Immunoinformatic Approach for Rational Identification of Immunogenic Peptides Against Host Entry and/or Exit Mpox Proteins and Potential Multiepitope Vaccine Construction.

COVID-19 has intensified humanity's concern about the emergence of new pandemics. Since 2018, epidemic outbreaks of the mpox virus have become worrisome. In June 2022, the World Health Organization declared the disease a global health emergency, with 14 500 cases reported by the Centers for Disease Control and Prevention in 60 countries.

Reactive oxygen species trigger inflammasome activation after intracellular microbial interaction.

The intracellular production of reactive oxygen species (ROS), composed of oxygen-reduced molecules, is important not only because of their lethal effects on microorganisms but also due to their potential inflammatory and metabolic regulation properties. The ROS pro-inflammatory properties are associated with the second signal to inflammasome activation, leading to cleaving pro-IL-1β and pro-IL18 before their secretion, as well as gasdermin-D, leading to pyroptosis. Some microorganisms can modulate NLRP3 and AIM-2 inflammasomes through ROS production: whilst Mycobacterium bovis, Mycobacterium kansasii, Francisella novicida, Brucella abortus, Listeria monocytogenes, Influenza virus, Syncytial respiratory virus, Porcine reproductive and respiratory syndrome virus, SARS-CoV, Mayaro virus, Leishmania amazonensis and Plasmodium sp.

Different drug approaches to COVID-19 treatment worldwide: an update of new drugs and drugs repositioning to fight against the novel coronavirus.

According to the World Health Organization (WHO), in the second half of 2022, there are about 606 million confirmed cases of COVID-19 and almost 6,500,000 deaths around the world. A pandemic was declared by the WHO in March 2020 when the new coronavirus spread around the world. The short time between the first cases in Wuhan and the declaration of a pandemic initiated the search for ways to stop the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or to attempt to cure the disease COVID-19.

Ivermectin-induced bacterial gut dysbiosis does not increase susceptibility to Pseudomonas aeruginosa lung infection but exacerbates liver damage.

Excessive use of medications, including the antiparasitic drug ivermectin, can lead to bacterial gut dysbiosis, an imbalance in the intestinal microbiome, which in turn may increase or decrease susceptibility to infectious processes. To better understand the effects of continuous ivermectin usage on the gut bacterial community, C57BL/6 isogenic mice were treated by gavage with ivermectin or saline. Ivermectin-induced bacterial gut dysbiosis is characterized by a decrease in Bacteroidetes, Firmicutes, Proteobacteria and Tenericutes and an increase in species of the phylum Verrucomicrobia.

Murine response to the opportunistic bacterium Pseudomonas aeruginosa infection in gut dysbiosis caused by 5-fluorouracil chemotherapy-induced mucositis.

Aims: This manuscript aims to explain the relationship between mucositis caused by 5-FU over gut bacterial species and susceptibility to opportunistic infection caused by P. aeruginosa.

Main Methods: BALB/c mice were intraperitoneally treated with PBS or 5-FU.

Antibiotic-induced gut dysbiosis and autoimmune disease: A systematic review of preclinical studies.

Antibiotic-induced gut dysbiosis is believed to be associated with the onset and development of autoimmune diseases. To evaluate microbiota's variations triggered by antibiotic therapy and its outcomes on autoimmune diseases, preclinical studies regarding these subjects were included in this review. The studies were selected on PubMed, Scopus and Web of Science from 2011 to 2021 by three researchers that extracted study data and risk of bias, which were verified by a further 3 independent researchers.

Epitope identification of SARS-CoV-2 structural proteins using in silico approaches to obtain a conserved rational immunogenic peptide.

The short time between the first cases of COVID-19 and the declaration of a pandemic initiated the search for ways to stop the spread of SARS-CoV-2. There are great expectations regarding the development of effective vaccines that protect against all variants, and in the search for it, we hypothesized the obtention of a predicted rational immunogenic peptide from structural components of SARS-CoV-2 might help the vaccine research direction. In the search for a candidate of an immunogenic peptide of the SARS-CoV-2 envelope (E), membrane (M), nucleocapsid (N), or spike (S) proteins, we access the predicted sequences of each protein after the genome sequenced worldwide.

Epitope-Based Vaccine of a Putative Small RNA Target Induces Protection and Less Tissue Damage in Mice.

spp. are Gram-negative, facultative intracellular bacteria that cause brucellosis in humans and animals. Currently available live attenuated vaccines against brucellosis still have drawbacks.

The role of IL-10 in immune responses against Pseudomonas aeruginosa during acute lung infection.

Pseudomonas aeruginosa is considered an opportunistic pathogen of great clinical importance. The clearance of this bacterium occurs through recognition of the pathogen by innate immune system receptors, leading to a lung inflammatory response. However, this response must be controlled via immunoregulatory pathways.

Amoxicillin-induced gut dysbiosis influences estrous cycle in mice and cytokine expression in the ovary and the caecum.

Problem: Gut dysbiosis is caused by several factors, including the use of antibiotics. Since intestinal dysbiosis is associated with a wide range of immunopathological and reproductive conditions, the main goal of this study was to evaluate amoxicillin-induced gut dysbiosis and its influence on the oestrous cycle in mice.

Method Of Study: Mice were treated with amoxicillin or PBS, and faecal microbiota was evaluated by 16S rDNA metagenomic sequencing.

Vancomycin-induced gut dysbiosis during Pseudomonas aeruginosa pulmonary infection in a mice model.

Pseudomonas aeruginosa is one of the most common opportunistic pathogens causing respiratory infections in hospitals. Vancomycin, the antimicrobial agent usually used to treat bacterial nosocomial infections, is associated with gut dysbiosis. As a lung-gut immunologic axis has been described, this study aimed to evaluate both the immunologic and histopathologic effects on the lungs and the large intestine resulting from vancomycin-induced gut dysbiosis in the P.

JVA, an isoniazid analogue, is a bioactive compound against a clinical isolate of the Mycobacterium avium complex.

Bacteria belonging to Mycobacterium avium complex are organisms of low pathogenicity that infect immunosuppressed individuals. Infection is treated with an antimicrobial macrolide, Clarithromycin (CAM) or Azitromycin, associated with Ethambutol and Rifabutin during 12 months. Regimen long duration and side effects hinder patient's commitment to treatment favoring emergence of antibiotic resistance.

Antibiotic-induced dysbiosis effects on the murine gastrointestinal tract and their systemic repercussions.

The gastrointestinal tract has become a focus of study recently. The crosstalk between microbiota, especially bacteria, and the intestinal mucosa has to be accurately balanced in order to maintain physiological homeostasis in the human body. This dynamic interaction results in different levels of short-chain fatty acids (SCFAs), IgA, and T cell lymphocyte subsets, which could lead the human body towards health or disease.

miR-181a-5p Regulates TNF-α and miR-21a-5p Influences Gualynate-Binding Protein 5 and IL-10 Expression in Macrophages Affecting Host Control of Infection.

is a Gram-negative intracellular bacterium that causes a worldwide zoonosis termed brucellosis, which is characterized as a debilitating infection with serious clinical manifestations leading to severe complications. In spite of great advances in studies involving host- interactions, there are many gaps related to modulation of the host immune response through regulatory mechanisms. Here, we deep sequenced small RNAs from bone marrow-derived macrophages infected with , identifying 69 microRNAs (miRNAs) that were differentially expressed during infection.

5-Lipoxygenase negatively regulates Th1 response during Brucella abortus infection in mice.

Brucella abortus is a Gram-negative bacterium that infects humans and cattle, causing a chronic inflammatory disease known as brucellosis. A Th1-mediated immune response plays a critical role in host control of this pathogen. Recent findings indicate contrasting roles for lipid mediators in host responses against infections.

Key role of Toll-like receptor 2 in the inflammatory response and major histocompatibility complex class ii downregulation in Brucella abortus-infected alveolar macrophages.

Alveolar macrophages (AM) seem to constitute the main cellular target of inhaled brucellae. Here, we show that Brucella abortus invades and replicates in murine AM without inducing cytotoxicity. B.

Lack of endogenous IL-10 enhances production of proinflammatory cytokines and leads to Brucella abortus clearance in mice.

IL-10 is a cytokine that regulates the balance between pathogen clearance and immunopathology. Brucella abortus is an intracellular bacterium that causes chronic disease in humans and domestic animals. Here we evaluated the contribution of IL-10 in host immune response and pathology during B.

Critical role of ASC inflammasomes and bacterial type IV secretion system in caspase-1 activation and host innate resistance to Brucella abortus infection.

Pathogens are detected by innate immune receptors that, upon activation, orchestrate an appropriate immune response. Recent studies revealed the intracellular signaling cascades involved in the TLR-initiated immune response to Brucella abortus infection. However, no report has elucidated the role of inflammasome receptors in Brucella recognition.

Toll-like receptor 6 plays an important role in host innate resistance to Brucella abortus infection in mice.

Brucella abortus is recognized by several Toll-like receptor (TLR)-associated pathways triggering proinflammatory responses that affect both the nature and intensity of the immune response. Previously, we demonstrated that B. abortus-mediated dendritic cell (DC) maturation and control of infection are dependent on the adaptor molecule MyD88.