Collagen-based products are found in different pharmaceuticals, medicine, food, and cosmetics products for a wide variety of applications. However, its use to prevent or improve the health of skin is growing dizzyingly. Therefore, this study investigated whether collagen peptides could induce fibroblast and keratinocyte proliferation and activation beyond reducing an inflammatory response induced by lipopolysaccharide (LPS). Human skin fibroblasts (CCD-1072Sk) and human keratinocytes (hKT-nh-skp-KT0026) were seeded at a concentration of 5 × 10⁴ cells/mL. LPS (10 ng/mL) and three doses of collagen peptides (2.5 mg/mL, 5 mg/mL, 10 mg/mL) were used. The readout parameters were cell proliferation; expression of inducible nitric oxide synthase (iNOS); expression of pro-collagen-1α by fibroblasts; and secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) by both cell types. The results demonstrated that all doses of collagen supplementation induced increased proliferation of both human fibroblasts (p < 0.01) and human keratinocytes (p < 0.001), while only the dose of 10 mg/mL induced an increased expression of pro-collagen-1α by fibroblasts. Similarly, only the dose of 10 mg/mL reduced LPS-induced iNOS expression in fibroblasts (p < 0.05) and keratinocytes (p < 0.01). In addition, collagen supplementation reduced the LPS-induced IL-1β (p < 0.05), IL-6 (p < 0.001), IL-8 (p < 0.01), and TNF-α (p < 0.05), and increased the TGF-β and VEGF expression in fibroblasts. Furthermore, collagen supplementation reduced the LPS-induced IL-1β (p < 0.01), IL-6 (p < 0.01), IL-8 (p < 0.01), and TNF-α (p < 0.001), and increased the TGF-β (p < 0.05) and VEGF (p < 0.05) expression in keratinocytes. In conclusion, collagen peptides were found to induce fibroblast and keratinocyte proliferation and pro-collagen-1α expression, involving increased expression of TGF-β and VEGF, as well as the suppression of an inflammatory response induced by LPS.

The present study investigated the anti-inflammatory effect of the probiotic Lacticaseibacillus rhamnosus (Lr) on lung inflammation induced by Lipopolysaccharide (LPS) of Escherichia coli in C57BL/6 mice. C57BL/6 mice were divided into four groups: control, LPS, Lr (1 day) + LPS, and Lr (14 days) + LPS. Total and differential cells from Bronchoalveolar Lavage Fluid (BALF) were counted in a Neubauer 40X chamber, and pro-and anti-inflammatory cytokines (IL-1β, IL-6, CXCL-1, TNF-α, TGF-β, and IL-10) were measured by ELISA assay. The analysis of whole leukocytes in blood was performed using the automated system Sysmex 800i. Morphometry of pulmonary tissue evaluated alveolar hemorrhage, alveolar collapse, and inflammatory cells. Pulmonary vascular permeability was assessed by Evans blue dye extravasation, and bronchoconstriction was evaluated in a tissue bath station. The transcription factor NF-kB was evaluated by ELISA, and its gene expression and TLR-2, TLR-4, MMP-9, MMP-12, and TIMP by PCR. The probiotic Lr had a protective effect against the inflammatory responses induced by LPS. Lr significantly reduced pro-inflammatory cells in the airways, lung parenchyma, and blood leukocytes. Furthermore, Lr reduced the production of pro-inflammatory cytokines and chemokines in BALF and the expression of TLRs, MMPs, and NF-kB in lung tissue and maintained the expression of TIMP in treated animals promoting a protective effect on lung tissue. The results of the study indicate that pre-treatment with the probiotic Lr may be a promising way to mitigate lung inflammation in endotoxemia.

Introduction: We sought to evaluate the effects of a 12-week pulmonary rehabilitation (PR) program on lung function, mechanics, as well as pulmonary and systemic inflammation in a cohort of 33 individuals with moderate to severe post-COVID-19. Material and Methods: The pulmonary rehabilitation (PR) program employed a combination of aerobic and resistance exercises. Thirty minutes of treadmill training at 75% of the maximum heart rate, combined with 30 min resistance training consisting of 75% of one maximum repetition, three times a week throughout 12 weeks. Results: PR improved the lung function, FVC (p < 0.02), FEV1 (p < 0.02), FEV1/FVC (p < 0.01), MEF25% (p < 0.006), MEF50% (p < 0.03), and MEF75% (p < 0.02). PR also positively influenced lung mechanics, reducing respiratory impedance (Z5Hz, p < 0.03), respiratory reactance (X5Hz, p < 0.01), resistance of the entire respiratory system (R5Hz, p < 0.03), central airway resistance (RCentral, p < 0.03), and peripheral airway resistance (RPeripheral, p < 0.02). Moreover, muscle strength gains were evident, with significant improvements observed in hand grip strength for both the right (p < 0.02) and left (p < 0.01) hands, as well as maximal inspiratory (p < 0.02) and expiratory (p < 0.03) pressures. Additionally, PR exhibited anti-inflammatory effects by reducing the pro-inflammatory cytokines IL-1β (p < 0.0001) and IL-6 (p < 0.0001) and increasing the anti-inflammatory IL-1RA (p < 0.0004) and IL-10 (p < 0.003) and anti-viral IFN-γ (p < 0.0002) and IFN-β (p < 0.008) cytokines in breath condensate and serum samples. Conclusions: Collectively, these findings highlight the effectiveness of PR in ameliorating COVID-19 sequel across respiratory system, skeletal muscle, and immune responses. This highlights its promising potential as a therapeutic intervention for individuals recovering from COVID-19.

The oxidative stress caused by systemic inflammatory response syndrome (SIRS), septic shock, and sepsis, is a risk factor triggering an increase in mortality in patients diagnosed with these pathologies. Selenium (Se) is an essential mineral that has antioxidant and cytoprotective functions, being strongly associated with the proper functioning of intracellular metabolic processes. In this context, the present study aims to investigate de therapeutic effects of intravenous selenium use considering pathologies such as SIRS, septic shock, sepsis, acute respiratory distress syndrome (ARDS), ventilator associated pneumonia (VAP), and coronavirus disease (COVID-19). This is an narrative literature review in which six main articles found in databases of SciELO, PubMed, and Google Scholar, were selected and analyzed. As a result, articles were found evidencing the benefit of Se in the inflammatory response, increasing the GPx-3 activity and decreasing the inflammatory cytokines, in addition to generating a lower risk of VAP, shortening the hospitalization time, and mortality. Thus, Se supplementation has beneficial evidence for acute respiratory diseases and should be considered as a viable option as adjuvant therapy.

Background: Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the overproduction of white blood cells, leading to symptoms such as fatigue, infections, and other complications. CML patients must take measures to prevent infections to mitigate the exacerbation of cancer cell proliferation and comorbidities. Methods: This study investigated whether vitamin C can suppress the hyperinflammatory activation of K-562 cells induced by lipopolysaccharide (LPS) and whether purinergic signaling (ATP and P2X7 receptor) and autophagy play a role in it. Two different doses of vitamin C (5 µg/mL and 10 µg/mL) were employed, along with the lysosome inhibitor chloroquine (CQ; 100 µM), administered 2 h prior to LPS stimulation (10 ng/mL) for a duration of 22 h in K-562 cells (3 × 10⁵ cells/mL/well). Results: Both doses of vitamin C reduced the release of interleukin-6 (IL-6) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) and tumor necrosis factor (TNF) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) induced by LPS. Furthermore, in LPS + CQ-stimulated cells, vitamin C at a concentration of 10 µg/mL inhibited the expression of LC3-II (p < 0.05). Conversely, both doses of vitamin C led to the release of the anti-inflammatory cytokine interleukin-10 (IL-10) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01), while only the 10 µg/mL dose of vitamin C induced the release of Klotho (10 µg/mL, p < 0.01). In addition, both doses of vitamin C reduced the accumulation of ATP (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) and decreased the expression of the P2X7 receptor at the mRNA level. Conclusions: Vitamin C inhibits the hyperinflammatory state induced by LPS in K-562 cells, primarily by inhibiting the ATP accumulation, P2X7 receptor expression, and autophagy signaling.

Even after virus elimination, numerous sequelae of coronavirus disease 2019 (COVID-19) persist. Based on accumulating evidence, large amounts of proinflammatory cytokines are released to drive COVID-19 progression, severity, and mortality, and their levels remain elevated after the acute phase of COVID-19, playing a central role in the disease’ sequelae. In this manner, bronchial epithelial cells are the first cells hyperactivated by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), leading to massive cytokine release, triggering the hyperactivation of leukocytes and other cells, and mediating COVID-19 sequelae. Therefore, proinflammatory cytokine production is initiated by the host. This in vitro study tested the hypothesis that ImmuneRecov™, a nutritional blend, inhibits the SARS-CoV-2-induced hyperactivation of human bronchial epithelial cells (BEAS-2B). BEAS-2B (5x10⁴/mL/well) cells were cocultivated with 1 ml of blood from a SARS-CoV-2-infected patient for 4 h, and the nutritional blend (1 µg/mL) was added in the first minute of coculture. After 4 h, the cells were recovered and used for analyses of cytotoxicity with the (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) (MTT) assay and the expression of the IL-1β, IL-6, and IL-10 mRNAs. The supernatant was collected to measure cytokine levels. SARS-CoV-2 incubation resulted in increased levels of IL-1β and IL-6 in BEAS-2B cells (p < 0.001). Treatment with the nutritional blend resulted in reduced levels of the proinflammatory cytokines IL-1β and IL-6 (p < 0.001) and increased levels of the anti-inflammatory cytokine IL-10 (p < 0.001). Additionally, the nutritional blend reduced the expression of the IL-1β and IL-6 mRNAs in SARS-CoV-2-stimulated cells and increased the expression of the IL-10 and IFN-γ mRNAs. In conclusion, the nutritional blend exerts important anti-inflammatory effects on cells in the context of SARS-CoV-2 infection.