Reduced Visceral Fat Weight and Body Weight Due to Ingestion of Fermented Collagen Peptide in High-Fat Diet-Fed Obese Mice.

Oral ingestion of collagen hydrolysate has various benecial effects. We developed a novel fermented collagen peptide (FCP), different from the conventional collagen peptides, by fermenting gelatin with Aspergillus sojae. This study aimed to investigate the effect of FCP in inhibiting fat accumulation under high-fat loading.

Sensitivity to a CD4 mimic of a consensus clone of monkey-adapted CCR5-tropic SHIV-MK38C.

By acclimatizing CCR5-tropic tier 1B SHIV-MK1 to rhesus monkeys, a tier 2 SHIV-MK38 strain with neutralization resistance and high replication ability was generated. In this study, we generated SHIV-MK38C, a monkey-infectious consensus molecular clone of SHIV-MK38. Analysis using pseudotype viruses showed that MK38C was tier 1C because it lacked the N169D mutation, which is the most important mutation for neutralization resistance.

Effect of Reducing Pigmentation by Collagen Peptide Intake: A Randomized, Double-Blind, Placebo-Controlled Study.

Introduction: We examined the effect of 5.0 g/day of collagen peptide (CP) or collagen peptide fermented with Aspergillus sojae (FCP) on skin pigmentation in healthy participants.

Methods: In this randomized, double-blind, placebo-controlled study, 44 men and women aged 25-63 years were placed into three groups by stratified random allocation and treated with CP, FCP, or placebo (PL) at 5.

Hybrids of Small-Molecule CD4 Mimics with Polyethylene Glycol Units as HIV Entry Inhibitors.

CD4 mimics are small molecules that inhibit the interaction of gp120 with CD4. We have developed several CD4 mimics. Herein, hybrid molecules consisting of CD4 mimics with a long alkyl chain or a PEG unit attached through a self-cleavable linker were synthesized.

Modulation of autoimmune pathogenesis by T cell-triggered inflammatory cell death.

T cell-mediated autoimmunity encompasses diverse immunopathological outcomes; however, the mechanisms underlying this diversity are largely unknown. Dysfunction of the tripartite linear ubiquitin chain assembly complex (LUBAC) is associated with distinct autonomous immune-related diseases. Cpdm mice lacking Sharpin, an accessory subunit of LUBAC, have innate immune cell-predominant dermatitis triggered by death of LUBAC-compromised keratinocytes.

Induction of neutralizing antibodies against tier 2 human immunodeficiency virus 1 in rhesus macaques infected with tier 1B simian/human immunodeficiency virus.

We previously developed CCR5-tropic neutralization-resistant simian/human immunodeficiency virus (SHIV) strains and a rhesus macaque model of infection with these SHIVs. We induced the production of neutralizing antibodies (nAbs) against HIV-1 by infecting rhesus macaques with different neutralization-resistant SHIV strains. First, SHIV-MK1 (MK1) (neutralization susceptible, tier 1B) with CCR5 tropism was generated from SHIV-KS661 using CXCR4 as the main co-receptor.

Evaluation of the immune response and protective effects of rhesus macaques vaccinated with biodegradable nanoparticles carrying gp120 of human immunodeficiency virus.

We previously reported that biodegradable amphiphilic poly(gamma-glutamic acid) nanoparticles (NPs) carrying the recombinant gp120 env protein of the human immunodeficiency virus type 1 (HIV-1) were efficiently taken up by dendritic cells, and induced strong CD8(+) T cell responses against the gp120 in mice. To evaluate gp120-carrying NPs (gp120-NPs) as a vaccine candidate for HIV-1 infection, we vaccinated rhesus macaques with these gp120-NPs and examined the immune response and protective efficacy against a challenge inoculation of simian and human immunodeficiency chimeric virus (SHIV). We found that gp120-NP vaccination induced stronger responses for both gp120-specific cellular and humoral immunity than gp120-alone vaccination.

Small intestine CD4+ cell reduction and enteropathy in simian/human immunodeficiency virus KS661-infected rhesus macaques in the presence of low viral load.

Human immunodeficiency virus type 1, simian immunodeficiency virus and simian/human immunodeficiency virus (SHIV) infection generally lead to death of the host accompanied by high viraemia and profound CD4(+) T-cell depletion. SHIV clone KS661-infected rhesus macaques with a high viral load set point (HVL) ultimately experience diarrhoea and wasting at 6-12 months after infection. In contrast, infected macaques with a low viral load set point (LVL) usually live asymptomatically throughout the observation period, and are therefore referred to as asymptomatic LVL (Asym LVL) macaques.

Small intestine CD4+ T cells are profoundly depleted during acute simian-human immunodeficiency virus infection, regardless of viral pathogenicity.

To analyze the relationship between acute virus-induced injury and the subsequent disease phenotype, we compared the virus replication and CD4(+) T-cell profiles for monkeys infected with isogenic highly pathogenic (KS661) and moderately pathogenic (#64) simian-human immunodeficiency viruses (SHIVs). Intrarectal infusion of SHIV-KS661 resulted in rapid, systemic, and massive virus replication, while SHIV-#64 replicated more slowly and reached lower titers. Whereas KS661 systemically depleted CD4(+) T cells, #64 caused significant CD4(+) T-cell depletion only in the small intestine.

A genetically engineered live-attenuated simian-human immunodeficiency virus that co-expresses the RANTES gene improves the magnitude of cellular immunity in rhesus macaques.

Regulated-on-activation-normal-T-cell-expressed-and-secreted (RANTES), a CC-chemokine, enhances antigen-specific T helper (Th) type-1 responses against HIV-1. To evaluate the adjuvant effects of RANTES against HIV vaccine candidate in SHIV-macaque models, we genetically engineered a live-attenuated SHIV to express the RANTES gene (SHIV-RANTES) and characterized the virus's properties in vivo. After the vaccination, the plasma viral loads were same in the SHIV-RANTES-inoculated monkeys and the parental nef-deleted SHIV (SHIV-NI)-inoculated monkeys.