Inflammatory bowel disease (IBD), which includes Crohn's disease (CD) and ulcerative colitis (UC), represents a group of chronic disorders characterized by inflammation of the gastrointestinal tract, typically with a relapsing and remitting clinical course. Mucosal macrophages play an important role in the mucosal immune system, and an increase in the number of newly recruited monocytes and activated macrophages has been noted in the inflamed gut of patients with IBD. Activated macrophages are thought to be major contributors to the production of inflammatory cytokines in the gut, and imbalance of cytokines is contributing to the pathogenesis of IBD. The intestinal inflammation in IBD is controlled by a complex interplay of innate and adaptive immune mechanisms. Cytokines play a key role in IBD that determine T cell differentiation of Th1, Th2, T regulatory and newly described Th17 cells. Cytokines levels in time and space orchestrate the development, recurrence and exacerbation of the inflammatory process in IBD. Therefore, several cytokine therapies have been developed and tested for the treatment of IBD patients.

Common polymorphisms in the fat mass and obesity-associated gene (FTO) have shown strong association with obesity in several populations. In the present study, we explored the association of FTO gene polymorphisms with obesity and other biochemical parameters in the Mexican population. We also assessed FTO gene expression levels in adipose tissue of obese and nonobese individuals. The study comprised 788 unrelated Mexican-Mestizo individuals and 31 subcutaneous fat tissue biopsies from lean and obese women. FTO single-nucleotide polymorphisms (SNPs) rs9939609, rs1421085, and rs17817449 were associated with obesity, particularly with class III obesity, under both additive and dominant models (P = 0.0000004 and 0.000008, respectively). These associations remained significant after adjusting for admixture (P = 0.000003 and 0.00009, respectively). Moreover, risk alleles showed a nominal association with lower insulin levels and homeostasis model assessment of B-cell function (HOMA-B), and with higher homeostasis model assessment of insulin sensitivity (HOMA-S) only in nonobese individuals (P dom = 0.031, 0.023, and 0.049, respectively). FTO mRNA levels were significantly higher in subcutaneous fat tissue of class III obese individuals than in lean individuals (P = 0.043). Risk alleles were significantly associated with higher FTO expression in the class III obesity group (P = 0.047). In conclusion, FTO is a major risk factor for obesity (particularly class III) in the MexicanMestizo population, and is upregulated in subcutaneous fat tissue of obese individuals.

The study identified bacterial species associated with obesity, metabolic complications and amino acid serum levels in Mexican children.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its associated coagulopathy are particularly worrisome in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), as these diseases carry an increased risk of thrombotic complications. Mathian et al recently reported the clinical course of COVID-19 in a series of 17 patients with SLE under chronic hydroxychloroquine therapy. 1 Of note, only one patient (6%) presented thrombosis despite the fact that four patients (24%) had a history of secondary APS, and five patients (29%) were receiving oral anticoagulants. Antiphospholipid (aPL) antibodies were not measured in these patients during active SARS-CoV-2 infection. 1 The American Society of Hematology recently stated that 'at the current time, there are only very limited data on aPL antibodies in COVID-19 and it is unclear if they represent an epiphenomenon or are actually involved in any haemostatic abnormalities seen in COVID-19 disease'. 2 Furthermore, almost all the available information refers to the lupus anticoagulant, with frequencies ranging from 45% to 87%. 3 4 This paucity of data led us to test a panel of aPL antibodies in blood specimens from 21 patients hospitalised in the intensive care unit between 12 and 19 April, due to severe or critical COVID-19, and received at our laboratory on 20 April to measure interleukin-6 levels. Anticardiolipin, anti-β 2 glycoprotein I, antiprothrombin, antiphosphatidylserine, antiphosphatidylinositol and antiannexin V antibodies were measured, each in IgM and IgG isotypes. Subsequently, demographic and clinical data were obtained from electronic medical records. Sera collected before the SARS-CoV-2 pandemic from 12 healthy individuals, matched for age and sex, were tested as controls.Pertinent results are summarised in table 1. The median age of patients was 62 years; 43% were men; and a high number of comorbidities were observed (median Charlson Comorbidity Index of 3). A total of 19 patients (90%) had shortness of breath on admission, and 12 (57%) eventually required invasive mechanical ventilation during hospitalisation. Elevated levels of D-dimer, ferritin and C reactive protein were found at presentation.Of the 21 patients with COVID-19 studied, 12 had at least one circulating aPL antibody, whereas only 1 of the 12 controls yielded a positive result (57% vs 8%; Fisher's exact test, p=0.009). The most frequently detected aPL antibodies were antiannexin V IgM (19%), anticardiolipin IgM (14%), antiphosphatidylserine IgM (14%), anticardiolipin IgG (10%) and antiphosphatidylserine IgG (10%) antibodies. One patient had triple positivity (8%); three patients had double positivity (25%); and the remaining eight had a single positivity (67%). Age and number of comorbidities tended to be lower in patients with aPL antibodies. In contrast, levels of D-dimer, ferritin and C reactive protein were higher both on admission and throughout the hospital stay in these patients. Elevated levels of interleukin-6 (>40 pg/mL) wer...

Coronavirus disease 2019 (COVID-19) was declared a pandemic and international health emergency by the World Health Organization. Patients with obesity with COVID-19 are 7 times more likely to need invasive mechanical ventilation than are patients without obesity (OR 7.36; 95% CI: 1.63–33.14, p = 0.021). Acute respiratory distress syndrome (ARDS) is one of the main causes of death related to COVID-19 and is triggered by a cytokine storm that damages the respiratory epithelium. Interleukins that cause the chronic low-grade inflammatory state of obesity, such as interleukin (IL)-1β, IL-6, monocyte chemoattractant peptide (MCP)-1, and, in particular, IL-17A and tumour necrosis factor alpha (TNF-α), also play very important roles in lung damage in ARDS. Therefore, obesity is associated with an immune state favourable to a cytokine storm. Our hypothesis is that serum concentrations of TNF-α and IL-17A are more elevated in patients with obesity and COVID-19, and consequently, they have a greater probability of developing ARDS and death. The immunobiology of IL-17A and TNF-α opens a new fascinating field of research for COVID-19.