ABSTRACT
Listeria monocytogenes is a food-borne bacterium that causes listeriosis upon the ingestion of contaminated food. Traditional methods to detect L. monocytogenes require pre-enrichment broths to increase its concentration. To improve the screening of contaminated food and prevent listeriosis outbreaks, rapid, specific and sensitive assays are needed to detect L. monocytogenes. This study developed a prototype lateral flow immunochromatographic assay (LFIA) employing antibodies against L. monocytogenes Internalin A (InlA) and Internalin B (InlB) proteins, that are involved in non-phagocytic cell invasion. The following antibodies were used to capture L. monocytogenes antigenic targets: mouse anti-Internalin A monoclonal antibody (MAb-2D12) conjugated to colloidal gold nanoparticles and a mouse anti-Internalin B polyclonal antibody. This test was able to detect pure L. monocytogenes from culture with a limit of detection (LOD) ranging from 5.9 × 103 to 1.5 × 104 CFU/mL. In milk artificially contaminated with L. monocytogenes, the LOD was 1 × 105 CFU/mL. This prototype test discriminated L. monocytogenes from other bacterial species (Listeria innocua, Enterobacter cloacae, Bacillus cereus). Results indicate that this LFIA developed using antibodies against L. monocytogenes InlA and InlB proteins is a sensitive and specific tool that can be potentially useful to rapidly detect L. monocytogenes in contaminated food. Supplementary Information: The online version contains supplementary material available at 10.1007/s13197-022-05597-9.
ABSTRACT
The triggering receptor expressed on myeloid cells-1 (TREM-1) is an innate immune receptor found in the surface of several immune and non-immune cells. Since its first description in 2000, this molecule and its soluble form (sTREM-1) have been implicated in many diseases with infectious and noninfectious origins. As an amplifier of inflammation, the membrane-associated TREM-1 (mTREM-1) isoform induces the production of pro-inflammatory mediators, thus contributing to the pathogenesis of diseases such as sepsis, arthritis, colitis and infections. In this context, many studies have used molecules capable of inhibiting TREM-1 activity as anti-inflammatory drugs. In this regard, a few peptides have been showing promising results in the amelioration of detrimental immune responses. Some commercially available drugs, including corticosteroids and antibiotics, with known anti-inflammatory effects, have also shown activity in TREM-1 signaling. Therefore, considering the potential of this receptor as a therapeutic target, the present review encompasses the main compounds explored so far in TREM-1 modulation, highlighting and critically discussing its effects and major drawbacks of such approaches.