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Background Burns cause the most severe injuries and are a major public health concern worldwide. It is common in third-world countries and it greatly increases mortality and illness there. Because of the long period of time spent in the hospital and the effort required to recover from a burn, it is one of the most costly injuries to treat. Objectives The aim of this study was to identify the priming factors related to burn injury among people in Bangladesh. Materials and Methods The study design was cross-sectional. Total 121 samples were selected conveniently for the study and the study was conducted in several hospital settings in Chittagong, Savar and Dhaka city like Chittagong Medical College Hospital, Enam Medical College Hospital, and Sheikh Hasina Burn Hospital. Data was collected by using a self-administered questionnaire. Statistical Analysis Descriptive and inferential statistics (chi-squared test) were used for data analysis that focused through tables. Results On average, people were 22.43 (14.399) years old. Of the total of 121 patients, 48.1% were female (n = 58) and 52.1% were male (n = 63). Among the participants, 56.2% (n = 68) were hurt accidentally, 33.9% (n = 41) were injured on the job, 2.5% (n = 3) were harmed intentionally, and 7.4% (n = 9) were injured while preparing food. In case of occurrence, 37.2% (n = 45) were burned by fire, 38.8% (n = 47) were electrical burn and 23.9% (n = 29) were chemical or scald type burn. Conclusions Most burn injuries are accidental, such as cooking fires, hot water, electric lines, and acid throwing that are significantly considered as the priming factors of burn injury among people in Bangladesh. The lack of awareness and ignorance causes these accidents and insufficient training causes most the electrical burns. [ABSTRACT FROM AUTHOR]

Innate cellular immune responses are a critical first-line defense against invading bacterial pathogens. Leukocyte migration from the bloodstream to a site of infection is mediated by chemotactic factors that are often host-derived. More recently, there has been a greater appreciation of the importance of bacterial factors driving neutrophil movement during infection. Here, we describe the development of a zebrafish infection model to study Acinetobacter baumannii pathogenesis. By using isogenic A. baumannii mutants lacking expression of virulence effector proteins, we demonstrated that bacterial drivers of disease severity are conserved between zebrafish and mammals. By using transgenic zebrafish with fluorescent phagocytes, we showed that a mutation of an established A. baumannii global virulence regulator led to marked changes in neutrophil behavior involving rapid neutrophil influx to a localized site of infection, followed by prolonged neutrophil dwelling. This neutrophilic response augmented bacterial clearance and was secondary to an impaired A. baumannii phenylacetic acid catabolism pathway, which led to accumulation of phenylacetate. Purified phenylacetate was confirmed to be a neutrophil chemoattractant. These data identify a previously unknown mechanism of bacterial-guided neutrophil chemotaxis in vivo, providing insight into the role of bacterial metabolism in host innate immune evasion. Furthermore, the work provides a potentially new therapeutic paradigm of targeting a bacterial metabolic pathway to augment host innate immune responses and attenuate disease. [ABSTRACT FROM AUTHOR]

Background. Infection with Vibrio cholerae induces durable immunity against subsequent disease, a process hypothesized to reflect anamnestic immune responses at the intestinal mucosa. The presence of antigen-specific memory B cells may therefore be a more direct measure of protection than serum antibody responses. Methods. We measured immunoglobulin (Ig) G memory B cells specific to cholera toxin B subunit (CTB) in 14 patients up to 90 days after V. cholerae O1 infection, by polyclonal stimulation of peripheral blood mononuclear cells followed by standard enzyme-linked immunospot assay. Results. All patients generated CTB-specific IgG memory B cell responses by day 30 (mean, 0.10% of total circulating IgG memory B cells; range, 0.037%-0.28%), which persisted to day 90 (mean, 0.07%; range, 0.003%- 0.27%). In contrast, circulating CTB-specific IgG antibody-secreting cells and serum vibriocidal and anti-CTB antibody responses peaked on day 7 and declined to undetectable or significantly lower levels by day 90. Conclusions. CTB-specific IgG memory B cell responses are detectable in the circulation at least 3 months after V. cholerae O1 infection and remain measurable even after serum antibody titers have declined to undetectable or considerably lower levels. This suggests that antigen-specific memory B cells may be an important long-term marker of the immune response to cholera. [ABSTRACT FROM AUTHOR]