Wound healing is a dynamic and complex process, characterized by the coordinated activities of multiple cell types, each with distinct roles in the stages of hemostasis, inflammation, proliferation, and remodeling. The cells of the immune system not only act as sentinels to monitor the skin and promote homeostasis, but they also play an important role in the process of skin wound repair. Skin-resident and recruited immune cells release cytokines and growth factors that promote the amplification of the inflammatory process. They also work with non-immune cells to remove invading pathogens and debris, as well as guide the regeneration of damaged host tissues. Dysregulation of the immune system at any stage of the process may lead to a prolongation of the inflammatory phase and the development of a pathological condition, such as a chronic wound. The present review aims to summarize the roles of different immune cells, with special emphasis on the different stages of the wound healing process.

Besides their primary role in hemostasis, platelets contain a plethora of immunomodulatory molecules that profoundly affect the entire process of wound repair. Therefore, platelet derivatives, such as platelet-rich plasma or platelet lysate, have been widely employed with promising results in the treatment of chronic wounds. Platelet derivatives provide growth factors, cytokines, and chemokines targeting resident and immigrated cells belonging to the innate and adaptive immune system. The recruitment and activation of neutrophils and macrophages is critical for pathogen clearance in the early phase of wound repair. The inflammatory response begins with the release of cytokines, such as TGF-β, aimed at damping excessive inflammation and promoting the regenerative phase of wound healing. Dysregulation of the immune system during the wound healing process leads to persistent inflammation and delayed healing, which ultimately result in chronic wound. In this review, we summarize the role of the different immune cells involved in wound healing, particularly emphasizing the function of platelet and platelet derivatives in orchestrating the immunological response.

Immigrants show higher adjusted diabetes prevalence than Italians, especially among South-East Asians followed by North and Sub-Saharan Africans. Diabetes progression is influenced by food behaviors, and diet control is a critical aspect in disease management. Food habits have many cultural and symbolic implications. Guidelines recommend that every patient should receive appropriate self-management education according to cultural and socioeconomic characteristics. This study aims to test whether a customized diet and transcultural mediator’s support can improve immigrants’ food habits. A pre-post quali-quantitative study was conducted among 20–79-year-old Bangladeshi and North African diabetic immigrants. The INMP transcultural mediator, an expert in the social and health care field, actively participates in clinical activity by decoding linguistic and cultural needs expressed by the foreigner patient. Five culturally tailored dietary profiles were designed according to international diabetes guidelines and adjusted to traditional food habits. Data were collected with two different semi-structured questionnaires. Changes in food consumption were assessed through McNemar’s test, while paired Wilcoxon Signed-Rank test was used to analyze pre and post intervention. Fifty-five patients were enrolled. At follow-up, cereals, meat, and potatoes intake significantly improved, and the number of adequate dietary habits for each patient increased significantly. Transcultural mediator support was 90% positively evaluated. Adherence to dietary control is favorably influenced by a transcultural intervention, which is based on clinical and socio-cultural criteria, in compliance with patient’s lifestyles.

Whilst the importance of keratinocytes as a first-line defense has been widely investigated, little is known about their interactions with non-resident immune cells. In this study, the impact of human keratinocytes on T cell effector functions was analyzed in an antigen-specific in vitro model of allergic contact dermatitis (ACD) to nickel sulfate. Keratinocytes partially inhibited T cell proliferation and cytokine production. This effect was dependent on the keratinocyte/T cell ratio and was partially reversible by increasing the number of autologous dendritic cells. The inhibition of T cell proliferation by keratinocytes was independent of the T cell subtype and antigen presentation by different professional antigen-presenting cells. Autologous and heterologous keratinocytes showed comparable effects, while the fixation of keratinocytes with paraformaldehyde abrogated the immunosuppressive effect. The separation of keratinocytes and T cells by a transwell chamber, as well as a cell-free keratinocyte supernatant, inhibited T cell effector functions to the same amount as directly co-cultured keratinocytes, thus proving that soluble factor/s account for the observed suppressive effects. In conclusion, keratinocytes critically control the threshold of inflammatory processes in the skin by inhibiting T cell proliferation and cytokine production.

Transient receptor potential ankyrin 1 (TRPA1) channels are expressed on the surface of different cell types, including immune cells. However, TRPA1’s role in the context of innate and adaptive immune responses has not been fully elucidated so far. In this study, we aimed at investigating the expression and function of TRPA1 channels on NK cells. Among NK cells, TRPA1 was highly expressed by the CD56^dimCD16⁺ subpopulation, but not by CD56^brightCD16⁻ cells, as detected by FACS. TRPA1 activation with the potent ligand allyl isothiocyanate (AITC) induces intracellular calcium flux in CD56^dimCD16⁺ cells, which was prevented by the TRPA1 antagonist HC-030031. AITC treatment increased the membrane around NKp44 and strongly decreased CD16 and CD8 expression, while CD158a, CD159a, NKG2d, NKp46 were substantially unaffected. Importantly, AITC increased the granzyme production and CD107 expression and increased NK cell-mediated cytotoxicity towards the K562 cell line and two different melanoma cell lines. In parallel, TRPA1 activation also plays regulatory roles by affecting the survival of NK cells to limit uncontrolled and prolonged NK cell-mediated cytotoxicity. Our results indicate that the activation of TRPA1 is an important regulatory signal for NK cells, and agonists of TRPA1 could be used to strengthen the tumor response of the immune system.

In many contexts, individuals with lower socioeconomic status, especially immigrants, have a higher burden of negative alcohol-related consequences and a higher probability of receiving a psychiatric diagnosis. This study aimed at exploring sociodemographic and clinical characteristics associated with harmful use of alcohol (HUA) among immigrant patients. A cross-sectional study was conducted in Rome (Italy) on a sample of 330 immigrant patients admitted to the gastroenterology outpatient clinic of the INMP (March 2013–October 2014). HUA was evaluated through the Alcohol Use Disorders Identification Test (AUDIT) questionnaire. The presence of psychiatric disorders was diagnosed through SCID I–II interviews. The association between sociodemographic characteristics and psychiatric disorders and HUA was evaluated through a multivariate log-binomial regression model. HUA was associated with unemployment, longer stay in Italy, mood disorder and not being married, especially among African immigrants. We provide original findings about a selected, hard-to-investigate population, suggesting priorities in interventions on HUA among specific vulnerable subgroups.