CUIDADOS DE ENFERMAGEM PRESTADOS A MULHERES COM HIPERTENSÃO GESTACIONAL E PRÉ-ECLAMPSIA

A hipertensão gestacional e pré-eclampsia estão entre as doenças que compõem as síndromes da gestação que podem levar a vários agravosa saúde da mãe e do bebê, e se caracterizam por hipertensão arterial e/ou proteinúria diagnosticada após a 20ª semana de gestação, que possui grande ocorrência. O objetivo deste estudo foi descrever e analisar a importância dos cuidados de enfermagem que devem ser prestados a mulheres com hipertensão gestacional/pré-eclampsiatendo em vista seu diagnóstico precoce e a identificação de possíveis complicações. Paraisto foi realizada uma revisão da literatura científica por meio da busca refinada de artigos relacionados à temática escolhida e foram utilizados 11 estudos para a elaboração deste trabalho acadêmico. Nos resultados foram identificados inúmeros cuidados de enfermagem que devem ser prestados: como controle de infecção, identificação do nível de ansiedade, controle de eletrólitos, balanço hídrico, aferição da pressão arterial,avaliação de proteinúria,  promoção do repouso entre outros. Sendo assim, este estudo reflete a importância das intervenções de enfermagem a mulheres com hipertensão gestacional/pré-eclampsia de modo a atenuar os desafios que enfrentam nesta etapa da vida

The Mechanism behind Bacterial Lipoprotein Release: Phenol-Soluble Modulins Mediate Toll-Like Receptor 2 Activation via Extracellular Vesicle Release from Staphylococcus aureus

Our study highlights the roles of surfactant-like molecules in bacterial inflammation with important implications for the prevention and therapy of inflammatory disorders. It describes a potential pathway for the transfer of hydrophobic bacterial lipoproteins, the major TLR2 agonists, from the cytoplasmic membrane of Gram-positive bacteria to the TLR2 receptor at the surface of host cells. Moreover, our study reveals a molecular mechanism that explains how cytoplasmic and membrane-embedded bacterial proteins can be released by bacterial cells without using any of the typical protein secretion routes, thereby contributing to our understanding of the processes used by bacteria to communicate with host organisms and the environment.The innate immune system uses Toll-like receptor (TLR) 2 to detect conserved bacterial lipoproteins of invading pathogens. The lipid anchor attaches lipoproteins to the cytoplasmic membrane and prevents their release from the bacterial cell envelope. How bacteria release lipoproteins and how these molecules reach TLR2 remain unknown. Staphylococcus aureus has been described to liberate membrane vesicles. The composition, mode of release, and relevance for microbe-host interaction of such membrane vesicles have remained ambiguous. We recently reported that S. aureus can release lipoproteins only when surfactant-like small peptides, the phenol-soluble modulins (PSMs), are expressed. Here we demonstrate that PSM peptides promote the release of membrane vesicles from the cytoplasmic membrane of S. aureus via an increase in membrane fluidity, and we provide evidence that the bacterial turgor is the driving force for vesicle budding under hypotonic osmotic conditions. Intriguingly, the majority of lipoproteins are released by S. aureus as components of membrane vesicles, and this process depends on surfactant-like molecules such as PSMs. Vesicle disruption at high detergent concentrations promotes the capacity of lipoproteins to activate TLR2. These results reveal that vesicle release by bacterium-derived surfactants is required for TLR2-mediated inflammation

Toll-like receptor 2 activation depends on lipopeptide shedding by bacterial surfactants

Sepsis caused by Gram-positive bacterial pathogens is a major fatal disease but its molecular basis remains elusive. Toll-like receptor 2 (TLR2) has been implicated in the orchestration of inflammation and sepsis but its role appears to vary for different pathogen species and clones. Accordingly, Staphylococcus aureus clinical isolates differ substantially in their capacity to activate TLR2. Here we show that strong TLR2 stimulation depends on high-level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activator Agr. PSMs are required for mobilizing lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane. Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2-deficient mice, but TLR2 is required for protection of mice against PSM-producing S. aureus. Thus, a crucial role of TLR2 depends on agonist release by bacterial surfactants. Modulation of this process may lead to new therapeutic strategies against Gram-positive infections