Salmonella Enteritidis Outer Membrane Protein-A Recombinant
Salmonella Typhi H Antigen Recombinant
Salmonella Typhi Haemolysin E Recombinant
Salmonella Typhi Outer Membrane Protein Recombinant
Salmonella Typhi Outer Membrane Protein 52kDa Recombinant
Salmonella Typhi (S. Typhi) is a Gram-negative bacterium that causes typhoid fever, a life-threatening illness. It belongs to the species Salmonella enterica subspecies enterica and is classified under the serovar Typhi . S. Typhi is highly adapted to humans and does not have a known animal reservoir .
Key Biological Properties: S. Typhi is a rod-shaped, flagellated bacterium that is capable of surviving in harsh environments. It forms biofilms, which contribute to its persistence and resistance to antibiotics .
Expression Patterns and Tissue Distribution: S. Typhi primarily infects the intestinal tract but can spread to the liver, spleen, bone marrow, and gallbladder . It is known for its ability to evade the host’s immune system and establish a systemic infection .
Primary Biological Functions: S. Typhi’s primary function is to infect and replicate within human hosts. It achieves this by invading intestinal epithelial cells and spreading through the bloodstream to other organs .
Role in Immune Responses and Pathogen Recognition: S. Typhi has evolved mechanisms to evade the host’s immune responses. It secretes a toxin that disrupts immune cell function, allowing the bacteria to spread and cause disease .
Mechanisms with Other Molecules and Cells: S. Typhi uses a type III secretion system (T3SS) to inject effector proteins into host cells, manipulating host cell processes to facilitate infection .
Binding Partners and Downstream Signaling Cascades: The bacterium’s toxin binds to specific sugars on the surface of immune cells, allowing it to enter and disable these cells . This interaction disrupts the host’s innate immune response and limits the development of adaptive immunity .
Regulatory Mechanisms Controlling Expression and Activity: S. Typhi tightly regulates the expression of its virulence factors to avoid detection by the host’s immune system . The regulatory protein TviA plays a crucial role in repressing the expression of the T3SS, preventing the activation of inflammatory responses .
Transcriptional Regulation and Post-Translational Modifications: The expression of virulence genes in S. Typhi is controlled at the transcriptional level by regulatory proteins like TviA . Post-translational modifications of these proteins further fine-tune their activity to ensure successful infection .
Biomedical Research: S. Typhi is used as a model organism to study host-pathogen interactions and the mechanisms of bacterial infection .
Diagnostic Tools: Serological tests, such as the Widal test, are used to detect antibodies against S. Typhi in patients . However, these tests have limitations and are often supplemented with molecular diagnostic techniques .
Therapeutic Strategies: Phage therapy is being explored as an alternative to antibiotics for treating S. Typhi infections, especially in the face of rising antibiotic resistance .
Role Throughout the Life Cycle: S. Typhi’s life cycle involves transmission through contaminated food or water, infection of the human host, and shedding of bacteria in feces . During infection, the bacteria can persist in the gallbladder, leading to chronic carriage and potential transmission to others .
S. Typhi’s ability to form biofilms and evade the immune system allows it to persist in the host and contribute to the spread of typhoid fever .