Human Intestinal Microvascular Endothelial Cells (HIMEC)

FA Treatment Restores Cell Viability and Inhibits TNF-α-Induced Cell Inflammation

Ulcerative colitis (UC) is a chronic inflammatory bowel disorder. Ferulic acid (FA), a traditional Chinese herb known for its antioxidant, anti-apoptotic, and anti-inflammatory properties, has an unclear role in UC. Yu et al. aimed to investigate FA's effects on UC.

In vivo, UC was induced in rats using 2,4,6-tribrobenzene sulfonic acid, followed by FA treatment. FA improved intestinal injury and reduced levels of inflammatory factors (IL-6, IL-12, IL-1β), apoptosis-related proteins (caspase-1, caspase-3), and the TXNIP/NLRP3 pathway in UC rats. To examine FA's effects on cell viability and inflammation, intestinal endothelial cells (HIMECs) were pretreated with various FA concentrations and TNF-α to induce damage. In control and solvent groups, cells grew normally, while TNF-α-treated cells showed reduced proliferation. FA treatment enhanced proliferation in a concentration-dependent manner (Fig. 1a). MTT assays indicated FA restored cell viability in TNF-α-treated HIMECs (Fig. 1b). ELISA results showed TNF-α increased IL-1β, IL-6, and IL-12, which FA subsequently reduced (Fig. 1c-e). These findings suggest FA improves cell viability and reduces TNF-α-induced inflammation.

Fig. 1. FA treatment restores the viability of HIMECs and inhibits TNF-α-induced cell inflammation (Yu S, Qian H, et al., 2022).

Plasmodium falciparum Parasite Lines Expressing DC8 and Group A PfEMP1 Bind to Brain, Intestinal, and Kidney Endothelial Cells

Cytoadhesion of Plasmodium falciparum-infected red blood cells cause microvascular blockages and organ issues. While the gastrointestinal tract acts as a primary sequestration site in fatal cerebral malaria, kidney complications are also seen in severe cases; however, detailed interactions at these sites are not well understood. Ortolan et al. studied parasite preferences for primary human microvascular endothelial cells from intestine (HIMEC) and kidney (HKMEC).

They examined CD36, ICAM-1, and EPCR expression on CD31⁺ human endothelial cells to determine parasite affinity for brain, gut, and kidney microvascular sites. Autopsies suggest higher parasite accumulation in peritubular capillaries versus glomerular ones. They compared endothelial cells from brain (HBMEC), intestine (HIMEC), and kidney (HKMEC) using flow cytometry, both under resting conditions and after TNF-α stimulation (Fig. 2). CD36 had low expression on HBMEC and HIMEC and was negligible on HKMEC, regardless of TNF-α stimulation (Fig. 3). EPCR was broadly expressed across HBMEC and HIMEC, slightly decreasing with TNF-α (Fig. 3). ICAM-1 showed low initial levels on cells but increased to nearly 100% after TNF-α treatment on all cell types (Fig. 3). HKMECs exhibited distinct receptor levels, likely due to their VEGF-enriched culture medium, which enhances ICAM-1 expression. Despite differences, intestinal and brain endothelial cells had similar receptor profiles.

Fig. 2. Representative flow cytometry gate strategies used for analyzing primary endothelial cell populations (Ortolan L S, Avril M, et al., 2022).

Fig. 3. Surface expression of CD36, EPCR, and ICAM-1 on primary human brain, intestinal and kidney endothelial cells (Ortolan L S, Avril M, et al., 2022).