Impact of an acceptance facilitating intervention on diabetes patients’ acceptance of Internet-based interventions for depression: A randomized controlled trial

Aims

To (1) determine diabetes patients’ acceptance of Internet-based interventions (IBIs) for depression, to (2) examine the effectiveness of an acceptance facilitating intervention (AFI) and to (3) explore subgroup specific effects.

Methods

141 diabetes patients from two inpatient rehabilitation units and one outpatient clinic in Germany were randomly allocated to an intervention (IG) and a no-intervention control group (CG). The IG received an AFI consisting of a personal information session before filling-out a questionnaire on patients’ acceptance of IBIs, predictors of acceptance (performance expectancy, effort expectancy, social influence, facilitating conditions, and Internet anxiety) as well as sociodemographic, depression-related and diabetes-related variables. The CG filled out the questionnaire immediately. Patients’ acceptance of IBIs was measured with a four-item scale (sum-score ranging from 4 to 20).

Results

The CG showed a low (50.7%) to medium (40.8%) acceptance with only 8.5% of all diabetes patients reporting a high acceptance of IBIs for depression. The AFI had no significant effect on acceptance (IG: M = 10.55, SD = 4.69, n = 70; KG: M = 9.65, SD = 4.27, n = 71; d = 0.20 [95%-CI: −0.13;0.53]) and the predictors of acceptance. Yet, subgroup analyses yielded a trend for depressed, diabetes-related distressed, female and younger (<59) participants and for those who do not frequently use the Internet to profit from the AFI.

Conclusion

Diabetes patients show a rather low acceptance toward IBIs for depression. Findings indicate that the AFI is likely to be effective in the subgroup of depressed, diabetes-related distressed, female or younger diabetes patients, but not in the whole target population. Hence, AFIs might need to be tailored to the specific needs of subpopulations.     

Lymphocyte CC chemokine receptor 9 and epithelial thymus-expressed chemokine (TECK) expression distinguish the small intestinal immune compartment: Epithelial expression of tissue-specific chemokines as an organizing principle in regional immunity

The immune system has evolved specialized cellular and molecular mechanisms for targeting and regulating immune responses at epithelial surfaces. Here we show that small intestinal intraepithelial lymphocytes and lamina propria lymphocytes migrate to thymus-expressed chemokine (TECK). This attraction is mediated by CC chemokine receptor (CCR)9, a chemoattractant receptor expressed at high levels by essentially all CD4(+) and CD8(+) T lymphocytes in the small intestine. Only a small subset of lymphocytes in the colon are CCR9(+), and lymphocytes from other tissues including tonsils, lung, inflamed liver, normal or inflamed skin, inflamed synovium and synovial fluid, breast milk, and seminal fluid are universally CCR9(-). TECK expression is also restricted to the small intestine: immunohistochemistry reveals that intense anti-TECK reactivity characterizes crypt epithelium in the jejunum and ileum, but not in other epithelia of the digestive tract (including stomach and colon), skin, lung, or salivary gland. These results imply a restricted role for lymphocyte CCR9 and its ligand TECK in the small intestine, and provide the first evidence for distinctive mechanisms of lymphocyte recruitment that may permit functional specialization of immune responses in different segments of the gastrointestinal tract. Selective expression of chemokines by differentiated epithelium may represent an important mechanism for targeting and specialization of immune responses.     

Practical preclinical model for assessing the potential for unconjugated hyperbilirubinemia produced by human immunodeficiency virus protease inhibitors

A practical preclinical model for the hyperbilirubinemia produced by human immunodeficiency virus protease inhibitors has been developed. Indinavir and atazanavir produced significant hyperbilirubinemia, whereas amprenavir, the negative control, was indistinguishable from the ritonavir booster dose. This model was used to disqualify an exploratory protease inhibitor from development.     

A skin-selective homing mechanism for human immune surveillance T cells

Effective immune surveillance is essential for maintaining protection and homeostasis of peripheral tissues. However, mechanisms controlling memory T cell migration to peripheral tissues such as the skin are poorly understood. Here, we show that the majority of human T cells in healthy skin express the chemokine receptor CCR8 and respond to its selective ligand I-309/CCL1. These CCR8(+) T cells are absent in small intestine and colon tissue, and are extremely rare in peripheral blood, suggesting healthy skin as their physiological target site. Cutaneous CCR8(+) T cells are preactivated and secrete proinflammatory cytokines such as tumor necrosis factor-alpha and interferon-gamma, but lack markers of cytolytic T cells. Secretion of interleukin (IL)-4, IL-10, and transforming growth factor-beta was low to undetectable, arguing against a strict association of CCR8 expression with either T helper cell 2 or regulatory T cell subsets. Potential precursors of skin surveillance T cells in peripheral blood may correspond to the minor subset of CCR8(+)CD25(-) T cells. Importantly, CCL1 is constitutively expressed at strategic cutaneous locations, including dermal microvessels and epidermal antigen-presenting cells. For the first time, these findings define a chemokine system for homeostatic T cell traffic in normal human skin.