Systematic Review of the Impact on Return to Work of Return-to-Work Coordinators.

Purpose We conducted a systematic review to understand the impact that return-to-work coordinators (RTWCs) have on return to work (RTW) outcomes for sick/injured workers. Methods MEDLINE, EMBASE, CINAHL, PsycINFO, Web of Science, and ABI Inform were searched from January 1, 2000 to September 16, 2020. Of 2,927 retrieved and screened citations, 14 quantitative articles fulfilled the eligibility and quality criteria. Quality assessment, data extraction, and evidence synthesis followed article screening. Results We focused on the impact of RTWCs for outcomes of work absence, RTW rates, quality of life, and cost-benefit. Our final synthesis included 14 articles. We found strong evidence that work absence duration was reduced when workers had face-to-face contact with a RTWC. As well, there was strong evidence linking face-to-face RTWC interventions with higher RTW rates and moderate evidence that this reduced intervention costs. RTWC interventions involving the identification of barriers and facilitators to RTW also showed promising results. However, only limited evidence was found that RTWCs improved quality of life for workers. Conclusions Our synthesis identifies key features of RTW interventions that improve RTW outcomes. Future high-quality research should measure long-term outcomes of RTWC interventions to evaluate sustainability and consider the nature of work. They should also focus on RTWC impact on worker quality of life assessments and for older workers and workers with chronic health conditions.

Manipulation of intestinal immune responses against ovalbumin by cholera toxin and its B subunit in mice.

We studied the effect of mucosal presentation of ovalbumin (OVA) conjugated to cholera toxin (CT) or cholera toxin B subunit (CTB) on the intestinal immune responses against OVA. Mice were primed intraperitoneally (i.p.) with OVA in a water-in-oil emulsion and boosted intraduodenally (i.d.) with OVA conjugated to CT or CTB in various molar ratios. Responses were evaluated by testing intestinal secretions for OVA-specific antibodies and by quantifying the OVA-specific antibody secreting cells (ASC) in the lamina propria of the small intestine. OVA-CT conjugates were tested in a molar ratio ranging from 1.8:1 to 4500:1. OVA-CTB conjugates were tested in a molar ratio ranging from 0.25:1 to 500:1. The optimum intestinal immune response was reached at a molar ratio of 1.8:1 for OVA-CT and 5:1 for OVA-CTB. The binding capacity of OVA-CTB, but not of OVA-CT, to GM1 ganglioside corresponded with the capacity to enhance the intestinal immune response. The effect of conjugating CTB or CT to OVA on the immune response against OVA was more striking when mice were not only boosted i.d., but also primed i.d. Both OVA-CT and OVA-CTB induced detectable immune responses, whereas free OVA did not. Therefore, the carrier effect of CT or CTB is essential to trigger a mucosal immune response against OVA when presented mucosally only. We conclude that enhancing antigen uptake greatly facilitates mucosal immune responses.

Quantification of antigen-specific antibody-secreting cells in the small intestine and other lymphoid organs of mice after oral booster immunization.

The intestinal immune response of mice against ovalbumin (OVA) was quantified by isolating lymphoid cells from the small intestine (SI) and testing them for antigen-specific immunoglobulin (Ig) secretion. The isolation procedure for functionally active lymphoid cells from the SI, originally developed to quantify the number of 'background' Ig-secreting cells in the SI, proved to be a useful method for evaluating antigen-specific intestinal immune responses quantitatively. The method was able to detect antigen-specific antibody-secreting cells (ASC) in the SI even when these cells occurred at a minimum frequency of only 0.006%. When mice were primed intraperitoneally (i.p.) with polymerized OVA and given an oral OVA booster immunization, OVA-specific ASC appeared in the SI from Day 3 after booster. After i.p. priming and an i.p. booster these cells could not be detected in the SI. The OVA-specific IgA-ASC responses in various organs after oral booster immunization were compared. From Day 5 after booster, when the response peaked, most OVA-specific IgA-ASC occurred in the SI. This suggested that these cells are mainly responsible for the OVA-specific antibodies demonstrated by ELISA in intestinal secretions from Day 6 after oral booster immunization. It is concluded that the quantitative method used in this study detects antigen-specific ASC in the SI with great sensitivity and could be used to evaluate immunization regimes aimed at inducing intestinal mucosal immune responses.