This study showed that the acute and chronic anti-inflammatory activity of P. aculeata leaves is very promising, and corroborates to better understand their ethnopharmacological applications.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged in December 2019 and rapidly outspread worldwide endangering human health. The coronavirus disease 2019 (COVID-19) manifests itself through a wide spectrum of symptoms that can evolve to severe presentations as pneumonia and several non-respiratory complications. Increased susceptibility to COVID-19 hospitalization and mortality have been linked to associated comorbidities as diabetes, hypertension, cardiovascular diseases and, recently, to obesity. Similarly, individuals living with obesity are at greater risk to develop clinical complications and to have poor prognosis in severe influenza pneumonia. Immune and metabolic dysfunctions associated with the increased susceptibility to influenza infection are linked to obesity-associated low-grade inflammation, compromised immune and endocrine systems, and to high cardiovascular risk. These preexisting conditions may favor virological persistence, amplify immunopathological responses and worsen hemodynamic instability in severe COVID-19 as well. In this review we highlight the main factors and the current state of the art on obesity as risk factor for influenza and COVID-19 hospitalization, severe respiratory manifestations, extrapulmonary complications and even death. Finally, immunoregulatory mechanisms of severe influenza pneumonia in individuals with obesity are addressed as likely factors involved in COVID-19 pathophysiology.

Breast cancer (BC) remains the leading cause of cancer-related deaths among women, and the chances to develop it are duplicated by obesity. Still, the impact of obesity during BC progression remains less understood. We investigated the role of obesity in tumor progression using the murine model of 4T1 mammary carcinoma in BALB/c female mice, previously high-fat-diet (HFD) fed. HFD induced obesity, metabolic impairment, and high serum and fat leptin levels. After injection of 4T1-cells, HFD-mice accelerated tumor progression and metastasis. 4T1-cells found within HFD-mice metastatic niches presented higher clonogenic potential. 4T1-cells treated in vitro with fat-conditioned medium derived from HFD-mice, increased migration capacity through CXCL12 and CCL25 gradients. In HFD-mice, the infiltration and activation of immune cells into tumor-sentinel lymph nodes was overall reduced, except for activated CD4+ T cells expressing low CD25 levels. Within the bone marrow, the levels of haematopoiesis-related IL-6 and TNF-α decreased after 4T1-cells injection in HFD-mice whereas increased in the controls, suggesting that upregulation of both cytokines, regardless of the tumor, is disrupted by obesity. Finally, the expression of genes for leptin, CXCR4, and CCR9 (receptors of CXCL12 and CCL25, respectively) was negatively correlated with the infiltration of CD8 T cells in human triple-negative BC tumors from obese patients compared to non-obese. Together, our data present early evidence of systemic networks triggered by obesity that promote BC progression to the metastatic niches. Targeting these pathways might be useful to prevent the rapid BC progression observed among obese patients.

Brazil has the second highest number of deaths due to COVID-19. Obesity has been associated with an important role in disease development and a worse prognosis. We aimed to explore epidemiological data from Brazil, discussing the potential relationships between obesity and COVID-19 severity in this country. We used a public database made available by the Ministry of Health of Brazil (182700 patients diagnosed with COVID-19). Descriptive statistics were used to characterize our database. Continuous data were expressed as median and analyzed by the nonparametric tests Mann–Whitney or one-sample Wilcoxon. The frequencies of categorical variables have been analyzed by chi-square tests of independence or goodness-of-fit. Among the number of deaths, 74% of patients were 60 years of age or older. Patients with obesity who died of COVID-19 were younger (59 years (IQR = 23)) than those without obesity (71 years (IQR = 20), P < 0.001 , and η2 = 0.0424). Women with obesity who died of COVID-19 were older than men (55 years (IQR = 25) vs. 50 (IQR = 22), P < 0.001 , and η2 = 0.0263). Furthermore, obesity increases the chances of needing intensive care unit (OR: 1.783, CI: 95%, and P < 0.001 ), needing ventilatory support (OR: 1.537, CI: 95%, and P < 0.001 and OR: 2.302, CI: 95%, and P < 0.001 , for noninvasive and invasive, respectively), and death (OR: 1.411, CI: 95%, and P < 0.001 ) of patients hospitalized with COVID-19. Our analysis supports obesity as a significant risk factor for the development of more severe forms of COVID-19. The present study can direct a more effective prevention campaign and appropriate management of subjects with obesity.

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