Clinical impact of vitamin D treatment in cystic fibrosis: a pilot randomized, controlled trial

BACKGROUND/OBJECTIVES: Vitamin D insufficiency in cystic fibrosis is common. Vitamin D3 is currently preferred over D2. We aimed to study the efficacy of vitamin D2 and D3 at increasing serum 25-hydroxyvitamin D (s25OHD) concentrations and their effect on respiratory health in cystic fibrosis. SUBJECTS/METHODS: Sixteen CF patients were randomized to receive vitamin D2 or D3 or to serve as controls. The starting dose of 5000 IU (< 16 years old) or 7143 IU/day (>= 16 years old) was further individually adjusted. Three months of intervention were followed by two of washout (ClinicalTrials. gov NCT01321905). RESULTS: To increase s25OHD, the mean daily dose of vitamin D2 and D3 had to be increased up to 15650 and 8184 IU, respectively. The combined group of vitamin D2 and D3 treated patients decreased plasma IL-8 (P < 0.05). Patients provided vitamin D3 improved FVC at the end of the trial (P < 0.05). Change in s25OHD was positively correlated with changes in the adult Quality-of-Life respiratory score at the end of supplementation (P = 0.006, r = 0.90), and with changes in FEV1 (P = 0.042, r = 0.62) and FVC (P = 0.036, r = 0.63) at one month of washout. CONCLUSIONS: Vitamin D supplementation may contribute to reduced inflammation and improved lung function in CF

Bacteroides are associated with GALT iNKT cell function and reduction of microbial translocation in HIV-1 infection.

Invariant natural killer T (iNKT) cells are innate-like T cells that respond to lipid antigens presented by CD1d. These immunoregulatory cells have the capacity for rapid cytokine release after antigen recognition and are essential for the activation of multiple arms of the immune response. HIV-1 infection is associated with iNKT cell depletion in the peripheral blood; however, their role in the gastrointestinal-associated lymphoid tissue (GALT) is less well studied. Our results show that iNKT cells are found at a higher frequency in GALT compared to blood, particularly in HIV-1 elite controllers. The capacity of iNKT cells to produce IL-4 and IL-10 in the GALT was associated with less immune activation and lower markers of microbial translocation, while Treg frequency showed positive associations with immune activation. We hypothesized that the composition of the microbiota would influence iNKT cell frequency and function. We found positive associations between the abundance of several Bacteroides species and iNKT cell frequency and their capacity to produce IL-4 in the GALT but not in the blood. Overall, our results are consistent with the hypothesis that GALT iNKT cells, influenced by certain bacterial species, may play a key role in regulating immune activation in HIV-1 infection

IFITM1 targets HIV-1 latently infected cells for antibody-dependent cytolysis.

HIV-1 persistence in latent reservoirs during antiretroviral therapy (ART) is the main obstacle to virus eradication. To date, there is no marker that adequately identifies latently infected CD4(+) T cells in vivo. Using a well-established ex vivo model, we generated latently infected CD4(+) T cells and identified interferon-induced transmembrane protein 1 (IFITM1), a transmembrane antiviral factor, as being overexpressed in latently infected cells. By targeting IFITM1, we showed the efficient and specific killing of a latently infected cell line and CD4(+) T cells from ART-suppressed patients through antibody-dependent cytolysis. We hypothesize that IFITM1 could mark natural reservoirs, identifying an immune target for killing of latently infected cells. These novel insights could be explored to develop clinical therapeutic approaches to effectively eradicate HIV-1

Dynamic MAIT cell response with progressively enhanced innateness during acute HIV-1 infection

10.1038/s41467-019-13975-9Nature Communications11127

Longitudinal Analysis of Peripheral and Colonic CD161+ CD4+ T Cell Dysfunction in Acute HIV-1 Infection and Effects of Early Treatment Initiation

10.3390/v12121426Viruses121

MicroRNAs 145 and 148a Are Upregulated During Congenital Zika Virus Infection.

Submitted by Fábio Marques ([email protected]) on 2019-07-04T13:28:28Z No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5)Approved for entry into archive by Regina Costa ([email protected]) on 2019-07-04T16:40:10Z (GMT) No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5)Made available in DSpace on 2019-07-04T16:40:10Z (GMT). No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5) Previous issue date: 2019Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Department of Microbiology, Immunology & Tropical Medicine, The George Washington University, Washington, DC, USA.Faculdade de Ciências Médicas de Campina Grande, Núcleo de Genética Médica, Centro Universitário UniFacisa, Campina Grande, Brasil.Instituto de Pesquisa Professor Amorim Neto, Campina Grande, Brasil.Serviço de Neurologia, Hospital Vera Cruz, Belo Horizonte, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Laboratório de Neuropatologia, Instituto Estadual do Cérebro, Rio de Janeiro, Brasil.Faculdade de Ciências Médicas de Campina Grande, Núcleo de Genética Médica, Centro Universitário UniFacisa, Campina Grande, Brasil./ Instituto de Pesquisa Professor Amorim Neto, Campina Grande, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Laboratório de Pesquisa Clínica em DST/AIDS. Rio de Janeiro, RJ, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil./ Departamento de Biologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brasil