Biology subjects

Serrato-Salas, J.

Publications and source records attributed to Serrato-Salas, J..

3 recordsLinked to original sources

bioRxiv2021

DENGUE VIRUS ALTERS SIALIC ACID RESIDUES CONFIGURATION IN MACROPHAGES

The activation of the innate immune response requires sialic acid residues removal. Nevertheless, it is unknown the role for these changes during the Dengue virus infection. We determine if during Dengue virus infection, the sialic acid residues alter on the macrophages. The human monocytic cell line THP-1 was differentiated into macrophages and were infected with Dengue virus. The changes in sialic acid were evaluated by lectin blot in the cellular lysate. The activity of neuraminidase was defined by RT-PCR and fluorescence assays. Macrophages infection with DENV-2 reduces -2,6 sialic acid residues at 24 h, and -2,3 sialic acid residues lower at 48 h in some proteins. Transcriptional profile and enzymatic activities of Neu-1 showed a narrow decrease. Sialic acid residues oscillation in varied conformations and times suggest it a role of a selective mechanism to remove these residues. The lesser participation of Neu-1 in this process could be concomitant to other similar enzymes such as sialyl-transferases, or the phenomenon requires minimal activity to have a relevant biological function.

immunology↗

bioRxiv2021

Down Regulation Of IL-1β Secretion By TGF-β1 In Macrophages Infected With Dengue Virus

Several pathogenic mechanisms have been linked to the severity of dengue virus infection, like viral cytotoxicity, underlying host genetics and comorbidities such as diabetes and dyslipidemia. It has been observed that patients with severe manifestations develop an uncontrolled immune response, with an increase in pro-inflammatory cytokines such as TNF, IL-1{beta}, IL-8, IL-6 and chemokines that damage the human microvascular endothelium, and also in anti-inflammatory cytokines IL-4, IL-10 and TGF-{beta}1. The role of TGF-{beta}1 on dengue is not clear; few studies have been published, and most of them from patient sera data, with both protective and pathological roles have described. The aim of this study was to evaluate the ability of TGF-{beta}1 to regulate the secretion of IL-1{beta} in macrophages infected by DENV using THP-1 cells treated with recombinant TGF-{beta}1 before or after DENV infection. By RT-PCR we did not observe a difference in IL-1{beta} expression between infected cells pretreated with TGF-{beta}1 and those that were not. However, secretion of IL-1{beta} was reduced only in cells stimulated with TGF-{beta}1 before infection, and not in those treated 2 hours post-infection. TGF-{beta}1 receptor blockage with SB505124 inhibitor, prior to the addition of TGF-{beta}1 and infection, abrogated the inhibitory effect of TGF-{beta}1. Our results suggest that DENV could regulate the function of TGF-{beta}1 on macrophages. This negative regulation of the TGF-{beta}1 pathway could be used by DENV to evade the immune response and could contribute to the immunopathology.

immunology↗

bioRxiv2021

Aedes aegypti Aag-2 culture cells enter endoreplication process upon pathogen challenge

Metamorphic insects apparently rely on a finite number of cells after emergence to counterbalance either commensal and pathogen presence. For hematophagous insects, blood-feeding is a crucial step for offspring development, therefore enteric cells repairing molecular mechanisms consists in fine regulated pathways to counterattack biotic and abiotic insults. Nevertheless, recent research suggests that midgut cells are capable to adapt their immune responses to pathogen challenges. Recently, Anopheles and Aedes mosquitoes have been observed to increase their DNA cell content upon encounter with parasites, bacteria and virus respectively. Genomic endoreplication is one of the most important processes in larval development for fast transcriptional activity and protein secretion. So, in this paper we explore the ability of Aedes aegypti Aag-2 culture cells to develop a likely endoreplication process to face pathogen presence. Aag-2 cells at 6 and 12 hours post-biotic insult enter a proliferation arrest and increases DNA content, these two phenomena recovers control levels at 24 h post-treatment. It requires more research data about the type of genomic regions that has been replicated in the process, and the concentration that antimicrobial molecules are released into culture media.

immunology↗