Depressive symptoms in youth are influenced by psychosocial stressors and cognitive vulnerabilities. Perceived everyday discrimination (PED) is a common stressor linked to mental health issues, while dysfunctional attitudes (DAs), per Beck's cognitive theory of depression, may mediate these effects. Additionally, depressive symptoms have been associated with physical health outcomes, such as inflammation. We examined relationships between PED, DAs, depressive symptoms, and interleukin-6 (IL-6), a marker of inflammation, in a sample of 98 youth (13-16 years old; 36.4% female, 63.6% male) from diverse racial/ethnic backgrounds (41.4% Black/African American, 34.8% White/European American, 7.1% Multiracial, 2% Hispanic, 1% Native American, 1% Other). Measures included the Everyday Discrimination Scale, Dysfunctional Attitudes Scale, Center for Epidemiological Studies Depression Scale, and saliva samples. Our regression analyses demonstrated that PED was significantly associated with both DAs and depressive symptoms as well as that DAs were significantly associated with depressive symptoms and IL-6, while neither PED nor depressive symptoms were significantly associated with IL-6. Consistent with the regressions, our mediation analyses revealed no significant indirect effects of PED on IL-6 through DAs, depressive symptoms, or their sequential combination. Our findings support the role of PED as a stressor within Beck's cognitive theory and expand the theory's application by linking DAs to inflammatory processes. Given these connections, nurses can play a crucial role in implementing cognitive interventions to mitigate the effects of DAs and advocating for systemic change to reduce discrimination.

Purpose:Colorectal cancer (CRC) is the third most common type of cancer worldwide. The link between inflammation and CRC is well established. Elevated levels of C-reactive protein (CRP) upon diagnosis is a known negative prognostic factor for CRC patients. Monomeric CRP (mCRP) has been demonstrated in tissues of several diseases associated with inflammation, including colon cancer (CC). mCRP possesses proinflammatory properties and is a possible mediator of tumor-promoting inflammation. This study aimed to detect and quantify circulating mCRP and assess potential correlations with clinical CRP and intra-tumoral mCRP in CC patients. Patients and Methods:Forty patients treated for stage II-III CC between 2012 and 2015 at Sorlandet Hospital, Norway, were included in the study. Twenty patients had CRP level <10 mg/l and 20 patients had CRP ≥10 mg/l, measured routinely at diagnosis (clinical CRP). EDTA plasma was used for mCRP detection by enzyme-linked immunosorbent assay (ELISA; n = 40) and mass spectrometry (MS; n = 20) (MS data are available via ProteomeXchange with identifier PXD046746). Tumor mCRP abundance was classified into three categories by reference scoring, using an antigen-retrieval technique on formalin-fixed paraffin-embedded tissue samples (n = 29). Results:Circulating mCRP levels were detectable by both ELISA and MS. Median mCRP level measured by ELISA was 2.55 ng/mL, while the MS analysis detected 19.02 ng/mL. Both analyses exhibited significant correlations with clinical CRP (ELISA, p = 0.012; MS, p < 0.001). Intra-tumoral mCRP correlated with circulating mCRP measured by MS (p < 0.001) and with clinical CRP (p < 0.001). Conclusion:To the authors' knowledge, this is the first report of mCRP in the circulation of cancer patients. By employing two different analytical methods, mCRP was reliably detected in CC patients. Patients with elevated circulating mCRP measured by MS had higher intra-tumoral mCRP abundance. The interesting correlation of circulating and intra-tumoral mCRP levels may represent another facet of the interplay between local and systemic inflammation in CC patients.

This study is based on the hopelessness theory of depression and previous research on perceived everyday discrimination (PED) and both depressive symptoms and Interleukin-6 (an inflammatory cytokine; IL-6) in adolescents. The purpose of this study is to examine the negative attribution, self, and consequence cognitive styles (CSs) proposed in the hopelessness theory as a possible mechanism underlying the association between PED and inflammation in adolescents and expand our understanding of the comorbidities between depressive symptoms and systemic inflammation (IL-6). This cross-sectional study featured a sample of 102 adolescents aged 13-16 (M = 14.10, SD = 0.52) who identified as White (47.5%), Black (41.4%), Mixed Race (7.1%), Latino (2%), and other (2%). Data analysis was conducted using PROCESS to compute regressions and effects between PED, negative CSs, depressive symptoms, and Interleukin-6. Results showed that negative attribution CS is the only negative CS associated with PED, depressive symptoms, and IL-6. Negative attribution CS is also the only negative CS of the three negative CSs that mediates both the association between PED and depressive symptoms and PED and IL-6 in our adolescent sample. Overall, these results indicate that individual negative CSs proposed in the hopelessness theory impact adolescents' physical and mental outcomes differently, which can inform targeted treatments. Nurses should provide cognitive-based interventions and promote societal-level change to reduce the experience and impact of PED on the mental and physical health of their adolescent patients.

PURPOSEAlthough the intestinal subtype of gastric cancer (GC) is most prevalent around the world, a relatively high prevalence of the diffuse subtype has been reported in some populations of Central American countries, including Guatemala. This study aimed to investigate whether differences exist in the prevalence of the two GC subtypes in the two main ethnic groups in Guatemala, namely Mayan and Mestizo (known as Ladino in Guatemala), between whom significant socioeconomic disparities exist, and to determine whether there is an association with Helicobacter pylori/CagA seropositivity.MATERIALS AND METHODSParticipants included 65 patients with GC and 135 age-/sex-matched controls. Data on ethnicity, H. pylori and CagA seropositivity status, as well as tumor subtype (diffuse or intestinal) were collected. Logistic regression models were fitted to examine the relationship between predictor variables (age, sex, ethnicity, H. pylori, and CagA) and the binary response variable (tumor type). Model selection was based on the Akaike information criterion.RESULTSThe prevalence of diffuse GC was found to be significantly higher in the Mayan compared with the Mestizo population in Guatemala. Although seropositivity for CagA was significantly higher in patients with GC, there were no significant differences between the two GC subtypes.CONCLUSIONThis study suggests that there are differences in the prevalence of intestinal and diffuse GC histologic subtypes between the two main ethnic groups in Guatemala. Further studies are warranted, given the potential higher prevalence of the more severe GC subtype in the most vulnerable population.

Streptococcus pneumoniae remains a primary pathogen in hospitalized patients with community-acquired pneumonia (CAP). The objective of this study was to define the epidemiology of pneumococcal pneumonia in Louisville, Kentucky, and to estimate the burden of pneumococcal pneumonia in the United States (US). This study was nested in a prospective population-based cohort study of all adult residents in Louisville, Kentucky, who were hospitalized with CAP from 1 June 2014 to 31 May 2016. In hospitalized patients with CAP, urinary antigen detection of 24 S. pneumoniae serotypes (UAD-24) was performed. The annual population-based pneumococcal pneumonia incidence was calculated. The distribution of S. pneumoniae serotypes was characterized. Ecological associations between pneumococcal pneumonia and income level, race, and age were defined. Mortality was evaluated during hospitalization and at 30 days, 6 months, and 1 year after hospitalization. Among the 5402 CAP patients with a UAD-24 test performed, 708 (13%) patients had pneumococcal pneumonia. The annual cumulative incidence was 93 pneumococcal pneumonia hospitalizations per 100,000 adults (95% CI = 91–95), corresponding to an estimated 226,696 annual pneumococcal pneumonia hospitalizations in the US. The most frequent serotypes were 19A (12%), 3 (11%), and 22F (11%). Clusters of cases were found in areas with low incomes and a higher proportion of Black or African American population. Pneumococcal pneumonia mortality was 3.7% during hospitalization, 8.2% at 30 days, 17.6% at 6 months, and 25.4% at 1 year after hospitalization. The burden of pneumococcal pneumonia in the US remains significant, with an estimate of more than 225,000 adults hospitalized annually, and approximately 1 out of 4 hospitalized adult patients dies within 1 year after hospitalization.

e15641 Background: Tumor-promoting inflammation is an established hallmark of cancer. C-reactive protein (CRP) is one of the most studied negative prognostic markers of the systemic inflammatory response (SIR) and known to be implicated in detrimental immune responses. Circulating CRP, as measured in routine practice, is a pentameric structure (pCRP). However, when pCRP binds to activated membranes, the protein dissociates into subunits termed monomeric CRP (mCRP). Pro-inflammatory characteristics of mCRP have been reported to be stronger than for pCRP. While a role for mCRP in cancer has been proposed, the circulating level of mCRP has never been investigated in cancer patients. Our aim was to detect and quantify plasma mCRP of patients diagnosed with stage II-III colon cancer (CC) and investigate possible correlations with other inflammatory markers. Methods: 40 patients treated for stage II-III CC between 2012 and 2015 at Sorlandet Hospital, Norway, were included in the study. 20 patients had pCRP level < 10 mg/L and 20 patients had pCRP > 10 mg/L, the latter interpreted as presence of SIR. Levels of pCRP and albumin were captured at the time of diagnosis. Pre-operative mCRP and the cytokines IL-6, IL-8 and TNFa were all measured using EDTA plasma samples. Pre-operative mCRP levels were measured by a specific ELISA employing reagents kindly provided by Drs. L. Potempa and I. Rajab (Roosevelt University, Schaumburg, IL). Results: Of the 40 patients, 47.5% were female, 57.5% had right-sided primary tumor and 50.0% were stage III. Median values (min-max) were for mCRP 2.55 ng/mL (0.00-10.9), pCRP 9.95 mg/L (0.50-136), IL-6 5.10 pg/mL (2.60-25.1), IL-8 4.95 pg/mL (0.40-32.4), TNFa 5.90 pg/mL (3.10-29.5) and albumin 40 g/L (29.0-46.0). Conclusions: To the authors’ knowledge, this is the first time mCRP has been reported in systemic circulation of cancer patients. Our study shows plasma mCRP to be quantifiable in CC patients, albeit at very low levels. This may be due to its reduced aqueous solubility and supports the notion of mCRP as a circulating particle-bound or tissue-associated isoform. However, despite low circulating mCRP levels and a small number of patients, mCRP still correlated with other well-known SIR markers with proven negative prognostic value in cancer patients, supporting its potential role as a pro-inflammatory player in CC. Further studies correlating SIR with circulating and tissue-bound mCRP are currently being performed. [Table: see text]

Our study is guided by Beck’s cognitive stress-vulnerability model of depression. We examined the associations between perceived everyday discrimination (PED) and TNF-⍺, an inflammatory biomarker associated with risk for severe illness, through the negative cognitive triad (NCT; negative thoughts about the self, world, and future) and depressive symptoms in adolescents. We utilized a sample of 99 adolescents (36.4

The differing roles of the pentameric (p) and monomeric (m) C-reactive protein (CRP) isoforms in viral diseases are not fully understood, which was apparent during the COVID-19 pandemic regarding the clinical course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Herein, we investigated the predictive value of the pCRP and mCRP isoforms for COVID-19 severity in hospitalized patients and evaluated how the levels of the protein isoforms changed over time during and after acute illness. This study utilized samples from a well-characterized cohort of Swedish patients with SARS-CoV-2 infection, the majority of whom had known risk factors for severe COVID-19 and required hospitalization. The levels of pCRP were significantly raised in patients with severe COVID-19 and in contrast to mCRP the levels were significantly associated with disease severity. Additionally, the pCRP levels remained elevated for at least six weeks post inclusion, which was longer compared to the two weeks for mCRP. Our data indicates a low level of inflammation lasting for at least six weeks following COVID-19, which might indicate that the disease has an adverse effect on the immune system even after the viral infection is resolved. It is also clear that the current standard method of testing pCRP levels upon hospitalization is a useful marker for predicting disease severity and mCRP testing would not add any clinical relevance for patients with COVID-19.

The pentraxin C-reactive protein (CRP) is a pentameric protein now known to be able to undergo dissociation into a monomeric, modified isoform, referred to as mCRP. In carefully assessing the bioactivities of each isoform, mCRP has strong pro-inflammatory activities while pCRP has mild anti-inflammatory activities. Systemic lupus erythematosus (SLE) is a disease characterized by a vast number of autoantibodies, including anti-CRP autoantibodies which have been associated with SLE disease activity and lupus nephritis. The origin of these autoantibodies is currently unknown. Extracellular vesicles (EVs) have been implicated in SLE pathogenesis as they can expose nuclear antigens on their outside surface, thereby being a potential adjuvant for the generation of autoantibodies. Herein, we studied exposure of both pCRP and mCRP on EVs in SLE plasma and the implications of each in disease activity, organ damage and clinical manifestations. We used flow cytometry to detect CRP isoforms on EV surfaces in 67 well-characterized SLE patients and 60 sex- and age-matched healthy controls. Autoantibodies against mCRP were measured using ELISA. We found an abundance of both pCRP and mCRP on SLE EVs compared to controls. Furthermore, mCRP+ but not pCRP+ EVs were elevated in patients with active disease and in anti-CRP positive patients. The proportions of mCRP+ EVs were lower in patients with acquired organ damage, especially in patients with lupus nephritis (LN), and displayed an inverse relationship with disease duration in LN and patients with active disease. Speculatively, these data suggest EV-bound mCRP as a relevant factor in SLE pathogenesis, which could contribute to development of anti-CRP autoantibodies by stimulating an immune response.

Presence of autoantibodies targeting nuclear constituents, i.e., double-stranded DNA and small nuclear ribonucleoproteins (snRNPs), remain a cornerstone in systemic lupus erythematosus (SLE).Fcγ receptor IIa (FcγRIIa) dependent uptake of nucleic acid containing immune complexes (ICs) by plasmacytoid dendritic cells (PDCs) can activate toll-like receptors (TLRs) such as TLR7 and TLR9 resulting in type I interferon (IFN) production.Previously, the classical liver-derived acute-phase reactant C-reactive protein (CRP) has been suggested to reduce ICinduced type I IFN production, whereas monomeric (mCRP) vs. pentameric (pCRP) mediated effects have not yet been unraveled.Herein, peripheral blood mononuclear cells (PBMCs) or enriched blood DCs from healthy volunteers were stimulated with SLE sera, snRNP-IgG (ICs), or TLR ligands with or without pCRP, mCRP, or anti-FcγRIIa antibody.Type I IFNs and cytokine responses were investigated using quantitative PCR, ELISA, and flow cytometry.pCRP inhibited IFN gene expression in PBMCs and enriched DCs after incubation with ICs, compared to ICs alone, whereas mCRP had significantly less inhibitory effect.The effect was independent on the order in which IC or CRP was added to the cells.In addition, pCRP inhibited IFN induced by other TLR stimulators, implicating broader inhibitory effects induced by pCRP.We demonstrate pronounced immunoregulatory functions of CRP whereas the inhibitory properties were evidently dependent on CRP's intact conformational state.The inhibition of type I IFNs was not due to competition of FcγRs, or binding of CRP to the ICs.Our findings have implications for autoimmune IC-mediated conditions imprinted by type I IFN gene dysregulation.

Purpose We examined the effect of informal cancer caregiver stress and negative attribution style (NAS) on depressive symptoms and salivary cortisol. Method The sample came from a hospital bone marrow unit and caregiver support organizations and included 60 informal cancer caregivers (51.7% partners) of individuals with cancer (provided care for a median of 27.5 h per week for 12 months) and 46 non-caregiver participants. In this cross-sectional study, participants completed questionnaires assessing NAS and depressive symptoms and provided saliva samples to measure cortisol. Results Linear regressions demonstrated that cancer caregiver stress ( p = 0.001) and the cancer caregiver stress by NAS interaction ( p = 0.017), but not NAS alone ( p = 0.152), predicted depressive symptoms. Caregivers independent of their NAS and non-caregivers high in NAS reported high depression while non-caregivers low in NAS reported low depression. Neither cancer caregiver stress ( p = 0.920) nor NAS alone ( p = 0.114), but their interaction, predicted cortisol ( p = 0.036). Higher NAS was associated with a higher cortisol in both groups while non-caregivers had higher cortisol than caregivers. Conclusions If the findings can be replicated, consideration of NAS in existing interventions to support informal cancer caregivers in managing chronic stress appears warranted.

Background Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by a large production of autoantibodies and deficient clearance of cellular waste. The disease typically oscillates between episodes of elevated disease activity and quiescent disease. C-reactive protein (CRP) is a pentameric acute-phase protein usually reflecting inflammation and tissue damage. However, despite increased inflammation and elevated interleukin-6, the levels of CRP typically remain low or only slightly raised in SLE. Under certain conditions, pentameric CRP (pCRP) can dissociate into its monomeric isoform (mCRP), which mainly has been ascribed pro-inflammatory properties. The present study aims to investigate the potential relationship between pCRP and mCRP, respectively, with disease activity and clinical features of SLE. Methods The levels of pCRP and mCRP were measured, by turbidimetry (high-sensitive) and sandwich enzyme-linked immunosorbent assay (ELISA) respectively, in serum samples from 160 patients with SLE and 30 patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV). Twenty-two of the SLE cases were selected for analysis at two time-points; quiescent disease and active disease. The two CRP isoforms were evaluated in relation to disease activity and clinical features in the two diseases. Results Levels of pCRP and mCRP were significantly lower in SLE than AAV ( p < 0.001) and the ratio of mCRP/pCRP was higher in SLE compared to AAV. The mCRP/pCRP ratio was higher for patients in remission and able to significantly separate between active/quiescent disease in paired, but not in non-paired, samples from patients with SLE. Significant correlations were observed with SLICC/ACR damage index for pCRP levels as well as inversely with the mCRP/pCRP ratio. Lower mCRP levels associated with malar rash. Conclusion As the interrelationship between the two isoforms appear to (a) discriminate between quiescent and active SLE and (b) differ between SLE and AAV, our data indicates that the two CRP isoforms could exert contrasting immunological effects and/or reflect different milieus. Given the biological effects of mCRP, it is possible that altered levels may indicate increased opsonization of immune complexes and apoptotic debris, and thereby prevent their deposition outside the reticuloendothelial system and manifestations such as lupus nephritis and lupus-related skin disease.

Background: The potential association of the ABO blood group with the risk of COVID-19 and its severity has attracted a lot of interest since the start of the pandemic. While a number of studies have reported an increased risk associated with blood type A and a reduced risk with type O, other studies have did not found a significant effect. This study aimed to define the prevalence of different ABO blood groups in hospitalized COVID-19 patients in the Louisville, KY area and to investigate whether an association exists between the blood group and disease severity. Methods: This was a retrospective observational study of 380 patients with SARS-CoV-2 infection hospitalized to eight of the adult hospitals in the city of Louisville. Patients were divided into four different groups according to their ABO blood type. Demographic characteristics and clinical variables, including laboratory data as well as clinical outcomes were compared. Results: Type O was the most common blood group among the hospitalized patients (51%) followed by type A (31%), B (14%) and AB (4%). The observed blood group distribution among the patients was not significantly different from the distribution expected when compared to a population of similar racial/ethnic composition. No significant associations were found between the blood group and comorbidities, inflammatory biomarkers as well as with recorded outcomes, including the mortality rate and the length of the hospital stay. Conclusions: The data from hospitalized patients in Louisville is is not consistent with the ABO blood group having a significant effect as a risk or severity factor for COVID-19, but it is representative in COVID-19 or its severity of its prevalence among different racial/ethnic populations.

It has become increasingly evident that a high percentage of patients that recover from acute COVID-19 infection continue to suffer from a variety of persistent symptoms even months after viral clearance, the most common ones being fatigue, dyspnea, anosmia, dysgeusia, cognitive dysfunction, and psychological problems, including anxiety and depression. This syndrome, known as Post-acute sequelae of COVID-19 (PASC), can severely affect the life quality and represents an important health care concern. The exact causes for the symptoms observed in patients with PASC remain to be adequately characterized, but are likely to be associated with multiple factors, including residual disease and/or inflammation, organ damage, effects of hospitalization and/or prolonged ventilation, as well as effects of social isolation and stress. This mini-review discusses evidence that may link both inflammatory and auto-immune processes in the pathophysiology of PASC.

This study analyzed the levels at admission of biomarkers for their association with and ability to predict risk of severe outcomes, including admission to the ICU, need for invasive mechanical ventilation (IMV), need for vasopressor use (VU), and in-hospital mortality (IHM) in 700 patients hospitalized with COVID-19. Biomarker data split by outcomes was compared using Mann-Whitney U tests; frequencies of biomarker values were compared using Chi-square tests and multivariable logistic regression analysis was performed to look at the impact of biomarkers by outcome. Patients that suffered IHM were more likely to have reduced platelet numbers and high blood urea nitrogen (BUN) levels among patients admitted to the ICU. Risk factors for mortality were related to hyper-coagulability (low platelet count and increased D-dimer) and decreased respiratory (PaO2/FiO(2) ratio) and kidney function (BUN). Association with risks of other severe outcomes were as follows: ICU with hyper-inflammation (IL-6) and decreased respiratory function; IMV with low platelet count, abnormal neutrophil-lymphocyte ratio with reduced respiratory function, VU with inflammatory markers (IL-6), and low platelet count with respiratory function. Our studies confirmed the association of biomarkers of hematological, inflammatory, coagulation, pulmonary and kidney functions with disease severity. Whether these biomarkers have any mechanistic or causal role in the disease progress requires further investigation.

The prevalence of non-alcoholic fatty liver disease (NAFLD) is higher in HIV-infected patients compared to the general population. While metabolic risk factors such as obesity, insulin resistance and the metabolic syndrome have been identified as key risk factors in all individuals, there is limited information regarding the mechanisms that contribute to the higher prevalence among individuals living with HIV, particularly among women and ethnic minorities. The aim of this study was to determine the association, over two time points, of a panel of biomarkers with liver steatosis in a cohort of HIV-seropositive women and age-matched negative controls and to investigate whether the association differed by HIV status. To this effect, plasma samples obtained from 105 HIV-positive and -negative participants enrolled in the Women's Interagency HIV study (WIHS) Washington DC site were assayed for biomarkers associated with inflammation, adipose tissue function, fibrinolysis, gut permeability and hepatocyte apoptosis/necrosis. Their association with liver steatosis, measured using Controlled-Attenuation Parameter (CAP) scores determined by transient elastography, were then analyzed. HIV positivity was associated with lower median IL-17A and higher IL-22 and sCD14 values. There were no statistically significant associations between HIV status, biomarkers or covariates with CAP measurement over two time points. However, IL-1β levels were associated with higher CAP scores at the second visit. Across all statistical models, an increase in BMI was associated with an increase in CAP measurements. No statistically significant associations were found between viral load history, CD4 + T-cell count, biomarkers and covariates, including ART use, on CAP measurements. These results confirm that BMI is a key risk factor for liver steatosis independent of HIV status. The potential contributions to NAFLD of differences in IL-1β, Th17-family cytokines and gut permeability between HIV-positive vs. negative individuals require further study.

El cáncer gástrico (CG) es la neoplasia del tubo digestivo más prevalente en el mundo, asociada a factores genéticos del hospedero y externos, como infección por Helicobacter pylori. La patogénesis incluye inflamación crónica mediada por citocinas del microambiente tumoral, detectables sistémicamente. Estudios previos reportan niveles séricos de citocinas y su contribución al diagnóstico de CG. El presente estudio analiza el perfil de citocinas del tipo de Th1(IFNγ), Th2(IL-4 e IL-10), Th17(Th-17A) y otras pro inflamatorias: IL-1β, IL-6 y TNF-α, en plasma de 70 casos de pacientes con CG comparándolos con 132 sujetos sanos equiparables en edad y sexo. Los casos provinieron del Hospital Roosevelt e Instituto Nacional de Cancerología de Guatemala (Incan) y formaron parte de un estudio previo. Se analizó la base de datos clínicos, patológicos y epidemiológicos. Se midieron los niveles de citocinas utilizando el sistema “MSD MULTI-SPOT Assay System”. La edad promedio de los casos fue 59.5 años, (DE 13.0), 51%, eran positivos para IgG anti H. pylori. Un 71% presentó adenocarcinoma grado III (Borrman), según clasificación de Lauren 55% tenían tipo intestinal. Las siete citocinas cuantificadas se encontraron significativamente elevadas (p < .05) en el plasma de los casos respecto a sus controles. Los casos de CG tipo difuso presentaron niveles de IFNγ significativamente elevados. Por regresión logística, las citocinas IL-6 e IL-10, están asociadas significativamente a CG (p < .05) independientemente del estatus de infección por H. pylori. Se destacan la IL-6 e IL-10 como las principales citocinas asociadas a la presencia de CG.

Although elevations in systemic suPAR levels have been associated with inflammatory conditions and with exposure to life stress and adversity, it is not yet clear whether acute psychological stress influences suPAR levels, either systemically and/or in saliva. The aim of this study was to investigate whether salivary suPAR levels are increased following exposure to acute psychological stress. Healthy subjects, aged 18-40 years, completed a laboratory psychological stressor and provided saliva samples before and after the stress test (60 min apart). Levels of suPAR as well as those of cytokines increased in the post-stress samples (all ps <.001). Baseline and post-stress IL-1 beta and TNF-alpha as well as post-stress IL-6 correlated significantly with suPAR (all ps <.01), but IL-10 and baseline IL-6 did not. These results show that suPAR levels in saliva are stress-reactive and suggest a potential application as stress biomarkers in saliva, particularly given the advantage of easily detectable concentrations.

Approximately 20% of patients infected with SARS-CoV-2 (COVID-19) develop potentially life-threatening pathologies involving hyperinflammation, cytokine storm, septic shock complications, coagulation dysfunction, and multiple organ failure. Blood levels of the prototypic acute phase reactant, C-reactive protein (CRP), which is hepatically synthesized and released in response to interleukin-6 stimulation, is markedly elevated in patients with COVID-19. Markedly high CRP levels correlate with poor prognosis for survival. Insights into CRP structure-function relationships have uncovered both pro- and anti-inflammatory isoforms that may be used to monitor the extent of tissue damage associated with COVID-19 pathologies and prognoses. Herein, rationale is given for interpretation of CRP blood levels as a simple, rapid, and cost-effective way to assess disease severity and help guide therapeutic options in COVID-19 patients.

Since December 2019, the SARS-CoV-2 (COVID-19) pandemic has extended its reach over most of the world, infecting over four million people and causing well over 300,000 deaths so far.[1] A significant percentage of infected patients develop severe symptoms and life-threatening conditions. While COVID-19 infection can affect all ages, available evidence points to older age and pre-existing comorbidities, such as hypertension, diabetes, and coronary heart disease, as important risk factors related to increased mortality rates.[2-4] Moreover, recent reports from China and the U.S. have suggested that susceptibility, and perhaps even mortality, to COVID-19 infection might be influenced by the ABO blood type. The purpose of the present minireview is to analyze the evidence published in the COVID-19 literature and to put it in the context of the existing knowledge about the association of blood group types and disease.