Streptococcus Pneumoniae Antibodies, Proteins & ELISA Kits

Streptococcus pneumoniae (pneumococci) is a gram-positive, facultative anaerobic bacteria. S. pneumoniae are round bacteria that tend to grow in chains, usually in lancet looking pairs called diplococci. There are 100 known serotypes of S. pneumoniae. The majority of serotypes cause disease, however, only a minority produce pneumococcal infections. Pneumococci inhabit the respiratory tract wherein infection occurs.

Colonization of the nasopharynx and oropharynx of healthy individuals leads to S. pneumoniae infection, inhalation of these colonies can cause infection in the lower airways. Although S. pneumoniae infection can occur in all populations, it is more common in patients with predisposed risk factors including; smokers, those who abuse alcohol or have asthma or COPD. In addition, patients over 65 years old or younger than 2 years old are at a higher risk of infection. Transmission of S. pneumoniae can occur via respiratory droplets from person-to-person contact, or autoinoculation from patients carrying S. pneumoniae bacteria in their upper respiratory tract.

S. pneumoniae is the most common pathogen to cause community-acquired pneumonia (CAP) worldwide. CAP is the 7th leading cause of death in the US costing up to $9 billion in hospitalizations each year. Currently, S. pneumoniae accounts for ~ 27% of pneumonia cases worldwide. There are two types of S. pneumoniae vaccine available in the US and Ireland; the pneumococcal conjugate vaccine (PCV13) and the pneumococcal polysaccharide vaccine (PPSV23).

Streptococcus pneumoniae is recognised by pattern recognition receptors (PRRs) which function in the control of host defence pathways. Toll-like receptors (TLRs), NOD-like receptors (NLRs) and RIG-I-like receptors (RLRs) are different classes of PRRs.

A major adhesin of pneumococci is the pneumococcal surface protein C (PspC). PspC interacts with the ectodomain of the human polymeric immunoglobulin receptor (pIgR). This interaction initiates host signal transduction cascades, thus, promoting bacterial colonization and internalization.

A combination of clinical signs and biomarkers have been implemented to assess the risk of pneumonia. High levels of C-reactive protein (CRP) and procalcitonin accompanied by unilateral hyperventilation have been associated with pneumonia. CRP values have been found to be particularly high in patients with S. pneumoniae or L. pneumophila. In addition, CRP values increased significantly with the severity of pneumonia, thus, CRP could be an effective biomarker to predict disease severity.

Another potential biomarker for pneumonia is triggering receptor expressed on myeloid cells-1 (TREM-1). TREM-1 is expressed on the surface of macrophages, neutrophils, and monocytes during acute inflammatory responses. Serum TREM-1 (sTREM-1) levels have been identified in patients with community-acquired pneumonia (CAP).

As previously mentioned, PRRs are responsible for the recognition of invading pathogens, such as S. pneumoniae. Once activated, PRRs function to regulate the production of inflammatory mediators such as IL-1B, IL-6, TNF Alpha, IFN Alpha, IFN Beta and CCL2. This occurs through stimulation of NF-kB and/or IRF3 or IRF7. The production of cytokines within the IL-1 family is controlled by PRRs on a post-translational level through the formation of inflammasomes. In addition to TLRs and NODs, the inflammasome-forming proteins NLRP3 and AIM2 contribute to the recognition of S. pneumoniae.

TLRs engage with adaptor molecules such as MyD88 and TRIF. MyD88 also mediates signaling downstream of IL-1 and IL-18 receptors. TLR2 functions in the recognition of components of the pneumococcal cell wall. In addition, TLR2 works in accordance with NOD2 to contribute to the clearance of pneumococcal colonization. TLR4 is activated by the exotoxin pneumolysin (PLY), a pneumococcal virulence factor. In the endosome, TLR9 detects pneumococcal DNA containing unmethylated CpG motifs.

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Immunometabolism plays a key role in human health and disease. It describes the series of changes that occur within the intracellular metabolic pathways of immune cells during activation.

Streptococcaceae use glycolysis for energy production. During S. pneumoniae infection, GLUT1-dependent glycolysis promotes the exacerbation of lung fibrogenesis via the activation of the AIM2 inflammasome. S. pneumoniae responds to exogenous fatty acids (FAs) by utilizing extracellular FAs for membrane phospholipid synthesis and suppressing its de novo biosynthetic pathway.

Research in mouse models of pneumonia infection indicated that pneumococcal strains lacking arginine biosynthesis genes were attenuated in growth and/or cleared from blood, lung, and cerebrospinal fluid. Thus, signifying the importance of pneumococcal arginine biosynthesis genes for patient outcome.  

Assay Genie provides Glycolysis, Arginase, Fatty Acid Oxidation and Glucose Uptake immunometabolism assay kits that would support Streptococcus Pneumoniae research.

The best studied and most widely used animal models for S. pneumoniae research are mouse, rat and rabbit models. Mouse models of pneumococcal pneumonia allow for the analysis of; levels of inflammation, the presence of bacteria in blood and lungs, and the histology of lung tissue. When compared to the mouse, rat and rabbit models are less commonly used in research. Having said that, their larger size enables researchers to collect more-substantial samples.

A non-human primate model of pneumococcal pneumonia is in high demand to study the underlying molecular mechanisms of severe infection. In addition, an NHP model would enable the identification of diagnostic tools, as well as, the exploration of potential therapeutic targets.

Assay Genie offer a wide range of animal model ELISA kits with the potential to support the advancing field of Streptococcus Pneumoniae research.