Many Streptococcal pathogens such as Streptococcus pyogenes, Streptococcus agalactiae, and Streptococcus pneumoniae share the perplexing ability to live as relatively harmless human colonizers in some cases, while causing severe and potentially life-threatening illnesses in other cases. When severe disease does occur as a result of Streptococcal infection, it is often marked by the induction of robust inflammatory responses in the infected host cells and surrounding tissues. The timing and type of inflammatory response can vary extensively, depending on factors such as which strain of the pathogen is involved, which types of host cells are affected, and whether the host has certain genetic features or other conditions that make them more susceptible to infection. In many cases, the activation of inflammatory signaling benefits the host by alerting the immune system to the presence of microbial invaders. In other cases, the magnitude or type of inflammatory response activated can harm the host, often by causing extensive tissue damage at the primary infection site, allowing for dissemination, and/or by triggering severe systemic outcomes such as septic shock.
Because of the complexity of the immune response to these microbial infections, it is often unclear whether the observed changes in specific inflammatory mediators will ultimately aid the host in clearing the infection or enhance the pathogenesis of the disease. The magnitude of the change in an inflammatory response induced by a pathogen is also frequently a critical aspect required to determine whether such changes are more beneficial to the host or the pathogen. Studies in cell culture models, animal models, or other experimental systems that are able to link the observed changes in these inflammatory responses to specific stages of microbial pathogenesis, such as uptake into host cells, intracellular survival, immune cell activation or recruitment, tissue destruction, or dissemination to various body sites often provide much-needed insight regarding the harm or benefit that results from these specific signaling changes. Tools such as neutralizing antibodies, small molecule inhibitors, and RNA-targeting mechanisms have been highly instrumental in allowing researchers to understand these relationships. Such connections are a key step toward the development of effective therapeutics that can temper the devastating effects of Streptococcal pathogens.
This Research Topic is dedicated to studies that explore the mechanisms by which Streptococcal pathogens manipulate host inflammatory signaling to colonize the host and/or cause disease. We welcome Original Research articles, Mini-Reviews, and Reviews that explore concepts related to one or more of the following:
(1) Streptococcal manipulation of host inflammatory signaling pathways
(2) Connections between specific inflammatory responses/pathways and key stages of pathogenesis during a particular type of Streptococcal infection
(3) Use of tools such as neutralizing antibodies, small molecule inhibitors, RNA-targeting mechanisms, and other approaches to identify possible therapeutic targets and/or strategies to counteract Streptococcal manipulation of host inflammatory signaling or other key steps of pathogenesis
Many Streptococcal pathogens such as Streptococcus pyogenes, Streptococcus agalactiae, and Streptococcus pneumoniae share the perplexing ability to live as relatively harmless human colonizers in some cases, while causing severe and potentially life-threatening illnesses in other cases. When severe disease does occur as a result of Streptococcal infection, it is often marked by the induction of robust inflammatory responses in the infected host cells and surrounding tissues. The timing and type of inflammatory response can vary extensively, depending on factors such as which strain of the pathogen is involved, which types of host cells are affected, and whether the host has certain genetic features or other conditions that make them more susceptible to infection. In many cases, the activation of inflammatory signaling benefits the host by alerting the immune system to the presence of microbial invaders. In other cases, the magnitude or type of inflammatory response activated can harm the host, often by causing extensive tissue damage at the primary infection site, allowing for dissemination, and/or by triggering severe systemic outcomes such as septic shock.
Because of the complexity of the immune response to these microbial infections, it is often unclear whether the observed changes in specific inflammatory mediators will ultimately aid the host in clearing the infection or enhance the pathogenesis of the disease. The magnitude of the change in an inflammatory response induced by a pathogen is also frequently a critical aspect required to determine whether such changes are more beneficial to the host or the pathogen. Studies in cell culture models, animal models, or other experimental systems that are able to link the observed changes in these inflammatory responses to specific stages of microbial pathogenesis, such as uptake into host cells, intracellular survival, immune cell activation or recruitment, tissue destruction, or dissemination to various body sites often provide much-needed insight regarding the harm or benefit that results from these specific signaling changes. Tools such as neutralizing antibodies, small molecule inhibitors, and RNA-targeting mechanisms have been highly instrumental in allowing researchers to understand these relationships. Such connections are a key step toward the development of effective therapeutics that can temper the devastating effects of Streptococcal pathogens.
This Research Topic is dedicated to studies that explore the mechanisms by which Streptococcal pathogens manipulate host inflammatory signaling to colonize the host and/or cause disease. We welcome Original Research articles, Mini-Reviews, and Reviews that explore concepts related to one or more of the following:
(1) Streptococcal manipulation of host inflammatory signaling pathways
(2) Connections between specific inflammatory responses/pathways and key stages of pathogenesis during a particular type of Streptococcal infection
(3) Use of tools such as neutralizing antibodies, small molecule inhibitors, RNA-targeting mechanisms, and other approaches to identify possible therapeutic targets and/or strategies to counteract Streptococcal manipulation of host inflammatory signaling or other key steps of pathogenesis
