Infants who require cardiopulmonary bypass for surgical repair of CHD are at high risk for secondary infections, which cause significant death and disability. The risk of secondary infection is increased by immune dysfunction. The intestinal microbiome calibrates immune function. Infants with CHD have substantial changes in their intestinal microbiome. We performed this scoping review to describe the current understanding of the relationship between the intestinal microbiome and immune function after pediatric cardiac surgery with cardiopulmonary bypass.

We searched the PubMed, Cumulative Index to Nursing and Allied Health Literature, Cochrane, and Scopus databases with the assistance of a medical librarian. We included trials that analysed intestinal microbiome composition and immune function after cardiac surgery with cardiopulmonary bypass in infants.

We found two observational cohorts and two interventional trials describing composition of intestinal microbiome and some measures of immune function after heart surgery with cardiopulmonary bypass in infants. A total of 114 children were analysed. Three trials were exclusively in infants, and one was in older children and infants. All trials found a differential composition of the intestinal microbiome in infants with CHD compared to those without CHD, and one described a robust correlation between composition of the intestinal microbiome with cytokine profile and adverse outcomes.

Despite robust preclinical data and data from other disease states, there is minimal data about the correlation between immune function and intestinal microbiome composition in infants with CHD after cardiopulmonary bypass.

A systematic review of case reports in spontaneous regression of head and neck squamous cell carcinoma (SCC) was carried out to investigate the pattern and characteristics of this phenomenon.

A systematic search of case studies of spontaneously regressed head and neck SCC was carried out in Ovid Embase, Ovid Medline and Pubmed. Methodological quality was assessed by ascertainment of diagnosis and overall details of reports. Outcomes included patient demographics, head and neck SCC characteristics and clinical course of disease.

A total of 8 cases were included and 50 per cent (n = 4) of the reported cases were SCC of the vocal folds. All cases received a surgical biopsy and three cases had possible febrile episodes preceding regression. The mean length of time to regression was 4.3 months.

Spontaneous regression in head and neck SCC is likely to be under-reported. A better understanding of how the host immune system can instigate an antitumour response will shed light on the development of novel treatments.

Zinc and copper are trace elements that have important roles in the function of the immune system. We aimed to compare serum zinc and copper levels in neonates with and without neonatal sepsis.

This case–control study examined 54 newborns with sepsis and 54 matched healthy controls admitted to the neonatal intensive care unit of Children’s Hospital, Bandar Abbas, Iran. Neonates with the diagnosis of sepsis were regarded as cases and those admitted for other reasons were regarded as controls. Maternal and neonatal serum zinc and copper were measured on admission. Copper, zinc, and copper/zinc ratio differences between case and control groups were analyzed.

Neonatal zinc levels were significantly lower in the sepsis group versus controls (88.65 ± 40.64 vs 143.48 ± 69.57μg/dL, p < 0.001). Sepsis group mothers had lower zinc (66.04 vs 83.37μg/dL, p = 0.008) and copper (124.09 vs 157.74μg/dL, p < 0.001). Neonatal copper levels were slightly lower in the sepsis group. Copper/zinc ratio was significantly higher in the sepsis group (p < 0.001). In the sepsis group, the interval to the resolution of sepsis symptoms was significantly shorter in neonates with excess compared to sufficient copper levels (P = 0.023).

Serum copper and zinc levels have an important role in the immune system’s response to the infection. Neonatal serum copper at levels higher than normal can lead to significantly shorter hospital stay. Also, higher Cu/Zn ratios can be found in neonatal sepsis, suggesting the potential utility of this index in the diagnosis of sepsis.

Terrorism and trauma survivors often experience changes in biomarkers of autonomic, inflammatory and hypothalamic-pituitary-adrenal (HPA) axis assessed at various times. Research suggests interactions of these systems in chronic stress.

This unprecedented retrospective study explores long-term stress biomarkers in three systems in terrorism survivors.

Sixty healthy, direct terrorism survivors were compared to non-exposed community members for cardiovascular reactivity to a trauma script, morning salivary cortisol, interleukin 1-β (IL-1β), and interleukin 2-R (IL-2R). Survivors’ biomarkers were correlated with psychiatric symptoms and diagnoses and reported functioning and well-being seven years after the Oklahoma City (OKC) bombing.

Main outcome measures were the Diagnostic Interview Schedule (DIS) Disaster Supplement for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) diagnoses, Impact of Events Scale-Revised (IES-R), Beck Depression Inventory-II (BDI-II), Distress and Functioning Scale (DAF), and General Physical Well-Being Scale.

Survivors had higher inflammatory IL-1β, lower anti-inflammatory IL-2R, lower cortisol, higher resting diastolic blood pressure (BP), and less cardiovascular reactivity to a trauma script than comparisons. Survivors’ mean posttraumatic stress (PTS) symptom levels did not differ from comparisons, but survivors reported worse well-being. None of survivors’ biomarkers correlated with PTS or depressive symptoms or diagnoses or reported functioning.

Alterations of biological stress measures in cardiovascular, inflammatory, and cortisol systems coexisted as an apparent generalized long-term response to terrorism rather than related to specific gauges of mental health. Potential interactions of biomarkers long after trauma exposure is discussed considering relevant research. Longer-term follow-up could determine whether biomarkers continue to differ or correlate with subjective measures, or if they accompany health problems over time. Given recent international terrorism, understanding long-term sequelae among direct survivors is increasingly relevant.

Ocrelizumab is an effective anti-CD20 therapy approved for Relapsing Remitting (RRMS) and Primary Progressive Multiple Sclerosis (PPMS). In clinical trials, a proportion of patients developed hypogammaglobulinemia which could contribute to infection risk. This study aimed to identify hypogammaglobulinemia and its risk factors and evaluate potentially associated serious infection risk in a real-world cohort of patients.

All MS patients treated with ocrelizumab in a Quebec City MS clinic from January 2017 to August 2021 were included and detailed patient characteristics were collected by chart review. Levels of immunoglobulins (IgM, IgA and IgG) were assessed prior to each treatment. Serious infection was defined as an infection requiring hospitalization or emergency room treatment. Association between hypogammaglobulinemia and serious infection was analyzed.

A total of 266 patients (average follow-up 2.05 years) were included (87% RRMS). After 6 infusions, 32.8%, 3.5% and 4.2% of patients had at least one IgM, IgA and IgG hypogammaglobulinemia event respectively. Aside from pre-treatment hypogammaglobulinemia, there were no variables associated with on-treatment hypogammaglobulinemia. There was a total of 21 serious infections (3.36 and 12.33 per 100-person-years in RRMS and PPMS). Developing hypogammaglobulinemia during treatment was not associated with serious infection. A regression analysis did not show associations between serious infection and key disease characteristics.

Similar to ocrelizumab extension studies, our cohort demonstrated a significant rate of hypogammaglobulinemia over time, mostly with IgM. No association was found between hypogammaglobulinemia and serious infection.

Schizophrenia affects approximately 1% of the world population, having a devastating impact not only in patients but in all society. As a result, it has been subject of extensive investigation and the presence of certain genes was associated with an increased risk of developing schizophrenia. However, the presence of these genes is not sufficient, therefore, other factors are necessarily involved.Observation of the association between schizophrenia and inflammatory states of the Central Nervous System led to the hypothesis that a dysfunction of the immune system may play a central role in this process.

In this work we intend to make a brief review of the existing literature related to the immunological theory of schizophrenia.

A bibliographic research was conducted in Medline library using the following terms: “schizophrenia and immune system”; “schizophrenia and inflammation” and “schizophrenia and neuroinflammation”.

The survey results reveal increasing evidence of the key role of the immune system in schizophrenia. Several studies show benefits of treatment with anti-inflammatory drugs in patients at an early stage of the disease. In the same way, it was verified that pro and anti-inflammatory cytokines influence glutamatergic transmission and tryptophan metabolism. Furthermore, the decrease in microglial activity appears to have a beneficial effect on schizophrenia.

Future will say if neuroimmunology mechanisms are primary or a secondary consequence in Schizophrenia. Recent discoveries in this area are encouraging and open the possibility of new therapeutic targets and new therapeutic approaches to this disease.

No significant relationships.

We have previously shown that the association between frequent cannabis use and psychosis is more likely in subgroups with low-grade inflammation than subgroups without (PMID: 33736715). The role of immune-related polymorphisms remains unknown.

To explore whether polymorphisms affecting the function of key immune regulatory proteins moderate the association between cannabis and psychosis, namely: ENTPD1 and NT5E, involved in the synthesis of CD39, CD73, respectively, and anti-inflammatory adenosine; CTLA4 and FOXP1, essential for Treg functional capacity.

We genotyped blood samples from 283 community-based controls and 140 recent-onset psychosis patients in Brazil (EU-GEI consortium, Ribeirão Preto/SP) for twelve polymorphisms (ENTPD1: rs3814159, rs3176891, rs10748643; NT5E: rs9444348, rs2295890; CTLA4: rs3087243, rs231775, rs5742909, rs4553808; FOXP1: rs6803008, rs6786408, rs830599; Illumina Human Core Exome-24). Cannabis frequency (daily, less than daily, never) was assessed by self-report (Cannabis Experience Questionnaire). Binary logistic regression models (OR,95%CI) included case status as the outcome, genotype (dominant model), cannabis frequency, and an interaction term between the two as exposure, adjusting for confounders (age, sex, ethnicity, tobacco smoking).

We found significant interactions between cannabis use and polymorphisms for ENTPD1 (rs3814159), NT5E (rs9444348), and FOXP1 (rs6786408). Less than daily or daily use were, in a dose-response fashion, only associated with psychosis in those with the variant and heterozygous genotypes; less than daily: ENTPD1 AG/GG (3.34,1.71-6.50); NT5E AG/AA (3.71,1.87-7.33); FOXP1 AC/CC (2.98,1.54-5.77); daily: ENTPD1 AG/GG (16.81;5.89-47.96); NT5E AG/AA (21.20,6.81-66.01); FOXP1 AC/CC (13.75,5.22-36.21).

Variation in genes that affect Treg function appears to modify the effect of cannabis consumption on psychosis in keeping with Treg hypofunction hypothesis (PMID:33713699).

No significant relationships.

Acute rheumatic fever is an autoimmune disease that develops due to streptococcal infection. The positive effect of breastfeeding on the development of the child’s immune system is well documented. In this study, we aimed to investigate the effect of breast milk intake period on the development of carditis.

Patients (n: 182) who were diagnosed with acute rheumatic fever between 2010 and 2019 were enrolled in the study. The patients were divided into groups according to carditis development. The demographic, socio-economic, and breastfeeding data were compared between groups.

The mean age of the patients was 10.5 ± 3.4, and 43.4 % (n: 79) of them were female. Independent predictors of the development of carditis in the first acute rheumatic fever episode were the number of children at home (OR: 1.773, CI 95%: 1.105, 2.845; p: 0.018) and breast milk intake less than 6 months (OR: 0.404, CI 95%: 0.174, 0.934; p: 0.034). Independent predictors of the development of carditis in any of the acute rheumatic fever episodes were the number of children at home (OR: 1.858, CI 95%: 1.100, 3.137; p: 0.021) and female gender (OR: 3.504, CI 95%: 1.227, 10.008; p: 0.019). The only independently predictor of the development of chorea during acute rheumatic fever was female gender (OR: 3.801, CI 95%: 1.463, 9.874; p: 0.006).

Although the occurrence of carditis is less common during the first acute rheumatic fever attack in patients with breast milk intake less than six months, this advantage is lost in recurrent attacks. This study showed that breast milk does not have a negative effect on acute rheumatic fever carditis.