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We examined the antibacterial action of several tannins on plasma coagulation by Staphylococcus aureus and the effect of conventional chemotherapy combined with tannic acid below the MIC. Coagulation was inhibited in plasma containing tannic acid (100 mg/L), gallic acid (5000 mg/L), ellagic acid (5000 mg/L), (–)-epicatechin (1500 mg/L), (–)-epicatechin gallate (500 mg/L) or (–)-epigallocatechin gallate (200 mg/L) after incubation for 24 h. All tannins inhibited coagulation at a concentration below the MIC. The MICs of oxacillin and cefdinir for S. aureus were reduced to ≤ 0.06 mg/L in Mueller–Hinton agar plates with tannic acid (100 mg/L) at a concentration below the MIC. The antistaphylococcal activity of tannic acid was reduced in plates with 10% rabbit blood, but not in those with 10% rabbit plasma. Membranous structures formed in a culture medium containing equal proportions of plasma and tryptic soy broth after incubation for 24 h. The colony counts of S. aureus in membranous structures in the medium containing oxacillin (40 mg/L) and tannic acid (100 mg/L) were c. 10-fold lower than those in medium containing oxacillin (40 mg/L) alone (P < 0.01). Tannic acid merits further investigation as a possible adjuvant agent against S. aureus skin infections treated with β-lactam antibiotics. [ABSTRACT FROM PUBLISHER]

The present study examined the effects of antimicrobial agents on a biofilm model of Staphylococcus aureus. A membranous structure (an immature biofilm) was formed on the coverslips of tissue culture dishes by S. aureus cells in plasma after incubation for 24 h. After incubation, the colony counts of S. aureus cells in the immature biofilms in plasma containing levofloxacin with 70% sucrose were about one-tenth of those in plasma containing levofloxacin without sucrose. The colony counts of S. aureus cells in the immature biofilms in plasma containing silver sulphadiazine or silver nitrate (at a silver concentration of 0.302%) were over 3000 times lower than those in control plasma without silver after incubation for 24 h. Plasma coagulation by S. aureus cells was not detected in plasma containing 70% sucrose 48 h after inoculation. The immature biofilms were incubated in plasma with and without 70% sucrose, and the immature biofilms were treated with 10% povidone-iodine for 2 min after incubation for 4 and 16 h. In this experiment, the colony counts of S. aureus cells in the immature biofilms incubated with 70% sucrose were about one-tenth of those in plasma without sucrose after incubation for 24 h. We suggest that levofloxacin or 10% povidone-iodine in combination with 70% sucrose and silver sulphadiazine or silver nitrate (at a silver concentration of 0.302%) are effective in eliminating S. aureus cells in a biofilm. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor focusing on tendon destruction induced by Panton-Valentine leukocidin-positive staphylococcus aureus.

Immune checkpoint inhibitors (ICIs) are effective against many advanced malignancies. However, many patients are nonresponders to immunotherapy, and overcoming this resistance to treatment is important. Boron neutron capture therapy (BNCT) is a local chemoradiation therapy with the combination of boron drugs that accumulate selectively in cancer and the neutron irradiation of the cancer site. Here, we report the first boron neutron immunotherapy (B-NIT), combining BNCT and ICI immunotherapy, which was performed on a radioresistant and immunotherapy-resistant advanced-stage B16F10 melanoma mouse model. The BNCT group showed localized tumor suppression, but the anti-PD-1 antibody immunotherapy group did not show tumor suppression. Only the B-NIT group showed strong tumor growth inhibition at both BNCT-treated and shielded distant sites. Intratumoral CD8+ T-cell infiltration and serum high mobility group box 1 (HMGB1) levels were higher in the B-NIT group. Analysis of CD8 + T cells in tumor-infiltrating lymphocytes (TILs) showed that CD62L- CD44 + effector memory T cells and CD69 + early-activated T cells were predominantly increased in the B-NIT group. Administration of CD8-depleting mAb to the B-NIT group completely suppressed the augmented therapeutic effects. This indicated that B-NIT has a potent immune-induced abscopal effect, directly destroying tumors with BNCT, inducing antigen-spreading effects, and protecting normal tissue. B-NIT, immunotherapy combined with BNCT, is the first treatment to overcome immunotherapy resistance in malignant melanoma. In the future, as its therapeutic efficacy is demonstrated not only in melanoma but also in other immunotherapy-resistant malignancies, B-NIT can become a new treatment candidate for advanced-stage cancers., (© 2024 The Author(s). Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.)

T-cell exhaustion is a major contributor to immunosuppression in the tumor microenvironment (TME). Blockade of key regulators of T-cell exhaustion, such as programmed death 1, can reinvigorate tumor-specific T cells and activate antitumor immunity in various types of cancer. In this study, we identified that CD106 was specifically expressed in exhausted CD8+ T cells in the TME using single-cell RNA sequencing. High CD106 expression in the TME in clinical samples corresponded to improved response to cancer immunotherapy. CD106 in tumor-specific T cells suppressed antitumor immunity both in vitro and in vivo, and loss of CD106 in CD8+ T cells suppressed tumor growth and improved response to programmed death 1 blockade. Mechanistically, CD106 inhibited T-cell receptor (TCR) signaling by interacting with the TCR/CD3 complex and reducing its surface expression. Together, these findings provide insights into the immunosuppressive role of CD106 expressed in tumor-specific exhausted CD8+ T cells, identifying it as a potential biomarker and therapeutic target for cancer immunotherapy. Significance: CD106 is specifically expressed in tumor-specific exhausted CD8+ T cells and inhibits the TCR signaling pathway by reducing surface expression of the TCR/CD3 complex to suppress antitumor immunity., (©2024 American Association for Cancer Research.)