Case of a Deep Neck Abscess During Treatment for COVID-19.

BACKGROUND COVID-19 is treated using antiviral and immunosuppressive drugs. Therefore, patients treated for COVID-19 may have an increased risk of secondary infection and a masked inflammatory response. We present a case of a deep neck abscess caused by pyogenic sternoclavicular arthritis during treatment for COVID-19. CASE REPORT A 55-year-old man with COVID-19 was admitted to the hospital with hypoxemia. He was then treated with remdesivir, tocilizumab, and dexamethasone and was placed in the prone position. When his condition stabilized, pain in the left shoulder appeared. There was no fever or elevation in inflammation markers, and he was administered analgesics. However, the pain worsened and redness of the left neck appeared. Plain computed tomography (CT) showed swelling of the left neck muscles. Because cellulitis was suspected, he was treated with antibiotics, but his symptoms did not improve. Three days after the plain CT, contrast-enhanced CT showed sternoclavicular arthritis, deep neck abscess, and mediastinal abscess. Therefore, an emergency incisional drainage was performed under general anesthesia. Wound cleaning and drainage were continued after surgery, and after drainage tubes were removed, the patient was discharged on postoperative day 17. CONCLUSIONS Cervical infections after COVID-19 treatment have been reported in a few cases. Particularly, deep neck abscesses require more attention since they could be fatal if not treated immediately. If a secondary infection is suspected in a patient treated with immunosuppressive drugs for COVID-19, a thorough physical examination should be performed to avoid misdiagnosis.

Determination of human γδ T cell-mediated cytotoxicity using a non-radioactive assay system.

The adoptive transfer of immune effector cells, such as CD8+ killer αß T cells, γδ T cells, NK (natural killer) cells, and genetically-modified T cells, has been receiving increasing attention. It is essential to determine cellular cytotoxicity so as to monitor the function and quality of ex vivo-expanded immune effector cells before infusion. The most common method is the [51Cr]-sodium chromate release assay. It is, however, preferable to avoid the use of radioactive materials in clinical laboratories. In order to establish a non-radioactive alternative to the standard radioactive assay, we previously synthesized a chelate-forming prodrug (BM-HT) and demonstrated that a combination of BM-HT and europium (Eu3+) was useful to determine NK cell-mediated cytotoxicity. In the present study, we examined whether or not this improved assay system could be used to determine the cellular cytotoxicity exhibited by Vγ2Vδ2+ γδ T cells. In addition, we compared Eu3+ and terbium (Tb3+) in the measurement of cellular cytotoxicity. Our assay system using BM-HT could be used successfully for the analysis of both γδ T cell receptor (TCR)- and CD16-mediated cytotoxicity. When the intensity of fluorescence was compared between Eu3+ and Tb3+, Tb3+ chelate was more sensitive than Eu3+ chelate, suggesting that the detection system using Tb3+ is superior to Eu3+ when tumor cells are not efficiently labeled with BM-HT. The method established herein is expected to promote the development of novel adoptive cell therapies for cancer.

Effect of IL-18 on the Expansion and Phenotype of Human Natural Killer Cells: Application to Cancer Immunotherapy.

When pathogenic stresses are recognized by innate immune cells, inflammasomes are assembled and caspase-1 is activated, resulting in the conversion of pro-IL-18 into mature IL-18. Because natural killer (NK) cells express IL-18 receptors, IL-18 may play roles in immune functions of NK cells. In the present study, we examined the effect of IL-18 on NK cells derived from lung cancer patients and healthy adult volunteers. When peripheral blood NK cells were stimulated with IL-2, the cells formed clusters beginning on day 5-6 and proliferated thereafter, in which the number of NK cells increased by 10-fold in 10 days. When IL-18 was added, cell clusters were observed as early as on day 4 and NK cells proliferated vigorously. On day 10, the expansion rate was 56-fold on average, showing that IL-18 promoted the expansion of NK cells. It was also notable that IL-18 enhanced the expression of CD80, CD86, HLA-DR and HLA-DQ on NK cells, suggesting that IL-18 conferred NK cells an APC-like phenotype. When cellular cytotoxicity was determined, APC-like NK cells efficiently killed tumor cells and anti-tumor activity was augmented by the addition of tumor antigen-specific mAbs. In addition, IFN-γ was produced by APC-like NK cells in response to tumor cells, and the cytokine production was further enhanced by mAbs. Taken together, IL-18 not only promoted the expansion of NK cells, but also changed the phenotype of NK cells. IL-2/IL-18-induced NK cells might, therefore, serve as a bridge between innate immunity and adaptive immunity and be useful for cancer immunotherapy.