Presentation Title

The role of Complement Receptor 4 in trogocytic killing of the parasite Trichomonas vaginalis by neutrophil-like cells

Faculty Mentor

Dr. Frances Mercer

Start Date

23-11-2019 10:45 AM

End Date

23-11-2019 11:30 AM

Location

110

Session

poster 4

Type of Presentation

Poster

Subject Area

biological_agricultural_sciences

Abstract

Trichomoniasis is a sexually transmitted infection, caused by Trichomonas vaginalis (Tv), that infects an estimated 3.7 million people in the United States. Roughly 70% of infected people do not show symptoms, and therefore do not seek further treatment. Tv is associated with infertility, spontaneous abortion, cervical cancers, and co-incident STIs, such as HIV. The current preferred treatment against Tv is Metronidazole, a non-specific antibiotic, which does not prevent reinfection and resistance against it is increasing. We recently showed that immune cells called neutrophils attack Tv through a recently discovered process called trogocytosis, in which the neutrophil “nibbles” the Tv until its membrane is breached. Trogocytosis is contact-dependent and is thought to be initiated by soluble proteins called opsonins priming the Tv for trogocytosis. We have shown that iC3b, an abundant opsonin in human serum, coats the surface of the parasite. This indicates the presence of a receptor on the host neutrophils that could bind iC3b. A receptor of interest is complement receptor (CR) 4, which is known to bind iC3b. We have shown that CR4 is present in neutrophil-like cells (NLCs), which we found to be a suitable model for studying the killing of Tv, as primary neutrophils are very short-lived. We hypothesize that the knockdown of CR4 will decrease the trogocytic activity of neutrophil-like cells and therefore enhance Tv survival. We will knockdown CR4 using CRISPR/Cas9, an innovative gene-editing method. The determination of which surface receptors are involved in initiating the trogocytic killing of Tv will better characterize this novel antimicrobial process, which may inform novel Tv therapies.

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Nov 23rd, 10:45 AM Nov 23rd, 11:30 AM

The role of Complement Receptor 4 in trogocytic killing of the parasite Trichomonas vaginalis by neutrophil-like cells

110

Trichomoniasis is a sexually transmitted infection, caused by Trichomonas vaginalis (Tv), that infects an estimated 3.7 million people in the United States. Roughly 70% of infected people do not show symptoms, and therefore do not seek further treatment. Tv is associated with infertility, spontaneous abortion, cervical cancers, and co-incident STIs, such as HIV. The current preferred treatment against Tv is Metronidazole, a non-specific antibiotic, which does not prevent reinfection and resistance against it is increasing. We recently showed that immune cells called neutrophils attack Tv through a recently discovered process called trogocytosis, in which the neutrophil “nibbles” the Tv until its membrane is breached. Trogocytosis is contact-dependent and is thought to be initiated by soluble proteins called opsonins priming the Tv for trogocytosis. We have shown that iC3b, an abundant opsonin in human serum, coats the surface of the parasite. This indicates the presence of a receptor on the host neutrophils that could bind iC3b. A receptor of interest is complement receptor (CR) 4, which is known to bind iC3b. We have shown that CR4 is present in neutrophil-like cells (NLCs), which we found to be a suitable model for studying the killing of Tv, as primary neutrophils are very short-lived. We hypothesize that the knockdown of CR4 will decrease the trogocytic activity of neutrophil-like cells and therefore enhance Tv survival. We will knockdown CR4 using CRISPR/Cas9, an innovative gene-editing method. The determination of which surface receptors are involved in initiating the trogocytic killing of Tv will better characterize this novel antimicrobial process, which may inform novel Tv therapies.