About this Research Topic
Streptococcus pneumoniae, a Gram-positive extracellular bacterium belonging to the mitis group, colonizes the human nasopharynx and is a leading cause of community-acquired pneumonia, meningitis, and bacteremia worldwide. Although approximately 20-40% of children carry this organism in their nasopharynx without clinical symptoms, S. pneumoniae is estimated to be responsible for the deaths of approximately 1,190,000 people annually from lower respiratory infection. In addition, antibiotic selective pressure has caused resistant pneumococcal clones to emerge and expand throughout the world, leading the World Health Organization to list S. pneumoniae as one of 12 priority antibiotic-resistant pathogens.
Prevention data from active bacterial core surveillance from 2009 to 2013 presented by the Centers for Disease Control indicate that pneumococcal conjugate vaccines are useful for preventing antibiotic resistance. While these vaccines target major serotypes, they cover a limited number of serotypes and thus generate selective pressure, with non-vaccine serotypes of S. pneumoniae increasing worldwide as a result. To establish novel effective infection control strategies, it is important to elucidate the detailed process of pneumococcal infection.
As the first step of pneumococcal infection, the bacterium colonizes the host mucosal surface of nasopharynx. Infection models using cultured human epithelial and/or endothelial cells have indicated various pneumococcal cell surface factors that contribute to colonization via molecular interactions with the extracellular matrix. During the process of infection, S. pneumoniae evades the host immune system and then replicates after colonization. During the early phase of infection, the innate immune system attempts to clear pathogens from tissues, with host immune factors such as pattern-recognition receptors detecting pathogenic bacteria and initiating inflammation. In cases of pneumococcal infection, non-conventional T-cells such as invariant NKT cells play an important role in host defense in addition to professional phagocytes. On the other hand, S. pneumoniae causes host cell death by the pore-forming toxin, pneumolysin, while pneumococcal cell surface proteins inhibit neutrophil phagocytosis and activity by the complement system. Although appropriate immune responses contribute to pneumococcal clearance, excessive inflammation can lead to serious tissue damage. An investigation of host regulation of immune responses against S. pneumoniae would contribute to better understanding of the infection process and host damage control.
This Research Topic encourages the collection of Original Research articles and Reviews on host-pathogen interactions regarding pneumococcal infection with a broad scope, including such topics as virulence factors, host immune responses, transmission, and superinfection, as well as others. Studies with cutting-edge techniques or unique approaches from a different perspective are welcome. We consider that this Research Topic will broaden our perspective related to the interaction of hosts and pathogens
Prevention data from active bacterial core surveillance from 2009 to 2013 presented by the Centers for Disease Control indicate that pneumococcal conjugate vaccines are useful for preventing antibiotic resistance. While these vaccines target major serotypes, they cover a limited number of serotypes and thus generate selective pressure, with non-vaccine serotypes of S. pneumoniae increasing worldwide as a result. To establish novel effective infection control strategies, it is important to elucidate the detailed process of pneumococcal infection.
As the first step of pneumococcal infection, the bacterium colonizes the host mucosal surface of nasopharynx. Infection models using cultured human epithelial and/or endothelial cells have indicated various pneumococcal cell surface factors that contribute to colonization via molecular interactions with the extracellular matrix. During the process of infection, S. pneumoniae evades the host immune system and then replicates after colonization. During the early phase of infection, the innate immune system attempts to clear pathogens from tissues, with host immune factors such as pattern-recognition receptors detecting pathogenic bacteria and initiating inflammation. In cases of pneumococcal infection, non-conventional T-cells such as invariant NKT cells play an important role in host defense in addition to professional phagocytes. On the other hand, S. pneumoniae causes host cell death by the pore-forming toxin, pneumolysin, while pneumococcal cell surface proteins inhibit neutrophil phagocytosis and activity by the complement system. Although appropriate immune responses contribute to pneumococcal clearance, excessive inflammation can lead to serious tissue damage. An investigation of host regulation of immune responses against S. pneumoniae would contribute to better understanding of the infection process and host damage control.
This Research Topic encourages the collection of Original Research articles and Reviews on host-pathogen interactions regarding pneumococcal infection with a broad scope, including such topics as virulence factors, host immune responses, transmission, and superinfection, as well as others. Studies with cutting-edge techniques or unique approaches from a different perspective are welcome. We consider that this Research Topic will broaden our perspective related to the interaction of hosts and pathogens
Keywords: Streptococcus pneumoniae, Host immunity, Virulence factor, Inflammation, Recognition mechanism
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