Proteolytic activity of secreted proteases from pathogenic leptospires and effects on phagocytosis by murine macrophages.

Leptospirosis is a zoonosis caused by spirochete Leptospira. Pathogenic leptospires evade the Complement System, enabling their survival upon contact with normal human serum in vitro. In a previous study, we demonstrated that proteases secreted by pathogenic leptospires cleave several Complement proteins, including C3 and the opsonins C3b and iC3b.

The Leptospira interrogans proteome's response to zinc highlights the potential involvement of this metal in translational-machinery and virulence.

Leptospires, as motile Gram-negative bacteria, employ sophisticated strategies for efficient invasion and dissemination within their hosts. In response, hosts counteract pathogens through nutritional immunity, a concept involving the deprivation of essential metals such as zinc. Zinc, pivotal in modulating pathogen-host interactions, influences proteins structural, catalytic, and regulatory functions.

O26 Polysaccharides as Key Players in Enteropathogenic Immune Evasion and Vaccine Development.

Enteropathogenic (EPEC) produce a capsule of polysaccharides identical to those composing the O-antigen polysaccharide of its LPS (lipopolysaccharide) molecules. In light of this, the impact of O26 polysaccharides on the immune evasion mechanisms of capsulated O26 EPEC compared to non-capsulated enterohemorrhagic (EHEC) was investigated. Our findings reveal that there was no significant difference between the levels in EPEC and EHEC of rhamnose (2.

Plasmid-encoded toxin of cleaves complement system proteins and inhibits complement-mediated lysis .

Plasmid-encoded toxin (Pet) is an autotransporter protein of the serine protease autotransporters of Enterobacteriaceae (SPATE) family, important in the pathogenicity of . The gene was initially found in the enteroaggregative (EAEC) virulence plasmid, pAA2. Although this virulence factor was initially described in EAEC, an intestinal pathotype, may also be present in other pathotypes, including extraintestinal pathogenic strains (ExPEC).

Sleep Pattern Interference in the Cognitive Performance of Lusitano Horses.

Like most mammalian, polyphasic sleep, equine sleep can be divided into two phases: the REM (rapid eye movement) phase and the NREM (non-rapid eye movement) phase. For this study, a randomized crossover experiment was conducted using ten purebred Lusitano horses, all dressage athletes aged from three to seven years old. The horses were filmed before the intervention to characterize their sleep patterns.

Cell lipid biology in infections: an overview.

Lipids are a big family of molecules with a vast number of functions in the cell membranes, within the cytoplasm, and extracellularly. Lipid droplets (LDs) are the most common storage organelles and are present in almost every tissue type in the body. They also have structural functions serving as building blocks of cellular membranes and may be precursors of other molecules such as hormones, and lipoproteins, and as messengers in signal transduction.

MPL36, a major plasminogen (PLG) receptor in pathogenic Leptospira, has an essential role during infection.

Leptospirosis, a zoonosis with worldwide distribution, is caused by pathogenic spirochetes belonging to the genus Leptospira. Bacterial outer membrane proteins (OMPs), particularly those with surface-exposed regions, play crucial roles in pathogen dissemination and virulence mechanisms. Here we characterized the leptospiral Membrane Protein L36 (MPL36), a rare lipoprotein A (RlpA) homolog with a C-terminal Sporulation related (SPOR) domain, as an important virulence factor in pathogenic Leptospira.

Sph2 and Sph2: Identification of B-Cell Linear Epitopes in Sphingomyelinase 2 (Sph2), Naturally Recognized by Patients Infected by Pathogenic Leptospires.

Sphingomyelin is a major constituent of eukaryotic cell membranes, and if degraded by bacteria sphingomyelinases may contribute to the pathogenesis of infection. Among spp., there are five sphingomyelinases exclusively expressed by pathogenic leptospires, in which Sph2 is expressed during natural infections, cytotoxic, and implicated in the leptospirosis hemorrhagic complications.

Characterization of a virulence-modifying protein of identified by shotgun phage display.

Pathogenic species of are etiologic agents of leptospirosis, an emerging zoonotic disease of worldwide extent and endemic in tropical regions. The growing number of identified leptospiral species sheds light to their genetic diversity and unique virulence mechanisms, many of them still remain unknown. Toxins and adhesins are important virulence factors in several pathogens, constituting promising antigens for the development of vaccines with cross-protection and long-lasting effect against leptospirosis.

Seroepidemiologic survey of the household contacts of leprosy patients.

Objective: Leprosy is a disabling infectious disease caused by Mycobacterium leprae. This study aimed to investigate the prevalence of leprosy among household contacts of leprosy patients.

Methods: This study is a serological survey in household contacts of leprosy patients who had been treated or were undergoing treatment in the city of Presidente Prudente, São Paulo, Brazil, from 2006-2016, using clinical examination and screening for anti- Phenolic glycolipid-I antibodies with Mycobacterium leprae-flow serology.

Leptolysin, a secreted metalloprotease of the pappalysin family with broad-spectrum activity.

Extracellular proteolytic enzymes are produced by a variety of pathogenic microorganisms, and contribute to host colonization by modulating virulence. Here, we present a first characterization of leptolysin, a metalloprotease of the pappalysin family identified in a previous exoproteomic study. Comparative molecular analysis of leptolysin with two other pappalysins from prokaryotes, ulilysin and mirolysin, reveals similarities regarding calcium, zinc, and arginine -binding sites conservation within the catalytic domain, but also discloses peculiarities.

O55 Polysaccharides Are Good Antigen Targets for the Formulation of Vaccines against O55 STEC and Capsulated aEPEC Strains.

The serogroup O55 of is composed of strains whose mechanisms of virulence are different from each other. Since the O55 polysaccharides are present in all O55 strains, and so are the polymers that compose the capsule of O55 atypical enteropathogenic (aEPEC), it was investigated whether anti-O55 antibodies were able to help the innate immune system to eliminate capsulated aEPEC and Shiga toxin-producing (STEC) belonging to the serogroup O55. The results demonstrate that the capsule of EPEC was able to inhibit the deposition of C3b on the bacterial surface and, as a consequence, their lysis by the alternative pathway of the complement system.

Correction: Prado, L.G.; Barbosa, A.S. Understanding the Renal Fibrotic Process in Leptospirosis. 2021, , 10779.

The authors wish to make the following corrections to this paper [...

Secreted Autotransporter Toxin (Sat) Mediates Innate Immune System Evasion.

Several strategies are used by to evade the host innate immune system in the blood, such as the cleavage of complement system proteins by secreted proteases. Members of the Serine Proteases Autotransporters of Enterobacteriaceae (SPATE) family have been described as presenting proteolytic effects against complement proteins. Among the SPATE-encoding genes (secreted autotransporter toxin) has been detected in high frequencies among strains of isolated from bacteremia.

The C-Terminal Domain of Zinc Transport Protein AdcA Binds Plasminogen and Factor H In Vitro.

Bacterial acquisition of metals from a host is an essential attribute to facilitate survival and colonization within an infected organism. , a bacterial pathogen of medical importance, has evolved its strategies to acquire multiple metals, including iron, manganese, and zinc. Other important strategies for the colonization and infection of the host have been reported for staphylococci and include the expression of adhesins on the bacterial surface, as well as the acquisition of host plasminogen and complement regulatory proteins.

Understanding the Renal Fibrotic Process in Leptospirosis.

Leptospirosis is a neglected infectious disease caused by pathogenic species of the genus . The acute disease is well-described, and, although it resembles other tropical diseases, it can be diagnosed through the use of serological and molecular methods. While the chronic renal disease, carrier state, and kidney fibrosis due to infection in humans have been the subject of discussion by researchers, the mechanisms involved in these processes are still overlooked, and relatively little is known about the establishment and maintenance of the chronic status underlying this infectious disease.

Chondrogenic potential of mesenchymal stem cells from horses using a magnetic 3D cell culture system.

Background: Mesenchymal stem cells (MSCs) represent a promising therapy for the treatment of equine joint diseases, studied due to their possible immunomodulatory characteristics and regenerative capacity. However, the source of most suitable MSCs for producing cartilage for regenerative processes in conjunction with biomaterials for an enhanced function is yet to be established.

Aim: To compare the chondrogenicity of MSCs derived from synovial fluid, bone marrow, and adipose tissue of horses, using the aggrecan synthesis.

Inactivation of the antimicrobial peptide LL-37 by pathogenic Leptospira.

Leptospires are aerobic, Gram-negative spirochetes with a high invasive capacity. Pathogenic leptospires secrete proteases that inactivate a variety of host's proteins including molecules of the extracellular matrix and of the human complement system. This strategy, used by several pathogens of medical importance, contributes to bacterial invasion and immune evasion.

The Role of Properdin in Killing of Non-Pathogenic .

Properdin (P) is a positive regulatory protein that stabilizes the C3 convertase and C5 convertase of the complement alternative pathway (AP). Several studies have suggested that properdin can bind directly to the surface of certain pathogens regardless of the presence of C3bBb. Saprophytic are susceptible to complement-mediated killing, but the interaction of properdin with spp.

Case for diagnosis. Eyelid edema and erythematous papules disseminated on the face.

Lupus miliaris disseminatus faciei or acne agminata is a chronic inflammatory disorder of the skin, considered an intriguing entity due to its pathogenesis, which is still largely speculative. It has been linked to tuberculosis, sarcoidosis, rosacea, and other granulomatous diseases, but it is considered an independent entity.

Contribution of Complement System pathways to the killing of Leptospira spp.

The Complement System (CS) plays an important role in the immune response against leptospirosis and can be activated by the Alternative and Lectin Pathways (Innate Immunity) and by the Classical Pathway (Acquired Immunity). Here we analyzed a broad range of nonpathogenic and pathogenic Leptospira strains considering their interaction with each CS pathway. We determined bacterial survival rate and CS protein deposition in the presence of purified proteins, specific component depleted sera and NHS treated with the chelating agents EDTA (inhibits all three activation pathways) or EGTA (inhibits the Classical and Lectin Pathways).

Complement Resistance Assays.

Like many other pathogens of medical importance, pathogenic Leptospira employ diverse strategies to circumvent Complement System activation. Under physiological conditions, this central humoral arm of innate immunity is tightly controlled by negative Complement regulatory proteins. However, upon infection, pathogenic microorganisms interfere with normal Complement host defense mechanisms by recruiting or mimicking Complement regulators and by secreting endogenous proteases or acquiring host's proteases that inactivate key Complement components.

Surface Protein Dispersin of Enteroaggregative Binds Plasminogen That Is Converted Into Active Plasmin.

Dispersin is a 10.2 kDa-immunogenic protein secreted by enteroaggregative (EAEC). In the prototypical EAEC strain 042, dispersin is non-covalently bound to the outer membrane, assisting dispersion across the intestinal mucosa by overcoming electrostatic attraction between the AAF/II fimbriae and the bacterial surface.