Despite the high prevalence of depression and post-traumatic stress disorder among first-generation Vietnamese Americans, their underutilization of mental health services continues to persist. The question of how culturally sensitive mental health services can be delivered to engage this population effectively in treatment has been a key issue for disparities research for the past several decades. Ample literature has identified individual, sociocultural and structural factors that influence mental health service use among this population, but very few studies have explored the perceptions of the clients themselves about mental illness or their pathways to care.

Twenty-one individual, inductive, and qualitative one-on-one interviews were conducted to address three aims: 1) to explore the conceptualizations of health among first-generation Vietnamese Americans living with depression and/or PTSD, 2) to illustrate the pathways through which this population obtained outpatient mental health services, and 3) to describe their expectations and perceptions of outpatient mental health treatment. Constructivist grounded theory (GT) guided all aspects of this study.

The participants were mostly female and ranged in age from 42 to 74 years. Two major themes, "bounded within these four walls" and finding one's way to "a place where I am respected," emerged as overarching processes through which the participants described their experiences. Their rich stories portrayed journeys through losing, finding and reclaiming their self worth -- journeys marked with losses, sacrifices, disruptions, stigma, resilience, coming to terms with their conditions, and managing their illnesses. These men and women remained optimistic on the road to reclaiming their sense of self worth, despite being crippled by their legacies of war, trauma, and migration to the United States. Their stories offer a culturally nuanced understanding of how participants explained their emotional discomforts, how they found their various ways to agencies that could help ease these discomforts, and the unexpected resources and relationships they gained from outpatient mental health care. This study's findings provide strong implications for social work research, practice, and policy that can help empower these individuals to find purpose and hope in their lives.

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Plasmacytoid dendritic cells (PDCs) are critical for defense against respiratory viruses because of their propensity to secrete high levels of type I interferons (IFN). The functions of PDCs in the lung can be influenced by airway epithelial cells. We examined the effect of human primary bronchial epithelial cells (PBECs) on PDC functions by performing RNA-sequencing of PDCs after co-culture with air liquid interface differentiated PBECs. Functional analysis revealed that PDCs co-cultured with PBECs displayed upregulation of type I IFN production and response genes. Upregulated transcripts included those encoding cytosolic sensors of DNA, ZBP-1,IRF-3, and NFkB as well as genes involved in amplification of the IFN response, such as IFNAR1, JAK/STAT, ISG15. In keeping with the RNA-seq data, we observe increased secretion of type I IFN and other cytokines in response to influenza in PDCs co-cultured with PBECs. The PDCs also primed Th1 responses in T cells. The enhanced response of PDCs co-cultured with PBECs was due to the action of growth factors, GMCSF, GCSF, and VEGF, which were secreted by PBECs on differentiation. These data highlight possible mechanisms to enhance the production of type-I IFN in the airways, which is critical for host defense against respiratory infections.

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Smoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the IL-22 pathway that protects lung function by increasing transepithelial resistance and epithelial cell regeneration and repair. Our results indicate that exposure to nicotine impairs the regenerative capacity of primary bronchial epithelial cells in scratch assays. IL-22 at 100 ng/ml significantly improved wound healing in epithelial cells; however, the exposure to nicotine hampered the IL-22-mediated effect of wound healing. Investigation into the mechanisms showed that IL-22 receptor, IL-22Rα1, was downregulated in the presence of nicotine as determined by q-PCR and flow cytometry. We also investigated the effect of nicotine on IL-22 production by T cells. Results indicate that nicotine inhibited the secretion of IL-22 from T cells in response to aryl hydrocarbon receptor (AHR) ligand, FICZ. Altogether, the data suggests that nicotine negatively influences the IL-22-IL-22R axis. This impairment may contribute to the nicotine-mediated detrimental effects on lung function.

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