Prevalence and risk factors of seafood-borne Vibrio vulnificus in Asia: a systematic review with meta-analysis and meta-regression.

Vibrio vulnificus is a free-living marine bacterium associated with the contamination of fish and shellfish-the most consumed seafood in Asia. Owing to its potentially lethal clinical consequences, the consumption of seafood contaminated with V. vulnificus has become a growing public health concern. This systematic review with meta-analysis and meta-regression aimed to integrate data on the prevalence of seafood-borne V. vulnificus specifically in Asia and assess the potential risk factors that can influence the outcomes. A comprehensive literature search of four electronic databases yielded 279 relevant studies, among which 38 fulfilled the inclusion criteria. These selected studies were subjected to risk-of-bias assessment and data extraction by three independent researchers. A meta-analysis of the eligible studies estimated the overall prevalence of seafood-borne V. vulnificus in Asia to be 10.47% [95% confidence interval (CI): 6.8-15.8%], with bivalve shellfish, such as oysters, mussels, clams, and cockles being the most contaminated seafood. The highest prevalence was reported in Japan, where 47.6% of the seafood samples tested positive for V. vulnificus. The subgroup and meta-regression analyses identified three potential covariates-detection method, publication year, and country-associated with between-study heterogeneity. Furthermore, data visualization displayed the variations in V. vulnificus prevalence across the studies, associated with differences in sample type, sample size, and sampling stage. This study provides valuable insights into the prevalence of V. vulnificus in fish and shellfish across the entire Asian continent and highlights the potential factors that cause variation in the prevalence rates among the studies. These findings underscore the importance of enhancing hygiene measures throughout the seafood supply chain to mitigate V. vulnificus infection risks and ensure the safety of consumers.

Integrating meta-analysis with a quantitative microbial risk assessment model to investigate Campylobacter contamination of broiler carcasses.

This study investigated the prevalence and associated risk factors of Campylobacter in South Korean broilers using a random-effects meta-analysis. Subsequently, to facilitate the design of preventive measures, the prevalence estimate from the meta-analysis was incorporated into a stochastic risk assessment model to quantify the Campylobacter contamination levels on broiler carcasses. The baseline model was developed based on the most common practices along the South Korean broiler processing line, with no interventions. Meta-analysis results revealed Campylobacter prevalence across the chicken supply chain in the following order: farms (60.6 % [57.3-63.4]), retail markets (43.90 % [24.81-64.99]), slaughterhouses (27.71 % [18.56-39.21]), and processing plants (14.50 % [3.96-41.09]). The model estimated a 52 % (36.1-70.8) Campylobacter prevalence at the end of chilling, with an average contamination level of 4.62 (2.50-6.74) log CFU/carcass. Sensitivity analysis indicated that Campylobacter fecal shedding (r = 0.95) and the amount of feces on bird exteriors (r = 0.17) at pre-harvest were the main factors for carcass contamination, while soft scalding (r = -0.22) and air chilling (r = -0.12) can serve as critical control points (CCPs) at harvest. Scenario analysis indicated that a combination of hard scalding, inside-outside bird washing, spray washing, and chlorinated water immersion chilling can offer a 30.9 % reduction in prevalence and a reduction of 2.23 log CFU/carcass in contamination levels compared to the baseline model. Apart from disinfection and sanitation interventions carried out during meat processing, the implementation of robust control measures is indispensable to mitigate Campylobacter prevalence and concentration at broiler farms, thereby enhancing meat safety and public health. Furthermore, given the high Campylobacter prevalence in the retail markets, future studies should explore the potential risk of cross-contamination at post-harvest stage.

T cell-intrinsic miR-155 is required for Th2 and Th17-biased responses in acute and chronic airway inflammation by targeting several different transcription factors.

Asthmatic airway inflammation is divided into two typical endotypes: Th2-mediated eosinophilic and Th1- or Th17-mediated neutrophilic airway inflammation. The miRNA miR-155 has well-documented roles in the regulation of adaptive T-cell responses and innate immunity. However, no specific cell-intrinsic role has yet been elucidated for miR-155 in T cells in the course of Th2-eosinophilic and Th17-neutrophilic airway inflammation using actual in vivo asthma models. Here, using conditional KO (miR155ΔCD4 cKO) mice that have the specific deficiency of miR-155 in T cells, we found that the specific deficiency of miR-155 in T cells resulted in fully suppressed Th2-type eosinophilic airway inflammation following acute allergen exposure, as well as greatly attenuated the Th17-type neutrophilic airway inflammation induced by repeated allergen exposure. Furthermore, miR-155 in T cells appeared to regulate the expression of several different target genes in the functional activation of CD4+ Th2 and Th17 cells. To be more precise, the deficiency of miR-155 in T cells enhanced the expression of c-Maf, SOCS1, Fosl2 and Jarid2 in the course of CD4+ Th2 cell activation, while C/EBPß was highly enhanced in CD4+ Th17 cell activation in the absence of miR-155 expression. Conclusively, our data revealed that miR-155 could promote Th2 and Th17-mediated airway inflammation via the regulation of several different target genes, depending on the context of asthmatic diseases. Therefore, these results provide valuable insights into actual understanding of specific cell-intrinsic role of miR-155 in eosinophilic and neutrophilic airway inflammation for the development of fine-tune therapeutic strategies.

Indoleamine 2,3-Dioxygenase in Hematopoietic Stem Cell-Derived Cells Suppresses Rhinovirus-Induced Neutrophilic Airway Inflammation by Regulating Th1- and Th17-Type Responses.

Asthma exacerbations are a major cause of intractable morbidity, increases in health care costs, and a greater progressive loss of lung function. Asthma exacerbations are most commonly triggered by respiratory viral infections, particularly with human rhinovirus (hRV). Respiratory viral infections are believed to affect the expression of indoleamine 2,3-dioxygenase (IDO), a limiting enzyme in tryptophan catabolism, which is presumed to alter asthmatic airway inflammation. Here, we explored the detailed role of IDO in the progression of asthma exacerbations using a mouse model for asthma exacerbation caused by hRV infection. Our results reveal that IDO is required to prevent neutrophilic inflammation in the course of asthma exacerbation caused by an hRV infection, as corroborated by markedly enhanced Th17- and Th1-type neutrophilia in the airways of IDO-deficient mice. This neutrophilia was closely associated with disrupted expression of tight junctions and enhanced expression of inflammasome-related molecules and mucin-inducing genes. In addition, IDO ablation enhanced allergen-specific Th17- and Th1-biased CD4+ T-cell responses following hRV infection. The role of IDO in attenuating Th17- and Th1-type neutrophilic airway inflammation became more apparent in chronic asthma exacerbations after repeated allergen exposures and hRV infections. Furthermore, IDO enzymatic induction in leukocytes derived from the hematopoietic stem cell (HSC) lineage appeared to play a dominant role in attenuating Th17- and Th1-type neutrophilic inflammation in the airway following hRV infection. Therefore, IDO activity in HSC-derived leukocytes is required to regulate Th17- and Th1-type neutrophilic inflammation in the airway during asthma exacerbations caused by hRV infections.