About this Research Topic
A majority of infectious diseases, especially systemic viral infections affect mainly infants and children, and a majority of adults have an immunity or tolerability to the infectious pathogens including colonized normal flora. Various clinical manifestations and host cell injury in infectious diseases are associated with host immune reactions to the etiologic substances from the infectious agents, including toxins and pathogen-associated molecular patterns (PAMPs), and/or from the injured host cells by infectious insults, including damage-associated molecular patterns (DAMPs). Although the substances have not yet been identified, advancement in scientific tools will aid in their discovery in the future. Acute or chronic infection-related immune-mediated diseases in childhood, such as Kawasaki disease (KD) or juvenile idiopathic arthritis (JIA) have been reported to be related with various infections, suggesting that the etiology of the diseases may be associated with immune reaction to the substances of host cell-origin including activated immune cells.
There are over hundreds of different types of normal flora or commensal microbials in humans, including bacteria, viruses, and fungi, in the upper respiratory tract (oropharynx), gastrointestinal tract, skin and genitourinary tract of the host. The ecologic system of these microbes (microbiota) is associated with a disordered state of the host, and the disturbance of relationship between microbiota and the host, that is, dysbiosis has been reported in autoimmune diseases such as inflammatory bowel disease and rheumatoid arthritis, obesity, and cancers. Microbiota differs in individuals, ethnic groups, and cultural environments, and can be changed due to environmental factors such as diets, antibiotic use, and possibly adaptation of a pathogen to the host. In an evolutional point of view, initially highly virulent pathogens, such as streptococcal species for scarlet fever and its complications, such as rheumatic fever and acute poststreptococcal glomerulonephritis, may be adapting and changing to normal flora in human species since decreasing cases with milder clinical manifestations have been observed over time. Although normal flora and host have a reciprocally helpful relationship, occasionally, some normal flora can cause infectious diseases or infection-related immune diseases when they invade and induce immune reactions in the host as shown acute pyelonephritis caused by Escherichia coli or postinfectious immune-mediated diseases.
The etiology and immunopathogenesis of KD, JIA, and other infection-related immune-mediated diseases in childhood remain to be solved. The immature immune status of some patients with these diseases may not efficiently control the etiologic substances produced after unknown pathogen infection. The epidemiological and clinical characteristics of a disease aid in presuming etiological agent(s) of the diseases.
This Research Topic welcomes original or review articles related to any aspects on the etiology of infection-related immune-mediated diseases, including KD and JIA, or the relationship between microbiota and these diseases.
There are over hundreds of different types of normal flora or commensal microbials in humans, including bacteria, viruses, and fungi, in the upper respiratory tract (oropharynx), gastrointestinal tract, skin and genitourinary tract of the host. The ecologic system of these microbes (microbiota) is associated with a disordered state of the host, and the disturbance of relationship between microbiota and the host, that is, dysbiosis has been reported in autoimmune diseases such as inflammatory bowel disease and rheumatoid arthritis, obesity, and cancers. Microbiota differs in individuals, ethnic groups, and cultural environments, and can be changed due to environmental factors such as diets, antibiotic use, and possibly adaptation of a pathogen to the host. In an evolutional point of view, initially highly virulent pathogens, such as streptococcal species for scarlet fever and its complications, such as rheumatic fever and acute poststreptococcal glomerulonephritis, may be adapting and changing to normal flora in human species since decreasing cases with milder clinical manifestations have been observed over time. Although normal flora and host have a reciprocally helpful relationship, occasionally, some normal flora can cause infectious diseases or infection-related immune diseases when they invade and induce immune reactions in the host as shown acute pyelonephritis caused by Escherichia coli or postinfectious immune-mediated diseases.
The etiology and immunopathogenesis of KD, JIA, and other infection-related immune-mediated diseases in childhood remain to be solved. The immature immune status of some patients with these diseases may not efficiently control the etiologic substances produced after unknown pathogen infection. The epidemiological and clinical characteristics of a disease aid in presuming etiological agent(s) of the diseases.
This Research Topic welcomes original or review articles related to any aspects on the etiology of infection-related immune-mediated diseases, including KD and JIA, or the relationship between microbiota and these diseases.
Keywords: Infectious diseases, Juvenile idiopathic arthritis, Kawasaki disease, Microbiota, Inflammatory bowel disease, Pathogen-associated molecular pattern, Damage-associated molecular pattern, Pathogenesis
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