Infectious Diseases Society of America.

Treating patients with severe sepsis.

TREM-1 is an important signaling receptor expressed on neutrophils and monocytes that plays an important role in systemic infections. Here, we review the intracellular signaling pathways that mediate the immunological effects of TREM-1. Because of the absence of signaling motifs, TREM-1 constitutively associates with DAP12 for induction of intracellular signals. After phosphorylation of DAP12, production of chemokines and cytokines is induced. Moreover, TREM-1 also modulates signaling pathways induced by known classes of PRRs, such as TLRs and NLRs. The exact mechanisms through which TREM-1 influences TLR and NLR pathways are still largely elusive.

https://jlb.onlinelibrary.wiley.com/doi/pdf/10.1189/jlb.0312145

TREM-1: intracellular signaling pathways and interaction with pattern recognition receptors

Meticillin-resistant Staphylococcus aureus (MRSA) strains are prevalent bacterial pathogens that cause both health care and community-associated infections. Increasing resistance to commonly prescribed antibiotics has made MRSA a serious threat to public health throughout the world. The USA300 strain of MRSA has been responsible for an epidemic of community-associated infections in the US, mostly involving skin and soft tissue but also more serious invasive syndromes such as pneumonia, severe sepsis and endocarditis. MRSA strains are particularly serious and potentially lethal pathogens that possess virulence mechanisms including toxins, adhesins, enzymes and immunomodulators. One of these is Panton–Valentine leukocidin (PVL), a toxin associated with abscess formation and severe necrotizing pneumonia. Earlier studies suggested that PVL was a major virulence factor in community-associated MRSA infections. However, some recent data have not supported this association while others have, leading to controversy. Therefore, investigators continue to search for additional mechanisms of pathogenesis. In this review, we summarize the current understanding of the biological basis of MRSA virulence and explore future directions for research, including potential vaccines and antivirulence therapies under development that might allow clinicians to more successfully treat and prevent MRSA infections.

/pdf/current-concepts-on-the-virulence-mechanisms-of-meticillin-4y5zf3gatt.pdf

Current concepts on the virulence mechanisms of meticillin-resistant Staphylococcus aureus.

Kucers’ The Use of Antibiotics is the definitive, internationally-authored reference, providing everything that the infectious diseases specialist and prescriber needs to know about antimicrobials in this vast and rapidly developing field. The much-expanded Seventh Edition comprises 4800 pages in 3 volumes in order to cover all new and existing therapies, and emerging drugs not yet fully licensed. Concentrating on the treatment of infectious diseases, the content is divided into four sections - antibiotics, anti-fungal drugs, anti-parasitic drugs, and anti-viral drugs - and is highly structured for ease of reference. Each chapter is organized in a consistent format, covering susceptibility, formulations and dosing (adult and pediatric), pharmacokinetics and pharmacodynamics, toxicity, and drug distribution, with detailed discussion regarding clinical uses - a feature unique to this title. Compiled by an expanded team of internationally renowned and respected editors, with expert contributors representing Europe, Africa, Asia, Australia, South America, the US, and Canada, the Seventh Edition adopts a truly global approach. It remains invaluable for anyone using antimicrobial agents in their clinical practice and provides, in a systematic and concise manner, all the information required when prescribing an antimicrobial to treat infection.

Kucers' the use of antibiotics : a clinical review of antibacterial, antifungal, antiparasitic and antiviral drugs

Triggering receptor expressed on myeloid cells-1 (TREM-1) is an amplifier of TLR-mediated inflammation during bacterial infections. Thus far, TREM-1 is primarily associated with unwanted signs of overwhelming inflammation, rendering it an attractive target for conditions such as sepsis. Respiratory tract infections are the leading cause of sepsis, but the biological role of TREM-1 therein is poorly understood. To determine the function of TREM-1 in pneumococcal pneumonia, we first established TREM-1 up-regulation in infected lungs and human plasma together with augmented alveolar macrophage responsiveness toward Streptococcus pneumoniae. Mice treated with an agonistic TREM-1 Ab and infected with S. pneumoniae exhibited an enhanced early induction of the inflammatory response that was indirectly associated with lower levels of negative regulators of TLR signaling in lung tissue in vivo. Later in infection, TREM-1 engagement altered S. pneumoniae-induced IRAK-M (IL-1R-associated kinase-M) kinetics so as to promote the resolution of pneumonia and remarkably led to an accelerated elimination of bacteria and consequently improved survival. These data show that TREM-1 exerts a protective role in the innate immune response to a common bacterial infection and suggest that caution should be exerted in modulating TREM-1 activity during certain clinically relevant bacterial infections.

/pdf/trem-1-activation-alters-the-dynamics-of-pulmonary-irak-m-2qrkfl2fr6.pdf

TREM-1 Activation Alters the Dynamics of Pulmonary IRAK-M Expression In Vivo and Improves Host Defense during Pneumococcal Pneumonia

Antimicrobial susceptibility and macrolide resistance genes in Streptococcus pyogenes collected in Austria and Hungary.

Plasma lipoproteins such as LDL (low-density lipoprotein) are important therapeutic targets as they play a crucial role in macrophage biology and metabolic disorders. The impact of lipoprotein profiles on host defense pathways against Gram-positive bacteria is poorly understood. In this report, we discovered that human serum lipoproteins bind to lipoteichoic acid (LTA) from Staphylococcus aureus and thereby alter the immune response to these bacteria. Size-exclusion chromatography and solid-phase-binding analysis of serum revealed the direct interaction of LTA with apolipoproteins (Apo) B100, ApoA1, and ApoA2. Only ApoB100 and the corresponding LDL exerted biological effects as this binding significantly inhibited LTA-induced cytokine releases from human and murine immune cells. Serum from hypercholesterolemic mice or humans significantly diminished cytokine induction in response to S. aureus or its LTA. Sera taken from the patients with familial hypercholesterolemia before and after ApoB100-directed immuno-apheresis confirmed that ApoB100 inhibited LTA-induced inflammation in humans. In addition, mice in which LDL secretion was pharmacologically inhibited, displayed significantly increased serum cytokine levels upon infection with S. aureus in vivo. The present study identifies ApoB100 as an important suppressor of innate immune activation in response to S. aureus and its LTA.

Apolipoprotein B100 is a suppressor of Staphylococcus aureus-induced innate immune responses in humans and mice

TLR 2 and CD14 Mediate Innate Immunity and Lung Inflammation to Staphylococcal Panton-Valentine Leukocidin In Vivo

Valentine Leukocidin In Vivo - Lung Inflammation to Staphylococcal Panton TLR 2 and CD14 Mediate Innate Immunity and

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