Bacterial infectious diseases are a class of diseases with specific pathogens. Current studies have shown the important application and signal transduction mechanism of exosomes in bacterial infectious diseases, but the studies are still limited. Therefore, the relationship between exosomes and bacterial infectious diseases should be further explored to provide new diagnosis and treatment ideas for clinicians. This paper reviews the mechanism and prospect of exosomes in bacterial infectious diseases caused by different pathogens. It summarizes the biological characteristics of exosomes. The mechanisms of bacterial infectious diseases, the primary pathways through which exosomes regulate various pathogens, and the modification of exosomes for anti-infection.
Humans ; Exosomes/metabolism* ; Signal Transduction ; Bacterial Infections/metabolism* ; Communicable Diseases

The process of macroautophagy (referred to hereafter as autophagy), is generally characterized by the prominent formation of autophagic vesicles in the cytoplasm. In the past decades, studies of autophagy have been vastly expanded. As an essential process to maintain cellular homeostasis and functions, autophagy is responsible for the lysosome-mediated degradation of damaged proteins and organelles, and thus misregulation of autophagy can result in a variety of pathological conditions in human beings. Although our understanding of regulatory pathways that control autophagy is still limited, an increasing number of studies have shed light on the importance of autophagy in a wide range of physiological processes and human diseases. The goal of the reviews in the current issue is to provide a general overview of current knowledge on autophagy. The machinery and regulation of autophagy were outlined with special attention to its role in diabetes, neurodegenerative disorders, infectious diseases and cancer.
Autophagy/*physiology ; Communicable Diseases/metabolism ; Diabetes Mellitus/metabolism ; Humans ; Models, Biological ; Neurodegenerative Diseases/metabolism

Alternative splicing (AS) is an evolutionarily conserved mechanism that removes introns and ligates exons to generate mature messenger RNAs (mRNAs), extremely improving the richness of transcriptome and proteome. Both mammal hosts and pathogens require AS to maintain their life activities, and inherent physiological heterogeneity between mammals and pathogens makes them adopt different ways to perform AS. Mammals and fungi conduct a two-step transesterification reaction by spliceosomes to splice each individual mRNA (named cis -splicing). Parasites also use spliceosomes to splice, but this splicing can occur among different mRNAs (named trans -splicing). Bacteria and viruses directly hijack the host's splicing machinery to accomplish this process. Infection-related changes are reflected in the spliceosome behaviors and the characteristics of various splicing regulators (abundance, modification, distribution, movement speed, and conformation), which further radiate to alterations in the global splicing profiles. Genes with splicing changes are enriched in immune-, growth-, or metabolism-related pathways, highlighting approaches through which hosts crosstalk with pathogens. Based on these infection-specific regulators or AS events, several targeted agents have been developed to fight against pathogens. Here, we summarized recent findings in the field of infection-related splicing, including splicing mechanisms of pathogens and hosts, splicing regulation and aberrant AS events, as well as emerging targeted drugs. We aimed to systemically decode host-pathogen interactions from a perspective of splicing. We further discussed the current strategies of drug development, detection methods, analysis algorithms, and database construction, facilitating the annotation of infection-related splicing and the integration of AS with disease phenotype.
Animals ; Alternative Splicing/genetics* ; RNA Splicing ; Spliceosomes/metabolism* ; RNA, Messenger/metabolism* ; Communicable Diseases/genetics* ; Mammals/metabolism*

Macrophage as a crucial component of innate immunity, plays an important role in inflammation and infection immunity. Notch signal pathway is a highly conserved pathway, which regulates cellular fate and participates in numerous pathological processes. At present, a lot of literature has confirmed the role of Notch signaling in regulating the differentiation, activation and metabolism of macrophage during inflammation and infection. This review focuses on how Notch signaling promotes macrophage pro-inflammatory and anti-infective immune function in different inflammatory and infectious diseases. In this regulation, Notch signaling interact with TLR signaling in macrophages or inflammatory-related cytokines including IL-6, IL-12, and TNF-α. Additionally, the potential application and challenges of Notch signaling as a therapeutic target against inflammation and infectious diseases are also discussed.
Humans ; Signal Transduction ; Macrophages ; Cytokines/metabolism* ; Inflammation/metabolism* ; Communicable Diseases ; Receptors, Notch/metabolism*

Introduction of double-stranded RNA (dsRNA) into some cells or organisms results in degradation of its homologous mRNA, a process called RNA interference (RNAi). The dsRNAs are processed into short interfering RNAs (siRNAs) that subsequently bind to the RNA-induced silencing complex (RISC), causing degradation of target mRNAs. Because of this sequence-specific ability to silence target genes, RNAi has been extensively used to study gene functions and has the potential to control disease pathogens or vectors. With this promise of RNAi to control pathogens and vectors, this paper reviews the current status of RNAi in protozoans, animal parasitic helminths and disease-transmitting vectors, such as insects. Many pathogens and vectors cause severe parasitic diseases in tropical regions and it is difficult to control once the host has been invaded. Intracellularly, RNAi can be highly effective in impeding parasitic development and proliferation within the host. To fully realize its potential as a means to control tropical diseases, appropriate delivery methods for RNAi should be developed, and possible off-target effects should be minimized for specific gene suppression. RNAi can also be utilized to reduce vector competence to interfere with disease transmission, as genes critical for pathogenesis of tropical diseases are knockdowned via RNAi.
Animals ; Communicable Diseases/*genetics/*parasitology ; Helminths/*genetics/metabolism ; Humans ; Insect Vectors/*genetics/metabolism ; Protozoa/*genetics/physiology ; *RNA Interference ; *Tropical Climate

Introduction of double-stranded RNA (dsRNA) into some cells or organisms results in degradation of its homologous mRNA, a process called RNA interference (RNAi). The dsRNAs are processed into short interfering RNAs (siRNAs) that subsequently bind to the RNA-induced silencing complex (RISC), causing degradation of target mRNAs. Because of this sequence-specific ability to silence target genes, RNAi has been extensively used to study gene functions and has the potential to control disease pathogens or vectors. With this promise of RNAi to control pathogens and vectors, this paper reviews the current status of RNAi in protozoans, animal parasitic helminths and disease-transmitting vectors, such as insects. Many pathogens and vectors cause severe parasitic diseases in tropical regions and it is difficult to control once the host has been invaded. Intracellularly, RNAi can be highly effective in impeding parasitic development and proliferation within the host. To fully realize its potential as a means to control tropical diseases, appropriate delivery methods for RNAi should be developed, and possible off-target effects should be minimized for specific gene suppression. RNAi can also be utilized to reduce vector competence to interfere with disease transmission, as genes critical for pathogenesis of tropical diseases are knockdowned via RNAi.
Animals ; Communicable Diseases/*genetics/*parasitology ; Helminths/*genetics/metabolism ; Humans ; Insect Vectors/*genetics/metabolism ; Protozoa/*genetics/physiology ; *RNA Interference ; *Tropical Climate

OBJECTIVETo purify Mannan-binding lectin (MBL) from human serum and detect its binding ability to several kinds of bacteria common in infectious diseases of children.

METHODSMBL was purified from human serum by affinity chromatography on mannan-Sepharose 4B column. Its binding ability to eight species, 97 strains of bacteria was detected by enzyme-linked lectin assay (ELLA).

RESULTSMBL has different binding ability to bacteria and shows strong binding ability to Klebsiella ornithinolytica and Escherichia coli, but shows relatively lower binding ability to Staphylococcus haemolyticus, Enterobacter cloacae and Staphylococcus epidermidis. To different isolates of Klebsiella pneumoniae, Haemophilus influenzae and Staphylococcus aureus, MBL shows quite different binding ability.

CONCLUSIONSMBL has different binding ability to different bacteria, and has relatively stronger binding ability to Gram-negative bacteria. Its binding ability to different isolates of certain kinds of bacteria is quite different.

Bacteria ; classification ; metabolism ; Child ; Child, Preschool ; Communicable Diseases ; microbiology ; Humans ; Mannose-Binding Lectin ; blood ; metabolism ; Protein Binding ; Species Specificity

Vitamin D deficiency is a global health problem that increases risk for metabolic bone diseases in children and adults as well as many chronic illnesses including autoimmune diseases, type 2 diabetes, cardiovascular disease, infectious disease, and cancer. This has raised important questions concerning the physiological and clinical impact of low vitamin D levels during pregnancy, with implications for functions of vitamin D. The review describes the pathways that are required for metabolism and function of vitamin D, the various clinical complications that have been linked to impaired vitamin D status during pregnancy, and effects of vitamin D supplementation on maternal and neonatal outcomes.
Adult ; Autoimmune Diseases ; Bone Diseases, Metabolic ; Cardiovascular Diseases ; Child ; Chronic Disease ; Communicable Diseases ; Diabetes, Gestational ; Female ; Humans ; Metabolism ; Pre-Eclampsia ; Pregnancy* ; Vitamin D Deficiency* ; Vitamin D* ; Vitamins*

Leprosy is an infectious diseases caused by Mycobacterium leprae. It is considered to be manifested in person with an impaired. immune system and is divided into two polar forms; the first being tuberculoid leprosy(TL) with nearly norrnal cell-mediated immunity(CMI) and the second heing lepromatous leprosy(LL) with deficient CMI. Adenosine deaminase(ADA) is an enzyme concerned with intermediary purine metabolism, which is known to be deficient in case of immunological dysfunction. To find out if there is any ADA deficiency in leprosy, the ADA activities in the lymphocytes of leprosy patients were compared with those of normal ones. The ADA activities in lymphocytes of normal subjects, TL patients and. LL patients were as follows; ID. 36-I-l. 90 units/10cells, 6. 35+0. 86units/10'cells and 4. 58+0. 52units/IO'cells respectively. The ADA activities in lymphocytes were revealed to be significantly different between normal subjects and LL patients(p<0. 01) and also between normal subjects and TL patients(p<0. 05). The lowered ADA activities in lymphocytes of leprosy patients, particularly in lepromatous leprosy, suggests a similar role in ADA for immunological response as demonstrated in severe combined immunodeficiency diseases.
Adenosine Deaminase* ; Adenosine* ; Communicable Diseases ; Humans ; Immune System ; Leprosy* ; Leprosy, Lepromatous ; Lymphocytes* ; Metabolism ; Mycobacterium leprae ; Severe Combined Immunodeficiency

As a member of the HSP90 family, heat shock protein (HSP) Gp96 is one of the most abundant proteins in the endoplasmic reticulum (ER), which displayed important molecular chaperones function in cells. Gp96 can stimulate the production of cytokines by activating the antigen presentation cells (such as dendritic cell, et al) in innate immunity. It is capable of eliciting an antigen-specific cytotoxic T lymphocyte (CTL) immune response to eliminate pathogens and tumors by facilitating antigen cross-presentation in adaptive immunity. Gp96 is also an ideal adjuvant in many recent researches. Here, we review the progress that addresses the role of biological characteristics, immunogenic mechanism that may be involved in the induction of anti-infection immune response and antitumor immunity, which may guide the new vaccine strategies with the knowledge of Gp96-antigen complexes.
Adjuvants, Immunologic ; genetics ; metabolism ; Antigen-Presenting Cells ; physiology ; Communicable Diseases ; immunology ; Dendritic Cells ; immunology ; Endoplasmic Reticulum ; immunology ; Humans ; Membrane Glycoproteins ; immunology ; Neoplasms ; immunology ; T-Lymphocytes, Cytotoxic ; immunology