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      Battle royale: Immune response on biofilms – host-pathogen interactions

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          Abstract

          <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" id="d3759003e125">The research interest of the scientific community in biofilm-forming microorganisms is growing due to the problems caused by their infections affecting humans and animals, mainly because of the difficulty of the host immune system in eradicating these microbial complex communities and the increasing antimicrobial resistance rates worldwide. This review describes the virulence factors and their interaction with the microbial communities of four well-known and highly biofilm-forming pathogens, more exactly, Pseudomonas aeruginosa, Escherichia coli, Staphylococcus spp., and Candida spp. The innate and adaptive immune responses caused by the infection with these microorganisms and their evasion to the host immune system by biofilm formation are discussed in the present work. The relevance of the differences in the expression of certain virulence factors and the immune response in biofilm-associated infections when compared to planktonic infections is usually described as the biofilm architecture protects the pathogen and alters the host immune responses, here we extensively discussed these mechanisms. </p>

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          Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management.

          Staphylococcus aureus is a major human pathogen that causes a wide range of clinical infections. It is a leading cause of bacteremia and infective endocarditis as well as osteoarticular, skin and soft tissue, pleuropulmonary, and device-related infections. This review comprehensively covers the epidemiology, pathophysiology, clinical manifestations, and management of each of these clinical entities. The past 2 decades have witnessed two clear shifts in the epidemiology of S. aureus infections: first, a growing number of health care-associated infections, particularly seen in infective endocarditis and prosthetic device infections, and second, an epidemic of community-associated skin and soft tissue infections driven by strains with certain virulence factors and resistance to β-lactam antibiotics. In reviewing the literature to support management strategies for these clinical manifestations, we also highlight the paucity of high-quality evidence for many key clinical questions.
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            Understanding the mechanism of IL-1β secretion

            The cytokine interleukin-1β (IL-1β) is a key mediator of the inflammatory response. Essential for the host-response and resistance to pathogens, it also exacerbates damage during chronic disease and acute tissue injury. It is not surprising therefore that there is a huge level of interest in how this protein is produced and exported from cells. However, the mechanism of IL-1β release has proven to be elusive. It does not follow the conventional ER-Golgi route of secretion. A literature full of disparate observations arising from numerous experimental systems, has contributed to a complicated mix of diverse proposals. Here we summarise these observations and propose that secretion of IL-1β occurs on a continuum, dependent upon stimulus strength and the extracellular IL-1β requirement.
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              Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey.

              Although activity that induced tumor regression was observed and termed tumor necrosis factor (TNF) as early as the 1960s, the true identity of TNF was not clear until 1984, when Aggarwal and coworkers reported, for the first time, the isolation of 2 cytotoxic factors: one, derived from macrophages (molecular mass 17 kDa), was named TNF, and the second, derived from lymphocytes (20 kDa), was named lymphotoxin. Because the 2 cytotoxic factors exhibited 50% amino acid sequence homology and bound to the same receptor, they came to be called TNF-α and TNF-β. Identification of the protein sequences led to cloning of their cDNA. Based on sequence homology to TNF-α, now a total of 19 members of the TNF superfamily have been identified, along with 29 interacting receptors, and several molecules that interact with the cytoplasmic domain of these receptors. The roles of the TNF superfamily in inflammation, apoptosis, proliferation, invasion, angiogenesis, metastasis, and morphogenesis have been documented. Their roles in immunologic, cardiovascular, neurologic, pulmonary, and metabolic diseases are becoming apparent. TNF superfamily members are active targets for drug development, as indicated by the recent approval and expanding market of TNF blockers used to treat rheumatoid arthritis, psoriasis, Crohns disease, and osteoporosis, with a total market of more than US $20 billion. As we learn more about this family, more therapeutics will probably emerge. In this review, we summarize the initial discovery of TNF-α, and the insights gained regarding the roles of this molecule and its related family members in normal physiology and disease.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Current Research in Immunology
                Current Research in Immunology
                Elsevier BV
                25902555
                2023
                2023
                : 4
                : 100057
                Article
                10.1016/j.crimmu.2023.100057
                10070391
                37025390
                78306ac7-f21b-4801-83b8-3341be901c97
                © 2023

                https://www.elsevier.com/tdm/userlicense/1.0/

                http://creativecommons.org/licenses/by/4.0/

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