Comparison of household income in in-hospital outcomes after implantation of left ventricular assist device.

INTRODUCTION: Due to the inability to keep up with the demand for heart transplantation, there is an increased utilization of left ventricular assist devices (LVAD). However, paucity of data exists regarding the association of household income with in-hospital outcomes after LVAD implantation. METHODS: Retrospective cohort study using the NIS to identify all patients ⩾18 years who underwent LVAD implantation from 2011 to 2017. Statistical analysis was performed comparing low household income (⩽50th percentile) and high income (>50th percentile). RESULTS: A total of 25,503 patients underwent LVAD implantation. The low-income group represented 53% and the high-income group corresponded to 47% of the entire cohort. The low-income group was found to be younger (mean age 55 ± 14 vs 58 ± 14 years), higher proportion of females (24% vs 22%), and higher proportion of blacks (32% vs 16%, p < 0.001 for all). The low-income group was found to have higher prevalence of hypertension, chronic pulmonary disease, smoking, dyslipidemia, obesity, and pulmonary hypertension (p < 0.001 for all). However, the high-income cohort had higher rate of atrial tachyarrhythmias and end-stage renal disease (p < 0.001). During hospitalization, patients in the high-income group had increased rates of ischemic stroke, acute kidney injury, acute coronary syndrome, bleeding, and need of extracorporeal membrane oxygenation (p < 0.001 for all). We found that the unadjusted mortality had an OR 1.30 (CI 1.21-1.41, p < 0.001) and adjusted mortality of OR 1.14 (CI 1.05-1.23, p = 0.002). CONCLUSION: In patients undergoing LVAD implantation nationwide, low-income was associated with increased comorbidity burden, younger age, and fewer in-hospital complications and all-cause mortality.

A Lutzomyia longipalpis Salivary Protein Induces Cross-Reactive Antibodies to Pemphigus Autoantigen Desmoglein 1.

Fogo selvagem (FS) is a blistering skin disease caused by pathogenic IgG4 autoantibodies to desmoglein 1 (DSG1). Preclinical FS and leishmaniasis are endemic to certain regions of Brazil and exhibit nonpathogenic anti-DSG1 antibodies. Recurring bites from Lutzomyia longipalpis, the sand fly vector of leishmaniasis, immunize individuals with L. longipalpis salivary antigens LJM17 and LJM11. We measured the antibody responses to LJM17, LJM11, and DSG1 in normal settlers and patients with FS from an endemic focus of FS and nonendemic control populations. We also immunized mice with these antigens and assessed the IgG response. Healthy individuals and patients with FS from endemic areas had significantly higher values of IgG4 anti-LJM17 antibodies than nonendemic controls (P < 0.001 for both). The levels of IgG anti-DSG1 and IgG4 anti-LJM17 and anti-LJM11 antibodies correlated positively in normal settlers and patients with FS. Mice immunized with recombinant LJM17 produced IgG1 antibodies (human IgG4 homolog) that strongly cross-reacted with recombinant DSG1; these IgG1 antibodies were inhibited by LJM17, LJM11, and DSG1 in a dose-dependent manner. However, they did not bind human or mouse epidermis by indirect immunofluorescence. Lastly, we identified short-sequence homologies of surface-exposed residues within the human DSG1 ectodomain and LJM17. Inoculation by LJM17 from L. longipalpis-elicited DSG1-cross-reactive IgG4 antibodies may lead to FS in genetically predisposed individuals.

Gut Microbes Egested during Bites of Infected Sand Flies Augment Severity of Leishmaniasis via Inflammasome-Derived IL-1ß.

Leishmania donovani parasites are the cause of visceral leishmaniasis and are transmitted by bites from phlebotomine sand flies. A prominent feature of vector-transmitted Leishmania is the persistence of neutrophils at bite sites, where they protect captured parasites, leading to enhanced disease. Here, we demonstrate that gut microbes from the sand fly are egested into host skin alongside Leishmania parasites. The egested microbes trigger the inflammasome, leading to a rapid production of interleukin-1ß (IL-1ß), which sustains neutrophil infiltration. Reducing midgut microbiota by pretreatment of Leishmania-infected sand flies with antibiotics or neutralizing the effect of IL-1ß in bitten mice abrogates neutrophil recruitment. These early events are associated with impairment of parasite visceralization, indicating that both gut microbiota and IL-1ß are important for the establishment of Leishmania infections. Considering that arthropods harbor a rich microbiota, its potential egestion after bites may be a shared mechanism that contributes to severity of vector-borne disease.