Analysis of Complement Factor H gene polymorphisms and their association with clinical manifestations ofleptospirosis.

Leptospirosis is caused by pathogenic leptospires, posing a significant public health problem. Host susceptibility to Leptospira infection is a multifactorial trait, and the host's genetic background can influence both the establishment of infection and the severity of the disease. Complement Factor H (FH) plays a crucial role in the interaction between pathogenic bacteria and the host.

Role of C-C chemokine receptor type 5 in pathogenesis of malaria and its severe forms.

Malaria is a mosquito-borne disease caused by Plasmodium parasites, responsible for a significant impact on public health in several tropical and sub-tropical countries. The majority of infection cases are classified as uncomplicated malaria, causing mild symptoms such as fever and headache. However, the disease may progress to severe malaria and death if the infection is not properly treated.

Unexplained fever with consumptive syndrome in the elderly: two cases of VEXAS syndrome with inflammasome dysregulation.

The aim of this study is to investigate the inflammasome dysregulation in peripheral blood leukocytes of VEXAS patients. The constitutive and in vitro triggered activation of inflammasome in PBMC and neutrophils was analyzed in two Brazilian patients with typical UBA1 mutations, and compared with healthy donors. Our findings highlight the constitutive activation of caspase-1 in VEXAS leukocytes, accompanied by increased plasma levels of IL-18.

Telemedicine for type 2 diabetes during COVID-19 pandemic: experience from a tertiary diabetes center.

Background: Telemedicine was largely employed during COVID-19 pandemic to guarantee continuity of care in a period of dramatic reduction of face-to-face visits. The aim of this study was to describe the clinical characteristics of a cohort of patients with type 2 diabetes followed by tele-visits and to evaluate the changes in the glyco-metabolic control during a 12-month follow-up.

Methods: This retrospective observational study included 136 adults aged >18 years with at least three tele-visits over a 12-month follow-up period, in a Diabetes Center of the Southern Italy, from April 2020 to March 2022.

Canonical Inflammasomes.

The innate immune response represents the first line of host defense, and it is able to detect pathogen- and damage-associated molecular patterns (PAMPs and DAMPs, respectively) through a variety of pattern recognition receptors (PRRs). Among these PRRs, certain cytosolic receptors of the NLRs family (specifically NLRP1, NLRP3, NLRC4, and NAIP) or those containing at least a pyrin domain (PYD) such as pyrin and AIM2, activate the multimeric complex known as inflammasome, and its effector enzyme caspase-1. The caspase-1 induces the proteolytic maturation of the pro-inflammatory cytokines IL-1ß and IL-18, as well as the pore-forming protein gasdermin D (GSDMD).

Cervical carcinoma induces NLRP3 inflammasome activation and IL-1ß release in human peripheral blood monocytes affecting patients' overall survival.

Purpose: Our group previously demonstrated that genetic variants in inflammasome genes contribute to protection against the establishment of human papilloma virus (HPV)-associated cervical carcinoma (CC). The objective of this study was to better understand the contribution of inflammasome and its cytokines in the CC microenvironment.

Methods: The inflammasome activation was analyzed in CC tumoral cell lines and healthy donors (HD)' monocytes in co-culture.

Severe COVID-19 patients show a dysregulation of the NLRP3 inflammasome in circulating neutrophils.

SARS-CoV-2 triggers inflammasome-dependent release of pro-inflammatory cytokine IL-1β and pyroptosis, therefore, contributes to the huge inflammatory response observed in severe COVID-19 patients. Less is known about the engagement of inflammasome in neutrophils, main players in tissue injury and severe infection. We studied the activation of the inflammasome in neutrophils from severe COVID-19 patients and assessed its consequence in term of cells contribution to disease pathogenesis.

A common variant close to the "tripwire" linker region of NLRP1 contributes to severe COVID-19.

Objective And Design: The heterogeneity of response to SARS-CoV-2 infection is directly linked to the individual genetic background. Genetic variants of inflammasome-related genes have been pointed as risk factors for several inflammatory sterile and infectious disease. In the group of inflammasome receptors, NLRP1 stands out as a good novel candidate as severity factor for COVID-19 disease.

Neuroimmunoendocrinology of SARS-CoV 2 Infection.

This review is aimed at illustrating and discussing the neuroimmune endocrinological aspects of the SARS-CoV-2 infection in light of the studies on this topic that have so far appeared in the literature. The most characteristic findings and pending controversies were derived by PubMed and Scopus databases. We included original and observational studies, reviews, meta-analysis, and case reports.

The inflammasomes: crosstalk between innate immunity and hematology.

Background: The inflammasome is a cytosolic multi-protein complex responsible for the proteolytic maturation of pro-inflammatory cytokines IL-1ß and IL-18 and of gasdermin-D, which mediates membrane pore formation and the cytokines release, or eventually a lytic cell death known as pyroptosis. Inflammation has long been accepted as a key component of hematologic conditions, either oncological or benign diseases.

Objectives: This study aims to review the current knowledge about the contribution of inflammasome in hematologic diseases.

In-vitro NLRP3 functional test assists the diagnosis of cryopyrin-associated periodic syndrome (CAPS) patients: A Brazilian cooperation.

Objective: To report our five-years experience on the use of NLRP3 inflammasome functional assays in the differential diagnosis of Brazilian patients with a clinical suspicion of CAPS.

Patients And Methods: The study included 9 patients belonging to 2 families (I, II) and 7 unrelated patients with a clinical suspicion of AID according to Eurofever/PRINTO classification, recruited between 2017 and 2022. The control group for the NLRP3 functional assay consisted of 10 healthy donors and for the CBA cytokines measurement of 19 healthy controls.

The genetics behind inflammasome regulation.

The inflammasome is a cytosolic multiproteic complex that promotes proinflammatory events through the release of the cytokines IL-1β and IL-18, and in some context by the induction of a lytic cell death called pyroptosis, in response to damage, infections, or changes in the homeostasis. Due to the powerful inflammatory effect, there are several regulatory mechanisms that are essential to modulate or limit the activation of the inflammasome. When these mechanisms fail, the deregulation of the complex leads or contributes to the development of a plethora of diseases characterized by constitutive and/or chronic inflammation, such as autoinflammatory, autoimmune, cardiovascular, neurodegenerative, and metabolic diseases, cancer, or even severe complications of infectious diseases.

Elucidating the 3D Structure of a Surface Membrane Antigen from as a Serodiagnostic Biomarker of Chagas Disease.

Chagas disease (CD) is a vector-borne parasitosis, caused by the protozoan parasite , that affects millions of people worldwide. Although endemic in South America, CD is emerging throughout the world due to climate change and increased immigratory flux of infected people to non-endemic regions. Containing of the diffusion of CD is challenged by the asymptomatic nature of the disease in early infection stages and by the lack of a rapid and effective diagnostic test.

Recessive NLRC4-Autoinflammatory Disease Reveals an Ulcerative Colitis Locus.

Purpose: NLRC4-associated autoinflammatory disease (NLRC4-AID) is an autosomal dominant condition presenting with a range of clinical manifestations which can include macrophage activation syndrome (MAS) and severe enterocolitis. We now report the first homozygous mutation in NLRC4 (c.478G > A, p.

Sepsis.

This article provides an overview of the history of the sepsis definitions as well as an overview of the current understanding of the pathogenesis of sepsis. The evolution of the treatment bundles is also presented.

Genetic contribution and functional impairment of inflammasome in sickle cell disease.

Background: Sickle cell disease (SCD), one of the most common single-gene disorders, is caused by mutations in the hemoglobin ß-chain gene. Clinical presentation is heterogeneous, and inflammation is a common condition. Thereby, we hypothesized that inflammasome and related cytokine IL-1ß could represent significant SCD pathogenesis contributors.

NLRP1 acts as a negative regulator of Th17 cell programming in mice and humans with autoimmune diabetes.

Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β cells. We show here that the protein NOD-like receptor family pyrin domain containing 1 (NLRP1) has a key role in the pathogenesis of mouse and human T1D. More specifically, downregulation of NLRP1 expression occurs during T helper 17 (Th17) differentiation, alongside greater expression of several molecules related to Th17 cell differentiation in a signal transducers and activators of transcription 3 (STAT3)-dependent pathway.

Common pathogen-associated molecular patterns induce the hyper-activation of NLRP3 inflammasome in circulating B lymphocytes of HIV-infected individuals.

Objective: Despite the antiretroviral treatment, people with HIV (PWH) still experience systemic chronic inflammation and immune-senescence, which represent risk factors for severe comorbidities and inefficient response to pathogens and vaccines. Given the dysregulation of NLRP3 inflammasome in PWH and the recently demonstrated role played by NLRP3 in B lymphocytes, we hypothesized that NLRP3 dysregulation in B cells can contribute to chronic inflammation and humoral dysfunction in PWH.

Design: NLRP3 inflammasome activation was evaluated in B lymphocytes and correlated with antibodies production and immunization response in PWH.

Inflammatory effect of Bothropstoxin-I from Bothrops jararacussu venom mediated by NLRP3 inflammasome involves ATP and P2X7 receptor.

Muscle tissue damage is one of the local effects described in bothropic envenomations. Bothropstoxin-I (BthTX-I), from Bothrops jararacussu venom, is a K49-phospholipase A2 (PLA2) that induces a massive muscle tissue injury, and, consequently, local inflammatory reaction. The NLRP3 inflammasome is a sensor that triggers inflammation by activating caspase 1 and releasing interleukin (IL)-1β and/or inducing pyroptotic cell death in response to tissue damage.

Sensing soluble uric acid by Naip1-Nlrp3 platform.

Uric acid (UA), a product of purine nucleotide degradation able to initiate an immune response, represents a breakpoint in the evolutionary history of humans, when uricase, the enzyme required for UA cleavage, was lost. Despite being inert in human cells, UA in its soluble form (sUA) can increase the level of interleukin-1β (IL-1β) in murine macrophages. We, therefore, hypothesized that the recognition of sUA is achieved by the Naip1-Nlrp3 inflammasome platform.