IAPV on the disruption of the honeybee gut microbiome balance. The progression of IAPV replication could, in turn, exacerbate antibiotic-induced gut microbiome dysbiosis in honeybees. Our research provides novel insights into the role of the gut microbiota in host-virus interactions, emphasizing the complex interplay between antibiotic use, gut microbiome health, and viral susceptibility in honeybees. We highlight the crucial role of a balanced gut microbiota in honey bees for their immune response against pathogens and emphasize the importance of careful, safe antibiotic use in beekeeping to protect these beneficial microbes.

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Preterm infants differ significantly from their term infant counterparts regarding bacterial colonization patterns related to maternal microbiota diversity, mode of delivery, feeding type, antibiotic exposure, and the environmental influences related to prolonged hospitalization in the neonatal intensive care unit (NICU). Necrotizing enterocolitis (NEC), a multifactorial intestinal disorder characterized by ischemic bowel disease, disproportionately impacts preterm infants and has a high disease burden. Recent studies in the basic, translational, and clinical scientific literature have advanced knowledge into this complex disease process. Despite the explosion of research into NEC, however, there is a still a great deal unknown about this devastating illness. Additionally, the disease morbidity and mortality for NEC remain high despite advances in therapy options. This chapter reviews the current literature into the preterm infant microbiome, pathogenesis of NEC, potential targets for altering preterm microbiome, influence of microbiome on other organ systems, long-term implications of microbiome dysbiosis, and future directions of study.

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OBJECTIVES: To investigate the correlation between periodontitis and cerebral small vessel disease (CSVD) from the clinical and microbiological aspects. SUBJECTS AND METHODS: Periodontitis patients (CP group, n = 31) and CSVD patients (CSVD group, n = 30) were examined for neurological and periodontal condition. Subgingival plaque was collected and performed using 16S rRNA sequencing. Logistic regression and LASSO regression were used to analyze the periodontal parameters and subgingival microbiota related to CSVD, respectively. Inflammatory factors in gingival crevicular fluid (GCF) were also detected and compared between the two groups. RESULTS: Clinical attachment level (CAL), teeth number and plaque index demonstrated a significant difference between CP and CSVD group, meanwhile, CAL was independently associated with CSVD. Besides, the microbial richness and composition were distinct between two groups. Five genera related to periodontal pathogens (Treponema, Prevotella, Streptococcus, Fusobacterium, Porphyromonas) were screened out by LASSO regression, suggesting a potential association with CSVD. Finally, the levels of inflammatory factors in GCF were statistically higher in CSVD group than those in CP group. CONCLUSIONS: Cerebral small vessel disease patients demonstrated worse periodontal condition, meanwhile the interaction between microbiota dysbiosis and host factors (inflammation) leading to a better understanding of the association between periodontitis and CSVD.

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Lung cancer has the highest mortality rate among all cancers worldwide. The 5-year overall survival rate for non-small cell lung cancer (NSCLC) is estimated at around 26%, whereas for small cell lung cancer (SCLC), the survival rate is only approximately 7%. This disease places a significant financial and psychological burden on individuals worldwide. The symbiotic microbiota in the human body has been significantly associated with the occurrence, progression, and prognosis of various diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. Studies have demonstrated that respiratory symbiotic microorganisms and their metabolites play a crucial role in modulating immune function and contributing to the pathophysiology of lung cancer through their interactions with the host. In this review, we provide a comprehensive overview of the microbial characteristics associated with lung cancer, with a focus on the respiratory tract microbiota from different locations, including saliva, sputum, bronchoalveolar lavage fluid (BALF), bronchial brush samples, and tissue. We describe the respiratory tract microbiota's biodiversity characteristics by anatomical region, elucidating distinct pathological features, staging, metastasis, host chromosomal mutations, immune therapies, and the differentiated symbiotic microbiota under the influence of environmental factors. Our exploration investigates the intrinsic mechanisms linking the microbiota and its host. Furthermore, we have also provided a comprehensive review of the immune mechanisms by which microbiota are implicated in the development of lung cancer. Dysbiosis of the respiratory microbiota can promote or inhibit tumor progression through various mechanisms, including DNA damage and genomic instability, activation and regulation of the innate and adaptive immune systems, and stimulation of epithelial cells leading to the upregulation of carcinogenesis-related pathways.

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Chronic alcohol consumption, an important risk factor for diseases and deaths, can cause intestinal microbiota dysbiosis and increase the infection of some opportunistic pathogens. However, the current studies on the effects of alcohol-induced intestinal microbiota dysbiosis on gut colonization of Klebsiella pneumoniae are still scarce. In the present study, we established a binge-on-chronic alcohol model in mice to identify the characteristics of alcohol-induced intestinal microbiome and metabolite dysbiosis using multi-omics and explored the effects and potential mechanisms of these dysbioses on the intestinal colonization of K. pneumoniae. The results show that chronic alcohol consumption alters the diversity and composition of gut microbiota (including bacteria and fungi), decreases the complexity of the interaction between intestinal bacteria and fungi, disturbs the gut metabolites, and promotes the colonization of K. pneumoniae on the gut of mice. The relevance analyses find that alcohol-induced gut microbiome dysbiosis has a strong correlation with the alteration of secondary bile acids. In vitro results suggest that the high concentration of lithocholic acid, a secondary bile acid, could significantly inhibit the proliferation of K. pneumoniae, and the adhesion of K. pneumoniae to Caco-2 cells. Our results indicate that alcohol-induced microbiome dysbiosis contributes to decreased levels of secondary bile acids, which was one of the main reasons affecting the colonization of K. pneumoniae in mice's intestines. Some secondary bile acids (e.g., lithocholic acid) might be a potential drug to prevent the colonization and spread of K. pneumoniae.IMPORTANCEAlcohol is one of the most commonly misused substances in our lives. However, long-term heavy drinking will increase the colonization of some opportunistic pathogens (e.g., Klebsiella pneumoniae) in the body. Here, we revealed that binge-on-chronic alcohol consumption disrupted the balance between gut bacteria and fungi, induced the gut microbiome and metabolites dysbiosis, and promoted the colonization of K. pneumoniae in the intestine of mice. In particular, alcohol-taking disrupted intestinal bile acid metabolism and reduced the lithocholic acid concentration. However, a high concentration of lithocholic acid can protect against intestinal colonization of K. pneumoniae by inhabiting the bacterial growth and adhesion to the host cell. Hence, regulating the balance of gut microbiota and intestinal bile acid metabolism may be a potential strategy for reducing the risk of K. pneumoniae infection and spread.

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BACKGROUND: Necrotic enteritis (NE) is a severe intestinal infection that affects both humans and poultry. It is caused by the bacterium Clostridium perfringens (CP), but the precise mechanisms underlying the disease pathogenesis remain elusive. This study aims to develop an NE broiler chicken model, explore the impact of the microbiome on NE pathogenesis, and study the virulence of CP isolates with different toxin gene combinations. METHODS: This study established an animal disease model for NE in broiler chickens. The methodology encompassed inducing abrupt protein changes and immunosuppression in the first experiment, and in the second, challenging chickens with CP isolates containing various toxin genes. NE was evaluated through gross and histopathological scoring of the jejunum. Subsequently, jejunal contents were collected from these birds for microbiome analysis via 16S rRNA amplicon sequencing, followed by sequence analysis to investigate microbial diversity and abundance, employing different bioinformatic approaches. RESULTS: Our findings reveal that CP infection, combined with an abrupt increase in dietary protein concentration and/or infection with the immunosuppressive variant infectious bursal disease virus (vIBDV), predisposed birds to NE development. We observed a significant decrease (p < 0.0001) in the abundance of Lactobacillus and Romboutsia genera in the jejunum, accompanied by a notable increase (p < 0.0001) in Clostridium and Escherichia. Jejunal microbial dysbiosis and severe NE lesions were particularly evident in birds infected with CP isolates containing cpa, netB, tpeL, and cpb2 toxin genes, compared to CP isolates with other toxin gene combinations. Notably, birds that did not develop clinical or subclinical NE following CP infection exhibited a significantly higher (p < 0.0001) level of Romboutsia. These findings shed light on the complex interplay between CP infection, the gut microbiome, and NE pathogenesis in broiler chickens. CONCLUSION: Our study establishes that dysbiosis within the jejunal microbiome serves as a reliable biomarker for detecting subclinical and clinical NE in broiler chicken models. Additionally, we identify the potential of the genera Romboutsia and Lactobacillus as promising candidates for probiotic development, offering effective alternatives to antibiotics in NE prevention and control.

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Copper oxide nanoparticles (CuO NPs) are being used in healthcare industries due to its antimicrobial properties. The increased consumption of NPs could lead to the rise of these NPs in the environment affecting the biological systems. Altered microbiome has been correlated to disease pathology in humans as well as xenobiotic toxicity in experimental animal models. However, CuO NPs-induced microbiome alterations in vertebrates have not been reported so far. In this study, for the first time, zebrafish larvae at 96 hpf (hours post fertilization) were exposed to CuO NPs for 24 h at 10, 20, and 40 ppm. After exposure, the control and treated larvae were subjected to 16S rRNA amplicon sequencing followed by relative taxa abundance, alpha and beta diversity analysis, single factor analysis, LEfSe, Deseq2, and functional profiling. No significant alteration was detected in the microbial richness and diversity, however, specific taxa constituting the core microbiome such as phylum Proteobacteria were significantly increased and Bacterioidetes and Firmicutes were decreased in the treated groups, indicating a core microbiota dysbiosis. Further, the family Lachnospiraceae, and genus Syntrophomonas involved in butyrate production and the metabolism of lipids and glucose were significantly altered. In addition, the opportunistic pathogens belonging to order Flavobacteriales were increased in CuO NPs treated groups. Moreover, the taxa involved in host immune response (Shewanella, Delftia, and Bosea) were found to be enriched in CuO NPs exposed larvae. These results indicate that CuO NPs exposure causes alteration in the core microbiota, which could cause colitis or inflammatory bowel disease.

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Evidence for the influence of chronic inflammation induced by microbial dysbiosis on aberrant DNA methylation supports a plausible connexion between disordered microbiota and precancerous lesions of gastric cancer (PLGC). Here, a comprehensive study including multi-omics data was performed to estimate the relationships amongst the gastric microbiome, inflammatory proteins and DNA methylation alterations and their roles in PLGC development. The results demonstrated that gastric dysbacteriosis increased the risk of PLGC and DNA methylation alterations in related tumour suppressor genes. Seven inflammatory biomarkers were identified for antrum and corpus tissues, respectively, amongst which the expression levels of several biomarkers were significantly correlated with the microbial dysbiosis index (MDI) and methylation status of specific tumour suppressor genes. Notably, mediation analysis revealed that microbial dysbiosis partially contributed to DNA methylation changes in the stomach via the inflammatory cytokines C-C motif chemokine 20 (CCL20) and tumour necrosis factor receptor superfamily member 9 (TNFRSF9). Overall, these results may provide new insights into the mechanisms that might link the gastric microbiome to PLGC. Supplementary Information: The online version contains supplementary material available at 10.1007/s43657-023-00118-w.

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The prevalence of obesity is growing worldwide and has been extensively linked to gut microbiota dysbiosis. In addition to exercise and physical activity, fiber-rich foods may be a first-line prophylactic to manage obesity. This study investigated in vivo dietary intervention with high-amylose maize starch (HAMS) and starch-entrapped microspheres (MS) to treat high-fat diet induced metabolic disorder and gut microbiome dysbiosis in mice. MS more efficiently controlled body weight as well as adipose tissue mass compared to HAMS. Furthermore, MS significantly reduced blood glucose, insulin, lipid and pro-inflammatory cytokine levels compared to the high-fat diet, while the effects of HAMS were less pronounced. The MS-altered gut microbiota composition favoring Streptococcaceae, Bacilli, Firmicutes and unclassified Clostridiales was predicted to promote fatty acid, pantothenate and Coenzyme A biosynthesis. In line with this, elevated fecal short chain fatty acid (SCFA), in particular, propionate concentration was observed in MS-fed mice. Our study provides novel insights into the mechanistic action of MS on intestinal homeostasis, providing a basis for future dietary therapeutic applications.

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Background: The mechanisms of hypertrophic scar formation and its tissue inflammation remain unknown. Methods: We collected 33 hypertrophic scar (HS) and 36 normal skin (NS) tissues, and detected the tissue inflammation and bacteria using HE staining, Gram staining, and transmission electronic microscopy (TEM), in situ hybridization and immunohistochemistry for MCP-1, TNF-α, IL-6 and IL-8. In addition, the samples were assayed by 16S rRNA sequencing to investigate the microbiota diversity in HS, and the correlation between the microbiota and the indices of Vancouver Scar Scale(VSS)score. Results: HE staining showed that a dramatically increased number of inflammatory cells accumulated in HS compared with NS, and an enhanced number of bacteria colonies was found in HS by Gram staining, even individual bacteria could be clearly observed by TEM. In situ hybridization demonstrated that the bacteria and inflammation cells co-localized in the HS tissues, and immunohistochemistry indicated the expression of MCP-1, TNF-α, IL-6, and IL-8 were significantly upregulated in HS than that in NS. In addition, there was a significantly different microbiota composition between HS and NS. At the phylum level, Firmicutes was significantly higher in HS than NS. At the genus level, S. aureus was the dominant species, which was significantly higher in HS than NS, and was strongly correlated with VSS indices. Conclusion: Microbiome dysbiosis, dominated by S. aureus, occurred in HS formation, which is correlated with chronic inflammation and scar formation, targeting the microbiome dysbiosis is perhaps a supplementary way for future scar management.

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Many factors may trigger intervertebral disc (IVD) structural failure (intervertebral disc degeneration (IDD) and endplate changes), including inflammation, infection, dysbiosis, and the downstream effects of chemical factors. Of these, microbial diversity in the IVD and elsewhere in the body has been considered as one of the potential reasons for disc structural failure. The exact relationships between microbial colonization and IVD structural failure are not well understood. This meta-analysis aimed to investigate the impact of microbial colonization and its location (such as skin, IVD, muscle, soft tissues, and blood) on IVD structural failure and corresponding low back pain (LBP) if any. We searched four online databases for potential studies. The potential relationships between microbial colonization in different sample sources (such as skin, IVD, muscle, soft tissues, and blood) and IDD and endplate change were considered as primary outcomes. Odds ratio (OR) and 95% confidence intervals (CI) for direct comparisons were reported. Grading of Recommendations Assessment, Development and Evaluation (GRADE) scale was used to assess the quality of evidence. Twenty-five cohort studies met the selection criteria. Overall pooled prevalence of microbial colonization in 2419 patients with LBP was 33.2% (23.6%-43.6%). The pooled prevalence of microbial colonization in 2901 samples was 29.6% (21.0%-38.9%). Compared with the patients without endplate change, the patients with endplate changes had higher rates of microbial colonization of disc (OR = 2.83; 95% CI = 1.93-4.14; I 2 = 37.6%; p = 0.108). The primary pathogen was Cutibacterium acnes which was present in 22.2% of cases (95% CI = 13.3%-32.5%; I 2 = 96.6%; p = 0.000). This meta-analysis and systematic review found low-quality grade evidence for an association between microbial colonization of disc with endplate changes. The primary pathogen was C. acnes. Due to lack of enough high-quality studies and methodological limitations of this review, further studies are required to improve our understanding of the potential relationships and mechanisms of microbiota, dysbiosis, IVD colonization and IVD structural failure.

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic is ongoing and multiple studies have elucidated its pathogenesis, however, the related- microbiome imbalance caused by SARS-CoV-2 is still not clear. In this study, we have comprehensively compared the microbiome composition and associated function alterations in the oropharyngeal swabs of healthy controls and coronavirus disease 2019 (COVID-19) patients with moderate or severe symptoms by metatranscriptomic sequencing. We did observe a reduced microbiome alpha-diversity but significant enrichment of opportunistic microorganisms in patients with COVID-19 compared with healthy controls, and the microbial homeostasis was rebuilt following the recovery of COVID-19 patients. Correspondingly, less functional genes in multiple biological processes and weakened metabolic pathways such as carbohydrate metabolism, energy metabolism were also observed in COVID-19 patients. We only found higher relative abundance of limited genera such as Lachnoanaerobaculum between severe patients and moderate patients while no worthy-noting microbiome diversity and function alteration were observed. Finally, we noticed that the co-occurrence of antibiotic resistance and virulence was closely related to the microbiome alteration caused by SRAS-CoV-2. Overall, our findings demonstrate that microbial dysbiosis may enhance the pathogenesis of SARS-CoV-2 and the antibiotics treatment should be critically considered.

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Microplastics (MPs) pollution in aquatic environment has attracted global attention in recent years. To evaluate the potential toxic effects of MPs in freshwater cultured fish, grass carps (Ctenopharyngodon idella) (body length: 7.7 ± 0.1 cm, wet weight: 6.28 ± 0.23 g) were exposed to different sizes (0.5 µm, 15 µm) and concentrations (100 µg/L, 500 µg/L) of polystyrene microplastics (PS-MPs) suspension for 7 and 14 days, followed by 7 days of depuration, detecting the variations in growth rate, histological structure, oxidative response and intestinal microbiome. Our results indicate that MP toxicity elicited significant size- and concentration-dependent responses by grass carp. MP exposure caused obvious decrease in growth rate on day 14 but not on day 7. Additionally, MPs with large size and high concentration caused more severe intestinal damage and less weight gain, while MP particles with small size and high concentration induced more severe liver congestion and stronger oxidative stress. MP exposure dramatically shifted the gut microbial composition, with the top 10 genera in abundance being associated with the diameter and concentration of the MPs. After 7 days of depuration, only superoxide dismutase and malondialdehyde in liver, showed a tendency to recover to the initial values. Even though the differences in the gut microbial community between the control and treatment groups disappeared, and the proportion of potential pathogenic bacteria in intestine was still high. Thus, it is clear that a short-term depuration period of 7 days is not enough for complete normalization.

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Oral cancer is one of the most common cancers worldwide and ranks fourth for the mortality rate of cancers in males in Taiwan. The oral microbiota is the microbial community in the oral cavity, which is essential for maintaining oral health, but the relationship between oral tumorigenesis and the oral microbiota remains to be clarified. This study evaluated the effect of microbiome dysbiosis on oral carcinogenesis in mice, and the impact of the microbiome and its metabolic pathways on regulating oral carcinogenesis. We found that antibiotics treatment decreases carcinogen-induced oral epithelial malignant transformation. Microbiome analysis based on 16S rRNA gene sequencing revealed that the species richness of fecal specimens was significantly reduced in antibiotic-treated mice, while that in the salivary specimens was not decreased accordingly. Differences in bacterial composition, including Lactobacillus animalis abundance, in the salivary samples of cancer-bearing mice was dramatically decreased. L. animalis was the bacterial species that increased the most in the saliva of antibiotic-treated mice, suggesting that L. animalis may be negatively associated with oral carcinogenesis. In functional analysis, the microbiome in the saliva of the tumor-bearing group showed greater potential for polyamine biosynthesis. Immunochemical staining proved that spermine oxidase, an effective polyamine oxidase, was upregulated in mouse oral cancer lesions. In conclusion, oral microbiome dysbiosis may alter polyamine metabolic pathways and reduce carcinogen-induced malignant transformation of the oral epithelium.

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Oral microbiome is a complex population of micro-organisms, which by cross-talking with the local immune system, plays a major role in the immune homeostasis of the oral cavity, further contributing in the physiology of the gastro-intestinal microbiota. Understanding their involvement in the onset and pathogenesis of oropharyngeal cancers is paramount, despite very few reports deal with the fundamental role exerted by oral microbiota disorders, such as dysbiosis and impairment in the oral microbiome composition as causative factors in the development of oropharyngeal tumors. Current research, via metabolomic or meta-transcriptomic analyses, is wondering how this complex microbial population regulates the immune homeostasis in oral and pharyngeal mucosa and whether changes in bacterial composition may give insights on the role of oral microbiome in the development of oropharyngeal tumors, so to prevent their occurrence.

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BACKGROUND: Evidence suggests that the pathogenesis of Parkinson's disease (PD) is initiated in the gut rather than in the brain. Thus, targeting the gut in early stages may have the potential to halt disease progression and alleviate symptoms. Various acupuncture techniques have been used to treat patients with PD and have shown promising results. However, previous acupuncture techniques focused on the brain and motor symptoms. We aimed to determine if targeting PD patients' gut-brain axis through electroacupuncture could be an effective, safe, and low-cost therapeutic option for management of non-motor and motor symptoms. METHODS: Thirty patients with mild to moderate PD were randomised into an intervention (n = 15) and a control group (n = 15). The intervention group received electroacupuncture twice a week for 30 min based on conventional drug treatment for 8 weeks. Conventional drug treatment was continued in the control group. The primary outcomes were changes in the score of clinical scales including the Non-motor Symptom Rating Scale (NMSS), PD Sleep Scale (PDSS), Bristol Stool Function Scale (BSFS), and Patient Associated Constipation and Quality of Life Scale (PAC-QOL). The secondary outcomes were the Unified PD Rating Scale (UPDRS) and Modified Hoehn-Yahr Staging Scale scores. Stool samples from the intervention group were collected before and after the procedure and were sent for gene sequencing. Adverse effects and personal impressions of the patients were noted during the course of the trial. RESULT: An 8-week course of scalp-abdominal electroacupuncture treatment was effective in improving the NMSS, PDSS, and UPDRS scores in patients with PD. Further, there was statistical significance in the two subdomains of NMSS, namely sleep/fatigue and miscellaneous, further implying the efficacy of acupuncture on sleep disturbance. However, although the current acupuncture treatment was gut targeted, it had no effect on BSFS or PAC-QOL. Apart from improved UPDRS motor scores and activities of daily living scores, acupuncture had no significant impact on scores of mentation, behaviour, mood, and therapy complications. Acupuncture did not alter the Hoehn and Yahr stage. Significant alterations in gut bacterial composition were detected in nine taxa at the genus level. The relative abundances of the genera Bacteroides and Parasutterella were significantly increased after the intervention, whereas the abundances of the genera Dialister, Hungatella, Barnesiella, Megasphaera, Allisonella, Intestinimon, and Moryella were significantly lower. CONCLUSION: An 8-week scalp-abdominal electroacupuncture treatment may be a complementary and alternative vehicle for PD patients. We detected nine taxa at the genus level which were significantly altered after treatment, emphasising the role of the gut-brain axis in the process.

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Tetracycline class antibiotics are widely used for multiple skin diseases, including acne vulgaris, acne rosacea, cutaneous infections, inflammatory dermatoses, and autoimmune blistering disorders. Concerns about antibiotic resistance and protecting the human/host microbiome beg the question whether broad-spectrum tetracyclines such as doxycycline and minocycline should be prescribed at such a high rate by dermatologists when a narrow-spectrum tetracycline derivative, sarecycline, exists. We evaluated the clinical effectiveness of oral sarecycline against cutaneous staphylococcal infections, eyelid stye, and mucous membrane pemphigoid to determine whether sarecycline is a viable option for clinicians to practice improved antibiotic stewardship. We observed significant improvement in staphylococcal infections and inflammatory dermatoses with courses of oral sarecycline as short as 9 days, with no reported adverse events. These clinical findings are consistent with in vitro microbiological data and anti-inflammatory properties of sarecycline. Our data provides a strong rationale for clinicians to use narrow-spectrum sarecycline rather than broad-spectrum tetracyclines as a first-line agent in treating staphylococcal skin infections and inflammatory skin diseases for which tetracyclines are currently commonly employed. Such advancement in the practice paradigm in dermatology will enhance antibiotic stewardship, reduce risk of antibiotic resistance, protect the human microbiome, and provide patients with precision medicine care.

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Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has affected millions of individuals with various implications. Consistent with the crucial role of the microbiome in determining health and disease in humans, various studies have investigated the gut and respiratory microbiome effect on the COVID-19. Microbiota dysbiosis might support the entry, replication, and establishment of SARS-CoV-2 infection by modulating various mechanisms. One of the main mechanisms that the modulation of respiratory microbiota composition during the COVID-19 infection affects the magnitude of the disease is changes in innate and acquired immune responses, including inflammatory markers and cytokines and B- and T-cells. The diversity of respiratory microbiota in COVID-19 patients is controversial; some studies reported low microbial diversity, while others found high diversity, suggesting the role of respiratory microbiota in this disease. Modulating microbiota diversity and profile by supplementations and nutrients can be applied prophylactic and therapeutic in combating COVID-19. Here, we discussed the lung microbiome dysbiosis during various lung diseases and its interaction with immune cells, focusing on COVID-19.

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