Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

The intramuscular administration of polymerized type I collagen (PTIC) for adult symptomatic COVID-19 outpatients downregulated hyperinflammation and improved symptoms. We inferred that LAIR1 is a potential receptor for PTIC. Thus, a binding assay and surface plasmon resonance binding assay were performed to estimate the affinity of the interaction between LAIR1 and PTIC. M1 macrophages derived from THP-1 cells were cultured with 2–10% PTIC for 24 h. Lysates from PTIC-treated THP-1 cells, macrophage-like cells (MLCs), M1, M1 + IFN-γ, and M1 + LPS were analyzed by Western blot for NF-κB (p65), p38, STAT1, and pSTAT1 (tyrosine⁷⁰¹). Serum cytokine levels and monocyte LAIR1 expressions (Mo1 and Mo2) were analyzed by luminometry and flow cytometry in symptomatic COVID-19 outpatients on PTIC treatment. PTIC-bound LAIR1 had a similar affinity to collagen in M1 macrophages. It downregulated pSTAT1 in IFN-γ-induced M1. COVID-19 patients under PTIC treatment showed a significant decrease in Mo1 percentages and cytokines (IP-10/MIF/eotaxin/IL-8/IL-1RA/M-CSF) associated with STAT1 and an increase in the Mo2 subset. The inflammatory mediators and Mo1 downregulation were related to better oxygen saturation and decreased dyspnea, chest pain, cough, and chronic fatigue syndrome in the acute and long-term phase of infection. PTIC is an agonist of LAIR1 and downregulates STAT-1 phosphorylation. PTIC could be relevant for treating STAT1-mediated inflammatory diseases, including COVID-19 and long COVID.

Background and aims: COVID-19 vaccination has proved to be effective to prevent symptomatic infection and severe disease even in immunocompromised patients including liver transplant patients. We aim to assess the impact of COVID-19 vaccination on the mortality and development of severe and critical disease in our center. Methods: A retrospective cohort study of LT patients in a reference center between March 2020 and February 2022. Demographic data, cirrhosis etiology, time on liver transplantation, immunosuppressive therapies, and vaccination status were recorded at the time of diagnosis. Primary outcome was death due to COVID-19, and secondary outcomes included the development of severe COVID-19 and intensive care unit (ICU) requirement. Results: 153 of 324 LT recipients developed COVID-19, in whom the main causes of cirrhosis were HCV infection and metabolic-associated fatty liver disease. The vaccines used were BNT162b2 (48.6%), ChAdOx1 nCoV-19 (21.6%), mRNA-1273 vaccine (1.4%), Sputnik V (14.9%), Ad5-nCoV-S (4.1%) and CoronaVac (9.5%). Case fatality and ICU requirement risk were similar among vaccinated and unvaccinated LT patients (adjusted relative case fatality for vaccinated versus unvaccinated of 0.68, 95% CI 0.14–3.24, p = 0.62; adjusted relative risk [aRR] for ICU requirement of 0.45, 95% CI 0.11–1.88, p = 0.27). Nonetheless, vaccination was associated with a lower risk of severe disease (aRR for severe disease of 0.32, 95% CI 0.14–0.71, p = 0.005). Conclusions: Vaccination reduces the risk of severe COVID-19 in LT patients, regardless of the scheme used. Vaccination should be encouraged for all.

The intramuscular administration of polymerized type I collagen (PTIC) for adult symptomatic COVID-19 outpatient downregulated hyperinflammation and improved symptoms. We inferred that LAIR-1 is a potential receptor for PTIC. Thus, binding assay and surface plasmon resonance binding assay were performed to estimate the affinity of the interaction between LAIR-1 and PTIC. M1-macrophage derived from THP-1 cells were cultured with 2-10% PTIC for 24 h. Lysates from PTIC-treated THP-1 cells, macrophages-like cells (MLCs), M1, M1+IFN-γ, and M1+LPS were analyzed by western blot for NF-κB(p65), p38, STAT-1, and pSTAT-1 (tyrosine701). Serum cytokine levels and monocyte LAIR-1 expression (Mo1 and Mo2) were analyzed by luminometry and flow cytometry in symptomatic COVID-19 outpatients on PTIC treatment. PTIC-bound LAIR-1 with a similar affinity to collagen in M1-macrophages. It downregulated pSTAT-1 in IFN-γ-induced M1. COVID-19 patients under PTIC treatment significantly decreased Mo1 percentage and cytokines (IP-10/MIF/eotaxin/IL-8/IL-1RA/M-CSF) associated with STAT-1 and increased Mo2 subset. The inflammatory mediators and Mo1 downregulation were related to better oxygen saturation and decreased dyspnea, chest pain, cough, and chronic fatigue syndrome in the acute and long-term phase of infection. PTIC is an agonist of LAIR-1 and downregulates STAT-1 phosphorylation. PTIC could be relevant for treating STAT-1-mediated inflammatory diseases, including COVID-19 and long-COVID.

Up to 15% of liver biopsies may reveal granulomas. The underlying causes vary geographically, with marked differences between high- and low-middle-income countries. No studies have examined the etiology of granulomatous liver disease (GLD) in Mexico. To describe the etiologic profile and clinical outcomes of patients diagnosed with GLD at a tertiary care center in Mexico. Retrospective cohort study of patients diagnosed with GLD by liver biopsy between 2001 and 2017. We identified 133 patients with GLD. The most common causes were infectious diseases (36.1%, n = 48; including 22 mycobacterial infections), foreign body reactions (21.1%, n = 28), and autoimmune disorders (15.0%, n = 20). The overall 6-month survival probability was 90.9% (95% confidence interval [CI], 86-95%), declining to 87.5% (95% CI, 82-93%) at 12 months. Patients with autoimmune etiologies had the best prognosis (100% survival at 6 and 12 months). In contrast, patients with neoplastic GLD had the poorest outcomes, with survival probabilities of 72.7% (95% CI, 50.6-100%) at 6 months and 63.6% (95% CI, 40.7-99.5%) at 12 months. Patients with idiopathic GLD had a favorable short-term prognosis, with a 12-month survival probability of 92%. In this cohort, infectious diseases were the most common cause of GLD. Prognosis varied by etiology, with idiopathic cases showing favorable short-term outcomes and neoplastic cases exhibiting poor survival rates.