Powerherbert9943

We developed a method to simultaneously quantify airway narrowing and muscle shortening using 2-photon microscopy and demonstrated that inhibition of α2β1 mitigated IL-13-enhanced airway narrowing without altering muscle shortening by impairing the tethering of muscle to the surrounding matrix. Our data identified cell matrix tethering as an attractive therapeutic target to mitigate the severity of airway contraction in asthma.BACKGROUNDThe COVID-19 vaccines currently in use require 2 doses to achieve optimal protection. Currently, there is no indication as to whether individuals who have been exposed to SARS-CoV-2 should be vaccinated, or whether they should receive 1 or 2 vaccine doses.METHODSWe tested the antibody response developed after administration of the Pfizer/BioNTech vaccine in 124 health care professionals, of whom 57 had a previous history of SARS-CoV-2 exposure with or without symptoms.RESULTSPostvaccine antibodies in SARS-CoV-2-exposed individuals increased exponentially within 5 to 18 days after the first dose compared to naive subjects (P less then 0.0001). In a multivariate linear regression (LR) model we showed that the antibody response depended on the IgG prevaccine titer and on the exposure to SARS-CoV-2. In symptomatic SARS-CoV-2-exposed individuals, IgG reached a plateau after the second dose, and those who voluntarily refrained from receiving the second dose (n = 7) retained their antibody response. Gastrointestinal symptoms, muscle pain, and fever markedly positively correlated with increased IgG responses. By contrast, all asymptomatic/paucisymptomatic and unexposed individuals showed an important increase after the second dose.CONCLUSIONOne vaccine dose is sufficient in symptomatic SARS-CoV-2-exposed subjects to reach a high titer of antibodies, suggesting no need for a second dose, particularly in light of current vaccine shortage.TRIAL REGISTRATIONClinicalTrials.gov NCT04387929.FUNDINGDolce & Gabbana and the Italian Ministry of Health (Ricerca corrente).Interstitial kidney inflammation is present in various nephritides in which serum interleukin 23 (IL-23) is elevated. Here we showed that murine and human renal tubular epithelial cells (TECs) expressing the IL-23 receptor (IL-23R) responded to IL-23 by inducing intracellular calcium flux, enhancing glycolysis, and upregulating calcium/calmodulin kinase IV (CaMK4), which resulted in suppression of the expression of the arginine-degrading enzyme arginase 1 (ARG1), thus increasing in situ levels of free L-arginine. Limited availability of arginine suppressed the ability of infiltrating T cells to proliferate and produce inflammatory cytokines. TECs from humans and mice with nephritis expressed increased levels of IL-23R and CaMK4 but reduced levels of ARG1. TEC-specific deletion of Il23r or Camk4 suppressed inflammation, whereas deletion of Arg1 exacerbated inflammation in different murine disease models. selleck chemicals llc Finally, TEC-specific delivery of a CaMK4 inhibitor specifically curbed renal inflammation in lupus-prone mice without affecting systemic inflammation. Our data offer the first evidence to our knowledge of the immunosuppressive capacity of TECs through a mechanism that involves competitive uptake of arginine and signify the importance of modulation of an inflammatory cytokine in the function of nonlymphoid cells, which leads to the establishment of an inflammatory microenvironment. New approaches to treat kidney inflammation should consider restoring the immunosuppressive capacity of TECs.Sepsis survivors exhibit impaired responsiveness to antigen (Ag) challenge associated with increased mortality from infection. The contribution of follicular dendritic cells (FDCs) in the impaired humoral response in sepsis-surviving mice is investigated in this study. We demonstrated that mice subjected to sepsis from cecal ligation and puncture (CLP mice) have reduced NP-specific high-affinity class-switched Ig antibodies (Abs) compared with sham-operated control mice following immunization with the T cell-dependent Ag, NP-CGG. NP-specific germinal center (GC) B cells in CLP mice exhibited reduced TNF-α and AID mRNA expression compared with sham-operated mice. CLP mice showed a reduction in FDC clusters, a reduced binding of immune complexes on FDCs, and reduced mRNA expression of CR2, ICAM-1, VCAM-1, FcγRIIB, TNFR1, IKK2, and LTβR compared with sham-operated mice. Adoptive transfer studies showed that there was no B cell-intrinsic defect. In summary, our data suggest that the reduced Ag-specific Ab response in CLP mice is secondary to a disruption in FDC and GC B cell function.Cystoisospora belli is a coccidian parasite that causes prolonged watery diarrhea especially among immunocompromised patients. Herein, we report a renal transplant patient who complaints of alternating diarrhea and review of literature related to cystoisosporiasis amongst the transplant recipients.

Leishmaniasis is a vector-borne disease caused by flagellated protozoans of the genus Leishmania. This study aimed to evaluate the epidemiological status of Visceral Leishmaniasis (VL) and Cutaneous Leishmaniasis (CL) among patients admitted to a university hospital in Istanbul, located in western Turkey.

This study included 160 and 77 patients with a pre-diagnosis of VL and CL, respectively, between January 2001 and December 2017. Detailed demographic data, including age, gender, nationality and the number and location of lesions were collected and recorded from the patient registries.

Among 160 bone marrow specimens that suspected as VL, 22 (13.7%) of the specimens that were evaluated with both culture and Giemsa staining detected as positive. Furthermore, 29 (37.7%) of the 77 patients suspected for CL showed evidence of Leishmania.

The increase in human immigration from neighbouring countries (with a high incidence of leishmaniasis) to Turkey might increase the risk of spreading the disease. This situation could result in a higher prevalence in metropolitan cities like Istanbul, where the country's population is concentrated.

The increase in human immigration from neighbouring countries (with a high incidence of leishmaniasis) to Turkey might increase the risk of spreading the disease. This situation could result in a higher prevalence in metropolitan cities like Istanbul, where the country's population is concentrated.