Febs Letters Impact Factor 2020

Febs Letters Impact Factor 2020 – A central role in our defense against infection. Its antibacterial effects have been known for over 100 years, but its importance in boosting immunity against pathogens has been relatively neglected. Only recently has it become clear that one of the major characteristics of pathogenic microorganisms is their ability to evade complement attack. All viruses, many bacteria, and certain organisms, fungi and protozoan parasites, can hide inside cells that are protected from antibodies, complement, and other humoral immune effector mechanisms. However, although most microorganisms have an extracellular morphology, some, such as viruses, cannot grow without the host’s replication machinery and intracellular protective environment.

This special issue of FEBS Letters contains 14 articles dedicated to the role of complement in microbial infection, and the SARS-CoV-2 pandemic has dramatically increased public interest in the organism and prevention of infection. It is particularly timely because the Below, we briefly summarize the role of complement in viral and bacterial infections, as described in individual articles belonging to this collection. The role of complement in is discussed in another article by Parente et al. [[1]] and he Kiyuka et al. [[2]], respectively.

Febs Letters Impact Factor 2020

Although Aspergillus is an opportunistic pathogen, it can cause multiple types of infections, especially in patients taking immunosuppressive drugs or suffering from immunocompromised individuals. The body is still active, but apparently Aspergillus can escape complement and cause invasive infections. There is a nature. Like C-reactive protein and PTX-3, there are various forms in fungi that interact with the complement system and pentraxin. Pentraxin works closely with the complement system by activating and regulating it. In an in-depth article, Parente et al. [[1]] Describe how Aspergillus can cope with these two her protein systems.

Polysaccharide Oxidation By Lytic Polysaccharide Monooxygenase Is Enhanced By Engineered Cellobiose Dehydrogenase

The causative agents of malaria, especially its most dangerous species, Plasmodium falciparum, are another group of complex organisms with different life forms. From Kiyu. [[2]] provides an update on what is currently known about complement evasion by the malaria parasite and how this information can be used to prepare efficient and functional vaccines.

As a medical problem, complement resistance is comparable to antimicrobial resistance (AMR). AMR is a “man-made” problem that has only emerged in the past 100 years, when antibiotics were adopted to treat infections in humans and animals. In contrast, complement resistance has evolved over a very long period of time. The emergence of complement-resistant pathogenic microorganisms coincided with the development of the complement system in different animals. Complement resistance in microorganisms has contributed to creating a repertoire of pathogenic microorganisms. AMR poses a threat because it loses the most commonly used tools against microbial infections caused by pathogenic and/or opportunistic organisms. The fact that opportunistic microbes such as Acinetobacter, Enterobacter sp., Klebsiella and Pseudomonas can cause infection usually depends on reduced host local or systemic immune activity. Second, even if a microbe is complement-sensitive, it can still cause infection.

Why is it important to study complement evasion mechanisms in microorganisms? Complement resistance is an important virulence mechanism for many pathogenic microorganisms. It is important to know the factors involved in the ability of microorganisms to evade complement-mediated opsonophagocytosis or direct killing, as well as other pathogenic mechanisms (e.g., adhesion, toxin production). This will aid in the development of vaccines, passive antibody therapies, or new types of antibiotics that may counter resistance mechanisms. Knowing how microbes and other organisms (such as blood-eating mites and insects) can inhibit complement may lead to new treatments for suppressing complement overactivity that occurs in many human diseases. Understanding how microbes deal with the complement system will help us understand the underlying mechanisms of the complement system itself and the relative contributions of its individual pathways and components. It also helps to

From a microbial perspective, complement resistance is important for the ability to survive and grow in animal hosts. Of course, many other factors are required. Microorganisms must possess the appropriate types of ligands for host receptors and other molecules for attachment and entry into cells and tissues. In many cases, toxins are required to provide sufficient debris for growth and nutrient delivery.In extreme cases, the toxins and infections themselves can be harmful to the host. The medical impact of microbial infections is enormous and is increasingly appreciated by the current SARS-CoV-2 pandemic. Although the interaction of SARS-CoV-2 with complement is still under study, a special issue of the current FEBS letter provides a panoramic view of what is currently known about the interaction between various microbes and the complement system. provide. This will be beneficial for research on other microbes, including coronaviruses, and other potential infectious threats in the future.

The Adipokine Nimrodb5 Regulates Peripheral Hematopoiesis In Drosophila

Viral complement resistance has been thoroughly discussed by Agrawal et al. [[3]]. Pathogenic bacteria are experts at stealing and misusing their host’s proteins, while pathogenic viruses typically steal their host’s genes and modify them for their own purposes. As demonstrated in this review, pathogenic viruses, such as poxviruses, mimic host complement regulatory proteins. In humans, regulators usually consist of a major structural unit, the complement regulatory protein repeat encoded on chromosome 1 of the so-called regulator of complement activation (RCA) gene cluster. In addition, a mimetic of the membrane attack complex inhibitor CD59 is found in the simian herpesvirus H. saimiri.

With the increasing emergence of problems caused by viruses, it is clear that there is a need to learn more about viral complement escape mechanisms.Dengue virus belongs to a large group of flaviviruses that cause various types of infections. (West Nile virus, yellow fever virus, and Zika virus). As described by Carr et al. [[4]], complement plays multiple roles in mosquito-borne dengue virus infection. In some cases, antibody-mediated immunity and complement can be protective, but in some cases they can significantly enhance the inflammatory response, leading to the serious complication of capillary leak syndrome. I have. The fact that viruses have developed multiple functional interactions with complement factors provides firm and unbiased evidence for the importance of complement as an immune defense mechanism.

This issue presents eight of his reviews on the interaction of complement with various bacteria. Staphylococci are masters of immune evasion, as shown in the article by de Vor et al. [[Five]]. They can block complement at many stages, stimulate neutrophils and form biofilms to protect them (eg on wound infections and implants). In this review, the reader can see the largest repertoire of complement inhibitors known in any bacterium and the mechanisms of biofilm generation. Interestingly, the latter represents a difference between S. epidermidis and S. aureus, making it a common cause of infection both at the surface and deep in tissue.

Streptococcus pneumoniae (pneumococcus) causes bacterial upper respiratory infections, pneumonia, sinusitis, and otitis media. It can also cause meningitis and septic infections. Pneumococcus and other streptococci are discussed by Syed et al. [[6]]. Like other pathogens, group A streptococci (Streptococcus pyogenes) and pneumococci utilize soluble complement inhibitors, particularly factor H for complement escape. For this they use specific surface proteins, most commonly M proteins or PspC family proteins. Other important virulence factors are cytolysin, streptolysin, and pneumolysin, which produce pores on cells somewhat similar to the complement membrane attack complex (MAC). The respiratory pathogens Haemophilus influenzae and Moraxella catarrhalis also utilize the soluble complement inhibitors C4bp and factor H for protection, as briefly presented by Riesbeck [[7]]. In addition, both have been found to bind vitronectin and may help prevent complement lysis due to killing these Gram-negative bacteria. Bacteria use multiple types of surface molecules for complement escape and adhesion to host cells.

Identification Of Diverse Lipid‐binding Modes In The Groove Of Zinc α2 Glycoprotein Reveals Its Functional Versatility

The Gram-negative bacteria Salmonella and Yersinia can cause both enteric and systemic infections. Krukonis and Thomson [[8]] describe the strategies underlying their ability to cause systemic infection and penetrate deep into tissues. These properties are largely based on their ability to hijack complement inhibitors, interfere with MAC formation, and proteolytically destroy complement proteins. As explained, various components of bacteria contribute to these functions.

Bacterial sepsis is a medical emergency. It can be caused by many bacteria, especially staphylococci, pneumococci, meningococci, or Gram-negative enteric bacteria. This is a situation where complement activation and other inflammatory mechanisms have become our enemy. Efforts have been made to find means to curb this overwhelming inflammatory condition. Mollnes and Huber-Lang [[ 9]] provides an update on ongoing attempts to save patients using state-of-the-art complement inhibitors and Toll-like receptor blockers.

Spirochetes constitute a peculiar group of bacteria with different characteristics. Barbosa et al. [[10]] Leptospiral species are a large group that includes both pathogenic and nonpathogenic agents. This allowed us to make meaningful comparisons of the ability to resist killing by complement, for example, in human serum. Not surprisingly, yet