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Background Lung fibrosis is a major concern in severe COVID-19 patients undergoing mechanical ventilation (MV). Lung fibrosis frequency in post-COVID syndrome is highly variable and even if the risk is proportionally small, many patients could be affected. However, there is still no data on lung extracellular matrix (ECM) composition in severe COVID-19 and whether it is different from other aetiologies of ARDS. Methods We have quantified different ECM elements and TGF-β expression in lung tissue of 28 fatal COVID-19 cases and compared to 27 patients that died of other causes of ARDS, divided according to MV duration (up to six days or seven days or more). In COVID-19 cases, ECM elements were correlated with lung transcriptomics and cytokines profile. Results We observed that COVID-19 cases presented significant increased deposition of collagen, fibronectin, versican, and TGF-β, and decreased decorin density when compared to non-COVID-19 cases of similar MV duration. TGF-β was precociously increased in COVID-19 patients with MV duration up to six days. Lung collagen was higher in women with COVID-19, with a transition of upregulated genes related to fibrillogenesis to collagen production and ECM disassembly along the MV course. Conclusions Fatal COVID-19 is associated with an early TGF-β expression lung environment after the MV onset, followed by a disordered ECM assembly. This uncontrolled process resulted in a prominent collagen deposition when compared to other causes of ARDS. Our data provides pathological substrates to better understand the high prevalence of pulmonary abnormalities in patients surviving COVID-19.

Despite scientific evidence and government actions aimed at reducing air pollution, it remains a major public health issue in large urban centers, compromising human health, particularly among the most vulnerable populations, including the elderly. Polyphenolic compounds are believed to have antiaging effects, reducing DNA damage and exhibiting anti‐inflammatory and antioxidant properties. The polyphenol resveratrol (Resv) has demonstrated protective effects in the lungs against harmful stimuli in adult mice; however, few studies have extended these investigations to elderly animals, which have reduced antioxidant responses. This study aimed to evaluate the effects of Resv on the lungs of 15‐month‐old mice exposed to diesel exhaust (DE). Animals were exposed to 1200 µg/m3 of PM2.5 over 30 consecutive days. Resv (1200 µg/m3) was administered for 40 days, beginning 10 days before DE exposure. We evaluated the inflammatory profile in bronchoalveolar lavage fluid (BALF) and serum; quantified macrophages; and assessed antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GR], glutathione‐S‐transferase [GST], and copper/zinc superoxide dismutase [Cu/Zn SOD]), 8‐OHdG, 8‐iso‐prostaglandin F2α (8‐isoprostane), collagen and elastic fiber content, and sirtuin protein levels (Sirt1, Sirt2, and Sirt6) in the lung parenchyma. Resv administration increased GR and Sirt1 levels and decreased Sirt2 levels. DE caused inflammatory changes in BALF and lung tissue, increased 8‐OHdG and 8‐isoprostane levels, and modulated antioxidant enzymes, sirtuins, and lung collagen. Resv administration after DE exposure did not significantly alter 8‐OHdG, antioxidant enzymes, sirtuins, or collagen levels in the lungs, but it reduced BALF cellularity and IL‐1β and 8‐isoprostane levels. Our data suggest moderate protective effects of Resv in aged lungs exposed to DE.

Elderly individuals were disproportionally affected during the COVID-19 pandemic, and more than 80% of the global COVID-19-related deaths between 2020 and 2021 occurred among people aged 60 years or older. Several cellular modifications in aged cells may lead to systemic inflammation and fibrotic responses. Age or exogenous insults induce cellular senescence, further increasing the release of pro-inflammatory mediators, leading to the condition known as inflammaging, that can contribute to disease severity. Older individuals presented signs of systemic hyperinflammation in severe COVID-19, but few studies analyzed the influence of age on lung tissue responses in cases of severe COVID-19. We hypothesized that age related alterations regarding innate/acquired immunity and cellular senescence in lung tissue of individuals without lung diseases could predispose to viral infection. We also aimed to identify how the aged lung responded to severe COVID-19 infection. We studied lung tissues from 19 individuals that died from non-pulmonary causes and 28 adult individuals who died from COVID-19 between March and May of 2020, divided according to their age (> or < 60 years). Tissue sections were stained, via immunohistochemistry, and 19 markers among immune cells, COVID-19 receptors, cytokines and senescence were analyzed in the lung parenchyma of both groups. In the COVID-19 group, the Luminex multiplex assay technique was used to detect a panel of 25 cytokines/chemokines. In control lungs, aged individuals had a lower TLR7 expression, without differences in other markers. Older patients had a shorter time between onset of symptoms and death, with a significant negative correlation with age. Unlike the adult younger group, older COVID − 19 patients presented significant differences in relation to their age matched controls in the expression of CD8 + T cells, IFN-α2, TLR7, pSTAT-3, p21 and p53. They also presented higher protein expression that IFN-α2 and TGF-beta than the adult COVID-19 group, with a trend to decreased CD20 + cell density in the lungs. Taken together, our data show age adversely affects the lung expression of key proteins related to COVID-19 susceptibility and severity, by perpetuating inflammation and increasing pro-fibrotic responses.

Background Studies in adult severe treatment-resistant asthma (STRA) have demonstrated heterogeneous pathophysiology. Studies in the pediatric age group are still scarce, and few include bronchial tissue analysis. Objective We investigated 6–18-year-old patients diagnosed with STRA in Sao Paulo, Brazil, by characterizing the different lung compartments and their correlations with asthma control and lung function. Methods Inflammatory profiles of 13 patients with a confirmed diagnosis of STRA were analyzed using blood, induced sputum, bronchoalveolar lavage, viral and bacterial screens and endobronchial biopsy. Inflammatory cells, cytokines, and basement membrane thickening were tested for correlations with the asthma control test (ACT) and spirometry and plethysmography parameters. Results Endobronchial biopsy specimens from 11 patients were viable for analysis. All biopsies showed eosinophilic infiltration. Submucosal (SM) eosinophils and neutrophils were correlated with worse lung function (pre-BD FEV1), and SM neutrophils were correlated with fixed obstruction (post-BD FEV1). Intraepithelial (IE) neutrophils were positively correlated with lung function (pre-BD sGaw). CD8 + T cells had the highest density in the IE and SM layers and were positively correlated with ACT and negatively correlated with the cytokines IL1β, IL2, IL5, IL7, IL10, IL12, IL17, GCSF, MCP-1, INF-δ, and TNFα in sputum supernatant. The ASM chymase + mast cell density correlated positively with quality-of-life score (pAQLQ) and ACT. Conclusion Eosinophils and SM neutrophils correlated with worse lung function, while IE neutrophils correlated with better lung function. Most importantly, CD8 + T cells were abundant in bronchial biopsies of STRA patients and showed protective associations, as did chymase + mast cells.

Background Pulmonary involvement in COVID-19 is characterized pathologically by diffuse alveolar damage (DAD) and thrombosis, leading to the clinical picture of Acute Respiratory Distress Syndrome. The direct action of SARS-CoV-2 in lung cells and the dysregulated immuno-coagulative pathways activated in ARDS influence pulmonary involvement in severe COVID, that might be modulated by disease duration and individual factors. In this study we assessed the proportions of different lung pathology patterns in severe COVID-19 patients along the disease evolution and individual characteristics. Methods We analysed lung tissue from 41 COVID-19 patients that died in the period March–June 2020 and were submitted to a minimally invasive autopsy. Eight pulmonary regions were sampled. Pulmonary pathologists analysed the H&E stained slides, performing semiquantitative scores on the following parameters: exudative, intermediate or advanced DAD, bronchopneumonia, alveolar haemorrhage, infarct (%), arteriolar (number) or capillary thrombosis (yes/no). Histopathological data were correlated with demographic-clinical variables and periods of symptoms-hospital stay. Results Patient´s age varied from 22 to 88 years (18f/23 m), with hospital admission varying from 0 to 40 days. All patients had different proportions of DAD in their biopsies. Ninety percent of the patients presented pulmonary microthrombosis. The proportion of exudative DAD was higher in the period 0–8 days of hospital admission till death, whereas advanced DAD was higher after 17 days of hospital admission. In the group of patients that died within eight days of hospital admission, elderly patients had less proportion of the exudative pattern and increased proportions of the intermediate patterns. Obese patients had lower proportion of advanced DAD pattern in their biopsies, and lower than patients with overweight. Clustering analysis showed that patterns of vascular lesions (microthrombosis, infarction) clustered together, but not the other patterns. The vascular pattern was not influenced by demographic or clinical parameters, including time of disease progression. Conclusion Patients with severe COVID-19 present different proportions of DAD patterns over time, with advanced DAD being more prevalent after 17 days, which seems to be influenced by age and weight. Vascular involvement is present in a large proportion of patients, occurs early in disease progression, and does not change over time.

Urban agriculture (UA) has been shown to provide several benefits to cities such as regional food production, increased biodiversity, and income generation, especially in peri‐urban areas. However, little is known about the impacts of UA within the urban sprawl of megacities in the Global South, which have different social and territorial configurations than cities in the Global North. This report aimed to characterize spaces, types and quantities of cultivated plants, cultivation practices, economic impacts, and socio‐environmental benefits of home and community gardens in the dense central areas of Sao Paulo megacity, with more than 11 million inhabitants and few planting spaces. An online survey applied to 143 gardeners in 2023 revealed that although having limited spaces (up to 10m2), 172 different food plants were cultivated, predominantly herbs, nonconventional food plants, and leafy vegetables. Sixty‐seven percent of the gardeners had in each meal up to 25% of the food consumed were garden products but most of them were not able to estimate the associated savings in weekly purchases. The gardens also attracted insects and animals, which were perceived positively by most people. Twenty‐two (16%) gardeners maintained beehives in domestic or community gardens, and more than 70% of the gardeners reported the practice of composting. While limited in scale, urban gardens in central and highly urbanized areas of Sao Paulo demonstrated potential to improve access to fresh food, enhance biodiversity, and promote sustainable practices. Our data helped to characterize the typology of UA from a megacity perspective for conditions prevailing in the Global South. Core Ideas Urban agriculture promotes agroecological practices. Urban gardens in central and highly urbanized areas improve access to fresh food. Characteristics of urban gardeners, such as production, types of cultivation, uses, and economic impacts. Plain Language Summary Urban agriculture promotes agroecological practices, enhances biodiversity, combats food insecurity, and improves socio‐environmental conditions. This report aimed to characterize spaces and cultivation practices, economic impacts, and socio‐environmental benefits of home and community gardens. A questionnaire was applied to gardeners, and data on demographics, types and quantities of cultivated plants, and associated impacts were collected. Results showed that although they have limited spaces (up to 10 m2), 172 different food plants were cultivated, predominantly herbs, nonconventional food plants, and leafy vegetables. Sixty‐seven percent affirmed that in each meal up to 25% of the food consumed contained garden products but most of them were not able to estimate the associated savings in weekly purchases. While limited in scale, urban gardens in central and highly urbanized areas demonstrate significant potential to improve access to fresh food and promote sustainable practices.

Aims To identify Rhizobium strains' ability to biocontrol Sclerotium rolfsii, a fungus that causes serious damage to the common bean and other important crops, 78 previously isolated rhizobia from common bean were assessed. Methods Dual cultures, volatiles, indole-acetic acid (IAA), siderophore production and 16S rRNA sequencing were employed to select strains for pot and field experiments. Results Thirty-three antagonistic strains were detected in dual cultures, 16 of which were able to inhibit ≥84% fungus mycelial growth. Antagonistic strains produced up to 36.5 μg mL−1 of IAA, and a direct correlation was verified between IAA production and mycelium inhibition. SEMIA 460 inhibited 45% of mycelial growth through volatile compounds. 16S rRNA sequences confirmed strains as Rhizobium species. In pot condition, common bean plants grown on S. rolfsii-infested soil and inoculated with SEMIA 4032, 4077, 4088, 4080, 4085, or 439 presented less or no disease symptoms. The most efficient strains under field conditions, SEMIA 439 and 4088, decreased disease incidence by 18.3 and 14.5% of the S. rolfsii-infested control. Conclusions Rhizobium strains could be strong antagonists towards S. rolfsii growth. SEMIA 4032, 4077, 4088, 4080, 4085, and 439 are effective in the biological control of the collar rot of the common bean.

Infection by Spodoptera frugiperda multiple nucleopolyhedrovirus (SfMNPV) profoundly alters the physiology of S. frugiperda (Lepidoptera: Noctuidae), promoting molecular responses that activate genes related to cellular defense. These responses demand substantial energy and lead to feeding dysfunction. Knowledge about the effects of SfMNPV on weight gain and leaf consumption rate is still incipient; in this context, we evaluated the survival rate, weight gain, leaf consumption rate, and body size of S. frugiperda exposed to different concentrations of SfMNPV. A completely randomized design was used in the laboratory. Treatments consisted of SfMNPV from the commercial product Cartugen®, diluted at different concentrations and applied on a Petri dish: 9.00 × 103, 1.80 × 104, 3.75 × 104, 7.50 × 104, 1.35 × 105, 2.25 × 105, and 3.75 × 105 occlusion bodies (OBs)/mL. Fifty first-instar larvae were used per treatment. The median lethal concentration was estimated at 1.32 × 105 OBs/mL (95% confidence interval = 1.22 × 105–1.43 × 105 OBs/mL). Nonlinear regression analysis of sublethal effects showed that the expected weight of the control (W0), the angular parameter (B), and the effective concentration capable of reducing larval weight by 50% (EC50) were 47.40 mg, 1.42, and 1.16 × 104 OBs/mL, respectively. Leaf consumption was inhibited at lower concentrations and increased at higher concentrations among surviving larvae, and larval growth (measured by head diameter, body length, and body width) was lower when larvae were exposed to SfMNPV than in the control. Our data suggest that SfMNPV at low concentrations causes dysfunctions that prevent normal development in surviving individuals, resulting in reduced consumption rate, body growth, and weight gain. Overall, our analysis indicates that the impact of SfMNPV extends beyond mortality; low concentrations can affect larval growth and feeding consumption rate in S. frugiperda.

Chronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE- induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.

Background Diesel exhaust particles (DEPs) are deposited into the respiratory tract and are thought to be a risk factor for the development of diseases of the respiratory system. In healthy individuals, the timing and mechanisms of respiratory tract injuries caused by chronic exposure to air pollution remain to be clarified. Methods We evaluated the effects of chronic exposure to DEP at doses below those found in a typical bus corridor in Sao Paulo (150 μg/m 3 ). Male BALB/c mice were divided into mice receiving a nasal instillation: saline (saline; n = 30) and 30 μg/10 μL of DEP (DEP; n = 30). Nasal instillations were performed five days a week, over a period of 90 days. Bronchoalveolar lavage (BAL) was performed, and the concentrations of interleukin (IL)-4, IL-10, IL-13 and interferon-gamma (INF-γ) were determined by ELISA-immunoassay. Assessment of respiratory mechanics was performed. The gene expression of Muc5ac in lung was evaluated by RT-PCR. The presence of IL-13, MAC2+ macrophages, CD3+, CD4+, CD8+ T cells and CD20+ B cells in tissues was analysed by immunohistochemistry. Bronchial thickness and the collagen/elastic fibers density were evaluated by morphometry. We measured the mean linear intercept (Lm), a measure of alveolar distension, and the mean airspace diameter (D0) and statistical distribution (D2). Results DEP decreased IFN-γ levels in BAL (p = 0.03), but did not significantly alter IL-4, IL-10 and IL-13 levels. MAC2+ macrophage, CD4+ T cell and CD20+ B cell numbers were not altered; however, numbers of CD3+ T cells (p ≤ 0.001) and CD8+ T cells (p ≤ 0.001) increased in the parenchyma. Although IL-13 (p = 0.008) expression decreased in the bronchiolar epithelium, Muc5ac gene expression was not altered in the lung of DEP-exposed animals. Although respiratory mechanics, elastic and collagen density were not modified, the mean linear intercept (Lm) was increased in the DEP-exposed animals (p ≤ 0.001), and the index D2 was statistically different (p = 0.038) from the control animals. Conclusion Our data suggest that nasal instillation of low doses of DEP over a period of 90 days results in alveolar enlargement in the pulmonary parenchyma of healthy mice.