2009/04/23 by Claudia Dumrese, Lutz Slomianka, Urs Ziegler +8 · 1 citation
Chemistry · Immunology and Microbiology · Medicine · #Biochemistry #Biology #Cell biology #Chemistry #Clostridium difficile and Clostridium perfringens research #Cysteine #Fusion protein #Galectins and Cancer Biology #Gene #Genetics #Helicobacter pylori #Helicobacter pylori-related gastroenterology studies #Immune system #Immunology #In vitro #Integrin alpha M #Macrophage #Microbiology #Phagocytosis #Phenotype
paper · doi:10.1016/j.febslet.2009.04.027
openalex publication_date 2009/04/23 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Helicobacter pylori genomes typically contain 8 or 9 genes that code for secreted and highly disulfide-bridged proteins designated Helicobacter cysteine-rich proteins (Hcp). Here we show that HcpA (hp0211) but not HcpC (hp1098) triggers the differentiation of human myeloid Thp1 monocytes into macrophages. Small amounts of HcpA cause the transition of round-shaped monocytes into cells with star-like morphologies, adherence to the culture dish surface, phagocytosis of opsonized fluorescent microspheres, and expression of the surface marker protein CD11b, all of which are indicative of a macrophage-like phenotype. We conclude that HcpA acts as a bacterial immune modulator similar to a eukaryotic cytokine.