Women become depressed more frequently than men, a consistent pattern across cultures. Inflammation plays a key role in initiating depression among a subset of individuals, and depression also has inflammatory consequences. Notably, women experience higher levels of inflammation and greater autoimmune disease risk compared to men. In the current review, we explore the bidirectional relationship between inflammation and depression and describe how this link may be particularly relevant for women. Compared to men, women may be more vulnerable to inflammation-induced mood and behavior changes. For example, transient elevations in inflammation prompt greater feelings of loneliness and social disconnection for women than for men, which can contribute to the onset of depression. Women also appear to be disproportionately affected by several factors that elevate inflammation, including prior depression, somatic symptomatology, interpersonal stressors, childhood adversity, obesity, and physical inactivity. Relationship distress and obesity, both of which elevate depression risk, are also more strongly tied to inflammation for women than for men. Taken together, these findings suggest that women’s susceptibility to inflammation and its mood effects may contribute to sex differences in depression. Depression continues to be a leading cause of disability worldwide, with women experiencing greater risk than men. Due to the depression-inflammation connection, these patterns may promote additional health risks for women. Considering the impact of inflammation on women’s mental health may foster a better understanding of sex differences in depression, as well as the selection of effective depression treatments.

Food-borne Salmonella spp., are a major cause of hospitalization and death. Adenosine, an important immune regulator of inflammation, limits tissue damage during infection. CD39 (nucleoside triphosphate dephosphorylase) combined with ecto-5′-nucleotidase (CD73) metabolizes ATP to adenosine. We studied the expressions of CD39 and CD73 in tissues, and T helper cells in mice after Salmonella infection and evaluated the role of CD73 in regulating immune responses and bacterial clearance in wild-type and CD73-deficient (CD73−/−) mice. Both CD39 and CD73 transcript levels declined in the infected wild-type mice. Compared to wild-type mice, tissues from infected CD73−/− mice had significantly higher expression of pro-inflammatory cytokines and reduced anti-inflammatory responses. CD73−/− mice were more resistant to infection and had a greater inflammatory responses and a significantly lower bacterial load in the liver compared to wild-type mice. Thus, CD73 expression attenuates inflammation during murine Salmonellosis and impairs immunity, leading to increased bacterial colonization and prolonged infection.

Abstract. Background: Law enforcement officers (LEOs) are responsible for maintaining public order and safety within communities. As a consequence of this obligation, LEOs are repeatedly exposed to a myriad of unavoidable occupational stressors, known to affect health behaviors and well-being. Importantly, LEO well-being has public safety implications as those reporting higher well-being exhibit more equitable police behavior relative to those reporting lower well-being. Aims: The present study aimed to identify factors that may be leveraged to enhance LEO well-being by investigating the indirect relation of health behaviors to well-being through psychological flexibility. Method: Path-analytic regression models were used to analyze cross-sectional data provided by LEOs recruited from three geographically dispersed police agencies ( N = 459; Male = 84.7%, White = 64.2%). Results: Results indicated psychological flexibility accounted for the relations of chronic pain and quality sleep to well-being. Regular exercise accounted for the largest proportion of well-being variance, though the indirect effect through psychological flexibility was not significant. Limitations: Inclusion of more comprehensive measures of well-being and health behaviors may further clarify the strength of relations reported herein. Conclusion: Enhancing flexible response styles may support high well-being in LEO populations who report poor sleep quality and chronic pain.

Foodborne Listeria monocytogenes (LM) causes serious illness & death every year in the US. Ingestion of LM can lead to septicemia, meningitis, & abortion. IL17 is secreted by T cells and regulates the production of CXC chemokines for monocyte and neutrophil recruitment to infected tissue. Foodborne LM infection occurs through the oral route, but mice are highly resistant to oral infection. Here, using a murinized LM strain, we explored the role of IL17RA signaling following oral LM infection. Mortality & body weight loss were compared after LM infection of C57BL/6 & IL17RA-KO mice. LM-specific proliferative responses of splenocytes isolated from infected mice were performed. Viable LM from liver & spleen tissue were enumerated. Neutrophil infiltration & inflammation were evaluated histologically. RT-PCR arrays were used to quantitate cytokine/chemokine mRNA expression in infected tissues. IL17RA-KO mice lost more body weight and died earlier following oral infection than infected WT mice. LM-Ag treated splenocytes from KO mice proliferated less vigorously than WT splenocytes. Tissues from infected IL17RA-KO mice had lower mRNA expression for IFN-γ, IL1-β & iNOS. Liver, spleen & gastric tissues from infected IL17RAKO mice showed increased necrotic tissue damage & increased LM burden. These results indicate that IL17RA signaling is important in host resistance to oral LM infection.

Salmonella spp. is responsible for the vast majority of foodborne illnesses in the US. Adenosine is an antiinflammatory mediator that limits tissue damage during inflammation. Surface enzymes CD39 & CD73 mediate the synthesis of extracellular adenosine & can regulate immune responses. We studied the expression of CD39 & CD73 in liver & spleen after infection of C57BL/6 mice with Salmonella enterica serotype Typhimurium (ST) & evaluated the role of CD73 after oral infection of wildtype & CD73-KO mice, in regulating immune responses & bacterial persistence. Liver & spleen cytokine mRNA expression was tested by RT-PCR. Cytokines were assayed by ELISA from cultured supernatant of activated splenocytes. Splenocyte-derived Th cells were tested for intracellular cytokines by FACS. Inflammatory responses in infected CD73-/- mouse livers were tested in H&E sections. Bacterial count was done from liver tissues. After ST infection of wildtype mice, both CD39 & CD73 transcript levels declined in spleen & liver. Splenocytes from ST-infected CD73-/- mice produced significantly more IFN-γ & IL17a. Infected CD73-/- mice had higher expressions of IFN-γ & TNF-α mRNA in liver. Histological examinations of liver sections showed significantly greater number of “inflammatory-foci”. Liver bacterial load was significantly lower in CD73-/-mice. CD73 expression contributes to adenosine accumulation that attenuates inflammation during Salmonellosis & may impair immunity to favor bacterial persistence.

Salmonella spp. is a leading cause of hospitalization & death in the US associated with foodborne illness. Salmonella causes acute gut inflammation. Adenosine is an antiinflammatory mediator that limits tissue damage during inflammation. Surface enzymes CD39 & CD73 mediate the synthesis of adenosine. We studied the expression of CD39 & CD73 in liver, spleen, & CD4+ Th cells after infection of C57BL/6 mice with Salmonella enterica serotype Typhimurium (ST) & evaluated the role of CD73 in regulating ST-induced inflammation. Proinflammatory cytokine mRNA expression was assayed by RT-PCR arrays & cytokine proteins were tested by FACS & ELISA after ST infection or ST antigen (Ag) treatment. Function of CD73 was tested by examining proinflammatory cytokine production with or without CD73-inhibitor treatment of activated splenocytes exposed to ST Ag. Inflammatory responses to ST infection in CD73-/- mice were evaluated in liver & spleen tissue in H&E sections & in activated CD4+ Th cells stained for intracellular IL17a & IFN-γ. ST Ag-treated & CD73-inhibited splenocytes produced more proinflammatory cytokines (IL17A). Splenocytes from ST-infected CD73-/- mice produced more IL17a cytokine & Th17 cells & infected CD73-/- mice also had greater infiltration of inflammatory cells in the liver. Extracellular adenosine synthesized by CD73 may regulate host inflammation during murine Salmonellosis.