PROJECT SUMMARY/ABSTRACT The number of immigrant families in the U.S. has rapidly increased across the last five years, with particular growth among Latinos from Central America (USCBP, 2016). Among Latino immigrant youth, posttraumatic stress symptoms (PSS) are a major public health concern—with our own pilot data showing that 60% of immigrant children and adolescents experience clinically significant PSS (Venta & Mercado, 2018), in contrast to less than 15% in non-immigrant groups (Foa et al., 2011). Our data indicate that the mean level of PSS is 161% - 204% higher in immigrant youth than prior estimates in non-immigrants (Venta & Mercado, 2018). Empirical and meta-analytic findings support an inflammatory hypothesis of PSS: elevations in systemic inflammatory biomarkers following trauma increase risk for persistent, impairing PSS (Gill et al., 2009). Conversely, close relationships—like those between parents and their children—have been repeatedly associated with reduced systemic inflammation (Fagundes et al., 2011). While the level of trauma exposure that immigrant children experience prior to migration represents a static risk factor for PSS, inflammatory response, in contrast, represents a dynamic risk factor that may be mitigated through close relationships, reducing likelihood of persistent PSS after migration. The broad aim of this proposal is to examine the physiological (i.e., increased inflammatory response) and relational (i.e., parent-child relationship as a buffer) bases of persistent PSS, a condition that is dramatically overrepresented in Latino immigrants. The study proposes to recruit N = 100 Latino recent immigrant families for new longitudinal research spanning twelve months. Methods assess multiple levels of analysis: an experimental task of caregiver mentalizing, a semi- structured interview of caregiver-child attachment security, self- and caregiver-reports of PSS, and a two-time point salivary test of inflammatory response. Specific Aim 1 is to test an inflammation-based hypothesis of PSS. Trauma exposure, inflammatory response (measured via saliva collected before and after a stress induction), and PSS will be assessed at baseline; PSS will be assessed again at six- and twelve-month follow- up. It is expected that trauma exposure will be associated with greater inflammation response at baseline, which, in turn, will be associated with persistent PSS. Specific Aim 2 is to examine the potential protective effects of the parent-child relationship in the inflammation-based hypothesis of PSS. Parent-child relationship factors (i.e., caregiver mentalizing and caregiver-child attachment) will be assessed at baseline and examined as moderators of the risk hypothesis posited in Aim 1. In sum, novel data collected in this study will test a physiological mechanism underlying a significant health disparity—that Latino immigrant youth are disproportionately affected by PSS— as well as test the protective role of putative intervention targets (i.e., parent-child relationships) in ameliorating risk for persistent PSS. The proposed study will enhance research opportunities for graduate and undergraduate students via paid, hands-on roles in high-impact research.

PROJECT NARRATIVE Latino immigrant children are disproportionately affected by posttraumatic stress symptoms, therefore there is a critical public health need to understand risk and protective factors related to the persistence of these symptoms in the post-migration U.S. context. The proposed study will test both a physiological mechanism underlying this disparity—increased inflammatory response—and the protective effects of parent-child relationship factors in mitigating risk for persistent posttraumatic stress symptoms post-migration; the sample is drawn from a population that is disproportionately affected by posttraumatic stress and rapidly growing in the U.S. and Texas (data collection site), recently immigrated Latino families. This study will provide novel data on a critical need in minority mental health, posttraumatic stress symptoms, by linking this outcome to a disease mechanism at the physiological level and to protective factors representing putative intervention targets for future research.