It has been known for many years that the interactions between bacterial pathogens and host epithelial cells can cause the induction of pro-inflammatory cytokines, and lead to changes in the expression of epithelial surface markers. Bacterial infections rely on the bacteria’s ability to evade the host cells recognition and interaction pathways, leading to host signaling and regulation such that the immune response is not activated.
Some bacteria have developed resistance to platelet antimicrobial properties and may now recruit platelets into the infection process. Platelets, without a doubt, play a crucial part in the innate immune system. Some of the worst effects of sepsis and IE may be avoided if bacteria block platelet activation. Furthermore, Salmonella bacteria have evolved a variety of strategies to evade or subvert immunity for their own advantage, and the anatomical site of infection frequently influences both the immune response and the bacterial destiny. Salmonella infection and the accompanying immune response are complex, especially given the systemic character of certain infections, in which various organs are likely to have varied levels of infection immunity.
Conversely, the host cells have dedicated regulation and signaling pathways for coping with intrusions by pathogens. In order to successfully invade of host cells, pathogenic bacteria can use surface macromolecules such as glycans and proteins in order to easily interact with and consequently subvert intracellular signaling machineries in the host, and avoid the triggering of an immune response.
What is not yet well known, are the specific mechanisms of recognition, binding, interaction, and adhesion of pathogenic bacteria, as well as host cellular regulation and signaling during bacterial infections. To interact with hosts, microorganisms synthesize glycans and glycan-binding proteins (known as lectins).
So far, there has been insufficient research into the discovery of adhesion factors implicated in pathogen-host cell interactions in epithelial cells. Furthermore, the information glycan-based pathogenesis and infectious illness symptoms provide is restricted. The majority of research into the pathogenesis of infectious bacteria has focused on the control of pathogenic factor expression after the start of symptoms. To initiate studies on glycan-based pathogenicity, researchers previously reported a methodologic and multi-omics analytical construction using a lectin-glycan interaction (LGI) concept, applied to enterohemorrhagic Escherichia coli. Researchers examine the strategies necessary for the prevention and treatment of infectious diseases, concentrating on the LGIs in the immune response of host glycans against harmful bacteria in the gut, to expand on systemic LGI in infectious diseases.
In hosts, the same machinery has evolved so that bacterial pathogens and hosts reciprocally utilize their own glycans and proteins to invade and protect, respectively.
Studying the initial steps in bacterial infections may help us to understand basic cell biology issues related to cellular interaction and signaling responses to membrane stress by pathogenic bacteria.
The aim of this Research Topic is therefore to explore
(i) emerging evidence for links between effector molecules for the adhesion of pathogenic bacteria to host cells,
(ii) the key role of these effector molecules at the crossroads of several pathways and
(iii) the host cellular regulation in pathogen-induced signaling
It has been known for many years that the interactions between bacterial pathogens and host epithelial cells can cause the induction of pro-inflammatory cytokines, and lead to changes in the expression of epithelial surface markers. Bacterial infections rely on the bacteria’s ability to evade the host cells recognition and interaction pathways, leading to host signaling and regulation such that the immune response is not activated.
Some bacteria have developed resistance to platelet antimicrobial properties and may now recruit platelets into the infection process. Platelets, without a doubt, play a crucial part in the innate immune system. Some of the worst effects of sepsis and IE may be avoided if bacteria block platelet activation. Furthermore, Salmonella bacteria have evolved a variety of strategies to evade or subvert immunity for their own advantage, and the anatomical site of infection frequently influences both the immune response and the bacterial destiny. Salmonella infection and the accompanying immune response are complex, especially given the systemic character of certain infections, in which various organs are likely to have varied levels of infection immunity.
Conversely, the host cells have dedicated regulation and signaling pathways for coping with intrusions by pathogens. In order to successfully invade of host cells, pathogenic bacteria can use surface macromolecules such as glycans and proteins in order to easily interact with and consequently subvert intracellular signaling machineries in the host, and avoid the triggering of an immune response.
What is not yet well known, are the specific mechanisms of recognition, binding, interaction, and adhesion of pathogenic bacteria, as well as host cellular regulation and signaling during bacterial infections. To interact with hosts, microorganisms synthesize glycans and glycan-binding proteins (known as lectins).
So far, there has been insufficient research into the discovery of adhesion factors implicated in pathogen-host cell interactions in epithelial cells. Furthermore, the information glycan-based pathogenesis and infectious illness symptoms provide is restricted. The majority of research into the pathogenesis of infectious bacteria has focused on the control of pathogenic factor expression after the start of symptoms. To initiate studies on glycan-based pathogenicity, researchers previously reported a methodologic and multi-omics analytical construction using a lectin-glycan interaction (LGI) concept, applied to enterohemorrhagic Escherichia coli. Researchers examine the strategies necessary for the prevention and treatment of infectious diseases, concentrating on the LGIs in the immune response of host glycans against harmful bacteria in the gut, to expand on systemic LGI in infectious diseases.
In hosts, the same machinery has evolved so that bacterial pathogens and hosts reciprocally utilize their own glycans and proteins to invade and protect, respectively.
Studying the initial steps in bacterial infections may help us to understand basic cell biology issues related to cellular interaction and signaling responses to membrane stress by pathogenic bacteria.
The aim of this Research Topic is therefore to explore
(i) emerging evidence for links between effector molecules for the adhesion of pathogenic bacteria to host cells,
(ii) the key role of these effector molecules at the crossroads of several pathways and
(iii) the host cellular regulation in pathogen-induced signaling
