Pregnancy Enables Antibody Protection Against Intracellular Infection

Pregnancy Enables Antibody Protection Against Intracellular Infection – Reproductive and respiratory syndrome attenuated live lineage 1 vaccine confers broad cross-protection against homologous and heterologous NADC30-like virus challenge in pigs

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Pregnancy Enables Antibody Protection Against Intracellular Infection

Pregnancy Enables Antibody Protection Against Intracellular Infection

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Human Pregnancy Levels Of Estrogen And Progesterone Contribute To Humoral Immunity By Activating Tfh/b Cell Axis

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Next Generation Of Immune Checkpoint Molecules In Maternal‐fetal Immunity*

Received: March 30, 2022 / Revised: May 8, 2022 / Approved: May 9, 2022 / Issued: May 10, 2022

Many bacterial infections are a major health problem worldwide, and the treatment of many of these infectious diseases is becoming increasingly difficult due to the development of a major threat, antibiotic resistance. A prophylactic vaccine against these bacterial infections is urgently needed. This is especially true for bacterial infections that are still neglected even though they affect a large part of the world’s population in poor sanitary conditions. An example of this is typhoid fever, a life-threatening disease also known as the “plague of war” caused by Rickettsia prowazekii, which may re-emerge in a war situation such as in Ukraine. However, vaccination against bacterial infections is a challenge. In general, bacteria are much more complex organisms than viruses and therefore more difficult targets. Unlike relatively simple viruses, bacteria possess a variety of antigens whose immunogenic potential is often unknown, and it is unclear which antigen could induce a protective and long-lasting immune response. Various vaccines against extracellular bacteria have been developed in the past and are still used successfully today, e.g. vaccine against tetanus, pertussis and diphtheria. Although induction of antibody production is usually sufficient for protection against extracellular bacteria, vaccination against intracellular bacteria is much more difficult because effective protection against these pathogens requires activation of T-cell-mediated responses, particularly cytotoxic CD8.

T cells. These responses are often not efficiently induced by vaccination with non-viable whole-cell antigens or subunit vaccines, so alternative methods of antigen delivery are required. This review provides an overview of current antibacterial vaccines and new approaches to vaccination with an emphasis on vaccination against intracellular bacteria.

Pregnancy Enables Antibody Protection Against Intracellular Infection

Among the most common bacterial pathogens in the western world today are Listeria, Salmonella (S.) enterica ssp., Helicobacter (H.) pylori, Escherichia (E.) coli, Staphylococcus (S.) aureus, Streptococcus (S.) pneumoniae (S .) pneumococci), Neisseria (N.) meningitidis (meningococcus) and Klebsiella (K.) pneumoniae. The causative agents of other bacterial diseases commonly encountered in hospitalization are Acinetobacter (A.) baumanii, Clostridioides (C.) difficile, and Pseudomonas (P.) aeruginosa. Previous infections with Clostridium (C.) tetanus (tetanus), Vibrio (V.) cholerae (cholera), Corynebacterium (C.) diphtheria (diphtheria), Bordetella (B.) pertussis (pertussis), and Salmonella enterica ssp. enterica serovar Typhi (typhoid) was a major health concern even before vaccines were developed against this pathogen.

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Most of these bacteria are free-living pathogens that are found in the environment and can reproduce in the extracellular space. When they enter the body, they are usually taken up and eliminated by macrophages such as macrophages (MØ), neutrophils and dendritic cells (DCs) and degraded in lytic compartments within these cells. However, these bacteria can be dangerous, eg. by releasing harmful toxins or causing severe inflammatory reactions that damage cells and tissues.

Unlike free-living bacterial pathogens, intracellular bacteria have evolved mechanisms to escape the degradation process in target cells in order to reproduce within these cells. The lifestyle of intracellular bacteria requires different immune defense mechanisms, especially the activation of T cells, especially CD8.

T cells. The following paragraphs summarize the knowledge of the lifestyle and immune defense mechanisms of these pathogens, as knowledge of the lifestyle of these bacteria, as well as the protective immune response, is an essential prerequisite for vaccine development.

While intracellular bacteria are found in the extracellular environment as well as within host cells, obligate intracellular bacteria are strictly dependent on host cells for survival and replication. Examples of pathogenic intracellular bacterial pathogens are Mycobacterium (M.) tuberculosis, N. meningitidis, Legionella (L.) pneumophila, Listeria (L.) monocytogenes, Shigella (S.) dysenteriae, Francisella (F.) tularensis, Bordetella (B. ) pertussis and Bacillus (B.) anthracis. In addition, S. aureus can infect host cells, although this mainly occurs extracellularly.

Mechanisms Of Immune Regulation By The Placenta: Role Of Type I Interferon And Interferon‐stimulated Genes Signaling During Pregnancy*

Only a few bacterial pathogens have an obligate intracellular lifestyle and are strictly dependent on host cells for reproduction. Examples of these obligate intracellular bacteria are Chlamydia ssp., Anaplasma ssp., Ehrlichia ssp., Coxiella ssp. and all rickettsia and orientia species. An overview of extracellular, selective, and essential intracellular bacterial pathogens and diseases can be found in Supplementary Table S1 (Table S1), which also provides information on currently available vaccines.

Intracellular bacteria use different strategies to escape phagolysosomal degradation to survive and reproduce in host cells. Depending on the species, bacteria reproduce freely either in the cytoplasm or in special cell compartments. Cytoplasmic replication is observed for L. monocytogenes, S. dysenteriae, B. anthracis, rickettsial species, Burkholderia (B.) pseudomallei and F. tularensis. L. monocytogenes, S. dysenteriae, B. anthracis and rickettsiae escape directly from the phagosomal vacuole [1], while B. pseudomallei and F. tularensis escape from the endosome at later stages. B. pseudomallei is released from late endosomes after fusion of phagosomes with early endosomes [2] while phagosomes containing F. tularensis transform into late endosomes, which become acidic before degradation to release bacteria into the cytoplasm [3]. Besides cellular replication, F. tularensis can also translocate into autolysose-like vesicles [ 2 ]. Other bacteria multiply in special vacuoles. L. pneumophila exits the endocytic pathway at the early endocytosis stage and utilizes vesicles from the endoplasmic reticulum (ER) to form ribosome-coated inclusion pods where bacteria replicate [ 2 ]. C. pneumoniae prevents phagosome fusion with early endosomes and collects vesicles from the Golgi to form compartments for replication [2] , while M. tuberculosis is found in early endosomes and inhibits fusion with lysosomes and acidification of the sac for replication [2] ] ]. In contrast, C. burnetii proliferates in phagolysosome-like acidic vacuoles after fusion of the late endosome with the lysosome [ 2 , 4 ]. Finally, S. enterica ssp. enterica proliferates in endosome-like vesicles that take up available lysosomal proteins but do not fuse with the lysosome, thereby excluding bacteria from degradation. These S. enterica containing vacuoles migrate and bind to the microtubule organizing center (MTOC) formed in the Golgi nucleus [ 2 , 5 ]. Figure 1 provides an overview of extracellular and intracellular bacterial pathogens, as well as immune mechanisms involved in defense and described in the next section.

Defense against extracellular and intracellular bacteria requires different immune systems. Protection against extracellular bacteria is mainly provided by antibodies produced by B cells and CD4.

Pregnancy Enables Antibody Protection Against Intracellular Infection

T helper cells that help B cells produce high-affinity class-switched IgG instead of IgM. Extracellular bacteria are taken up by macrophages such as MØ and DCs, which also serve as antigen-presenting phagocytic cells (APCs). During phagocytosis of the pathogen, macrophages containing bacteria mature by fusing with endosomes and eventually lysosomes. It provides an acidic environment and various enzymes involved in bacterial death and decomposition. In addition, the membrane of the phagolysosomal compartment of APCs contains preformed major histocompatibility complex class II (MHCII) molecules. It is loaded with peptides derived from degraded proteins of the pathogen and transported to the cell surface where CD4 is located.

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T cells can recognize bound peptide antigens through the T cell receptor (TCR). Activated APCs that recognize and encounter bacteria upregulate the expression of costimulatory molecules (CD80/CD86) needed to activate T cells and release cells that allow T cells to differentiate into T cells.

In addition to 17, IL-22, which releases IL-17 and TNFα, produces cytokines that act on non-immune cells. T

17 differentiation also requires the release of IL-23 or the presence of TGFb and IL-6 [10]. Active CD4

T cells also produce IL-2, which acts as a growth and survival factor.

Vitamins, Microelements And The Immune System: Current Standpoint In The Fight Against Coronavirus Disease 2019

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