scholarly journals Timely and early respiratory rehabilitation in patients with covid 19 pneumonia in a referral hospital

2021 ◽  
Vol 21 (4) ◽  
pp. 887-889
Author(s):  
Antonio O. Morales Avalos ◽  
Felix K. Llanos Tejada ◽  
Juan A. Salas Lopez ◽  
Aldo R. Casanova Mendoza

SARS-CoV-2 is a beta-coronavirus of the same subgenus as SARS and MERS viruses, they share the same gene binding receptor, angiotensin converting enzyme (ACE2). (1) The spectrum of disease severity is varied, with the mild form being the most frequent (81%), and severe disease present in 14% of cases, with critical presentation being present in 5%, with a mortality of 2.3%.(2) The post-pneumonia respiratory sequela caused by beta-Coronaviruses is diffuse alveolar damage with fibrotic lesions; the pathophysiological mechanism is multifactorial, which involves activation of transforming growth factor beta (TGF-β)(3), IL1, IL6, MCP1 and TNF-α secondary to epithelial injury and subsequent inflammation. In addition, exposure to high O2 concentrations and effects of barotrauma, caused by advanced oxygen/ventilatory support, activate the pro-fibrotic TGF-β pathway, resulting in aberrant repair characterized by exaggerated deposition of fibroblasts, myofibroblasts and collagen. Forty-seven percent and 25% of patients who survive moderate to severe COVID-19 pneumonia have decreased carbon monoxide diffusion and predicted total lung capacity, respectively. (4)

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Jing-Wen Xu ◽  
Yun-Lun Li ◽  
Shi-Jun Zhang ◽  
Wen-Qing Yang ◽  
Wen-Ting Nie ◽  
...  

Essential hypertension (EH) is a risk factor for some severe diseases. This study aimed to screen out serum special proteins and seek interaction between them, which would provide new therapeutic targets and elucidate the comprehensive pathophysiological mechanism for EH. Patients with EH (Group A, n=47) and healthy controls (HC) (Group B, n=47) were recruited in this study. Serums from the two groups were analyzed with isobaric tags for relative and absolute quantitation coupled two-dimensional liquid chromatography followed by electrospray ionization-tandem mass spectrometry technique, while the candidate special proteins were verified with ELISA and western blot. A total of 404 proteins were identified, of which 30 proteins were upregulated (>1.2-fold, p<0.05) and 81 proteins were downregulated (<0.833-fold, p<0.05) compared with HC group. With GO, KEGG analysis, and literature retrieval, 4 proteins, cathepsin G, transforming growth factor beta-1, hyaluronidase-1, and kininogen-1, were found jointly involved in the renin-angiotensin-aldosterone system and kallikrein-kinin system. The profiles of these 4 candidate proteins were confirmed with ELISA and western blot. The concentration variation of these 4 proteins could better predict the occurrence and illustrate the pathophysiological mechanism of EH. And their discovery may help pave the way for exploring new therapies of EH.


2014 ◽  
Vol 5 (4) ◽  
pp. 409-419 ◽  
Author(s):  
R.S. Steinberg ◽  
M. Lima ◽  
N.L. Gomes de Oliveira ◽  
A. Miyoshi ◽  
J.R. Nicoli ◽  
...  

The effect of intestinal colonisation on the immune system was investigated in germ-free mice monoassociated with Lactobacillus strains isolated from calf faeces. Single doses of Lactobacillus acidophilus L36 or Lactobacillus salivarius L38 were administered to germ-free mice by intragastric gavage. Ten days later, the mice were euthanised. Gene expression levels of interleukin 5 (IL-5), IL-6, IL-10, IL-12b, IL-17a, gamma interferon (IFN-γ), transforming growth factor beta 1 (TGF-β1), and tumour necrosis factor alpha (TNF-α) were quantified in segments of the small and large intestines by real time quantitative polymerase chain reaction. All the mice were colonised rapidly after Lactobacillus administration with intestinal counts ranging from 6.53 to 8.26 log cfu/g. L. acidophilus L36 administration increased the expression of cytokines involved with the Th2 (IL-5, IL-6 and TGF-β1) and Th17 (IL-17a, TNF-α and IL-6) inflammatory response, whereas L. salivarius L38 appeared to stimulate a pattern of less diversified cytokines in the intestine. Intragastric gavage of L. acidophilus L36 and L. salivarius L38 induced similar levels of colonisation in the digestive tracts of germ-free mice but stimulated different immune responses in the intestinal mucosa. The different immunomodulation patterns might facilitate the potential use of these lactobacilli as probiotics to treat distinct pathological conditions, for example protection against Citrobacter rodentium infection by stimulating IL-17 production.


2020 ◽  
Author(s):  
Caroline Busatta Vaz de Paula ◽  
Marina Luise Viola Azevedo ◽  
Seigo Nagashima ◽  
Ana Paula Camargo Martins ◽  
Mineia Alessandra Scaranello Malaquias ◽  
...  

Abstract Background: The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification.Objective: To analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury.Methods: Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC).Results and conclusion: Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages was observed in the COVID-19 group when compared to both the H1N1 and the CONTROL groups. Different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-COV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. The understanding and management of the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.


Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1158
Author(s):  
Wei Chen ◽  
Prabhu Balan ◽  
David G. Popovich

Pro-inflammatory cytokines and anti-inflammatory cytokines are important mediators that regulate the inflammatory response in inflammation-related diseases. The aim of this study is to evaluate different New Zealand (NZ)-grown ginseng fractions on the productions of pro-inflammatory and anti-inflammatory cytokines in human monocytic THP-1 cells. Four NZ-grown ginseng fractions, including total ginseng extract (TGE), non-ginsenoside fraction extract (NGE), high-polar ginsenoside fraction extract (HPG), and less-polar ginsenoside fraction extract (LPG), were prepared and the ginsenoside compositions of extracts were analyzed by HPLC using 19 ginsenoside reference standards. The THP-1 cells were pre-treated with different concentrations of TGE, NGE, HPG, and LPG, and were then stimulated with lipopolysaccharide (LPS). The levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and anti-inflammatory cytokines, such as interleukin-10 (IL-10), and transforming growth factor beta-1 (TGF-β1), were determined by enzyme-linked immunosorbent assay (ELISA). TGE at 400 µg/mL significantly inhibited LPS-induced TNF-α and IL-6 productions. NGE did not show any effects on inflammatory secretion except inhibited IL-6 production at a high dose. Furthermore, LPG displayed a stronger effect than HPG on inhibiting pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) productions. Particularly, 100 µg/mL LPG not only significantly inhibited the production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, but also remarkably enhanced the production of anti-inflammatory cytokine IL-10. NZ-grown ginseng exhibited anti-inflammatory effects in vitro, which is mainly attributed to ginsenoside fractions (particularly less-polar ginsenosides) rather than non-saponin fractions.


1998 ◽  
Vol 66 (8) ◽  
pp. 3562-3568 ◽  
Author(s):  
Guixiang Dai ◽  
David N. McMurray

ABSTRACT Protein malnutrition leads to multiple detrimental alterations of host immune responses to mycobacterial infection. In this study, we demonstrated that splenocytes from low-protein (LP) guinea pigs vaccinated 6 weeks previously with attenuated Mycobacterium tuberculosis H37Ra failed to control the accumulation of virulentM. tuberculosis H37Rv in cocultured autologous peritoneal macrophages, despite the fact that they were able to control the accumulation of virulent tubercle bacilli in cocultured syngeneic peritoneal macrophages from normally nourished guinea pigs as successfully as did those from high-protein (HP) counterparts. Vaccine-induced growth control of virulent M. tuberculosisH37Rv in these cocultures appeared to be mediated by CD4 lymphocytes but not CD8 cells. Tuberculin (purified protein derivative [PPD])-induced lymphoproliferation was markedly impaired in vaccinated LP guinea pigs, and the depletion of CD4 lymphocytes significantly decreased lymphocyte proliferation whereas CD8 cell depletion did not. Protein malnutrition also impaired the abilities of cells from vaccinated LP guinea pigs to produce cytokines, including interferon, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β), in response to PPD, despite the demonstration of higher serum levels of TNF-α and TGF-β after an intravenous injection of PPD into LP guinea pigs. In contrast, peritoneal macrophages from protein-malnourished guinea pigs produced a higher level of TGF-β 4 days after infection in vitro with M. tuberculosis H37Rv than did those from protein adequate controls. These results suggest that dietary protein malnutrition impairs vaccine-induced resistance to M. tuberculosis, in part, by altering the cytokine profile to favor macrophage deactivation.


2021 ◽  
Vol 31 (3) ◽  
pp. 311-319
Author(s):  
A. A. Dei ◽  
B. I. Geltser ◽  
M. V. Antonyuk ◽  
T. A. Gvozdenko ◽  
E. P. Kalinina ◽  
...  

Aim. Assessment of the role of cytokine-mediated changes in the development of respiratory muscle (RM) dysfunction in patients with community-acquired pneumonia (СAP). Methods. 84 men aged 18 – 26 years with a median of age 19.5 [18.4; 22.8]. Mild to moderate CAP (MCAP) was diagnosed in 62 (73.8%) patients and severe (SCAP) in 22 (26.2%). The expiratory (MEP, MRPDout) and inspiratory (MIP, MRPDin. SNIP) strength indices of RM were recorded on a MicrоRPM apparatus (CareFusion, UK). The severity of endogenous intoxication was verified using the following indices: hematologic (HII), leukocyte (LII), and nuclear. Serum concentrations of interleukins-2, -8, -10, basic fibroblast growth factor, transforming growth factor-beta, tumor necrosis factor-alpha (TNF-α), and a soluble receptor for TNF-α. Data processing was performed by cluster and correlation analysis methods. Results. Three clusters of patients with CAP were identified by the characteristic combinations of indicators of RM strength, endogenous intoxication, and cytokine status. The first cluster had MCAP, the second – both MCAP and SCAP, the third – SCAP. In the first cluster, dysfunction of expiratory RM prevailed, and in the second and third – dysfunction of inspiratory RM. In the midst of CAP, significant negative correlations of RM strength indicators with LII, HII, TNF-α, IL-10, IL-8, and IL-2 levels were recorded. The endogenous intoxication indices reached control values in all patients during recovery. The first cluster showed a decrease in the level of analyzed cytokines against isolated dysfunction of expiratory RM. The second cluster showed a tendency toward restoration of TNF-α and IL-8 levels, and only their SNIP index was normal. The third cluster showed minimal medians of RM strength against the continuing imbalance in the profile of pro- and anti-inflammatory cytokines during recovery. Conclusion. RM dysfunction in CAP is associated with cytokine-mediated dysfunction. The degree of cytokine involvement in this process depends on the severity of endogenous intoxication and the volume of alveolar inflammation.


2012 ◽  
Vol 40 (02) ◽  
pp. 295-308 ◽  
Author(s):  
Yan Liu ◽  
Hui Zhao ◽  
Jie Zhang ◽  
Ping Zhang ◽  
Ming Li ◽  
...  

The regulatory effect of Liuwei Dihuang Pills (LDP) was studied on cytokines in mice with experimental autoimmune encephalomyelitis (EAE), a model for human multiple sclerosis (MS), induced by immunization with MOG35-55 and complete Freund's adjuvant (CFA) supplemented with pertussis toxin (PTX). LDP was administrated orally for 40 days, and prednisone acetate (PA) was used as a control. The pathological changes in the spinal cords of mice were observed by light microscope with hematoxylin-eosin (HE) staining and transmission electron microscope (TEM). The protein and mRNA expression of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) in the spinal cords were assessed by immunohistochemistry and RT-PCR assay, and the cyclic adenosine monophosphate (cAMP) in mice plasma was measured by radioimmunoassay (RIA) on days 12, 25 and 40 post-immunization (PI). The results showed that inflammatory cells, demyelination and axonal loss were reduced, and that the protein and mRNA expression of TNF-α and the ratio of TNF-α/TGF-β were obviously decreased, to different extents. However, the levels of cAMP were enhanced in LDP-treated groups. These findings suggested that LDP regulates the cytokine balance in favor of T helper 1 (Th1)/regulatory T (Treg) cells, which depend on enhancement of cAMP levels. LDP has a potential role in the treatment of MS and other demyelinating diseases of the central nervous system.


2020 ◽  
Vol 9 (12) ◽  
pp. 4010
Author(s):  
Li-Han Hsu ◽  
Thomas C. Soong ◽  
Nei-Min Chu ◽  
Chung-Yu Huang ◽  
Shu-Huei Kao ◽  
...  

Patients with malignant pleural effusion (MPE) who underwent successful pleurodesis survive longer than those for whom it fails. We hypothesize that the therapy-induced inflammatory responses inhibit the cancer progression, and thereby lead to a longer survival. Thirty-three consecutive patients with MPE that were eligible for bleomycin pleurodesis between September 2015 and December 2017 were recruited prospectively. Nineteen patients (57.6%) achieved fully or partially successful pleurodesis, while 14 patients either failed or survived less than 30 days after pleurodesis. Two patients without successful pleurodesis were excluded because of missing data. Interleukin (IL)-1 beta, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor in the pleural fluid were measured before, and after 3 and 24 h of pleurodesis. Their pleurodesis outcome and survival were monitored and analyzed. Patients who underwent successful pleurodesis had a longer survival rate. Patients without successful pleurodesis had significantly higher TNF-α and IL-10 levels in their pleural fluid than in the successful patients before pleurodesis. Following pleurodesis, there was a significant increment of IL-10 in the first three hours in the successful patients. In contrast, significant increments of TNF-α and IL-10 were found in the unsuccessful patients between 3 and 24 h after pleurodesis. The ability to produce specific cytokines in the pleural space following pleurodesis may be decisive for the patient’s outcome and survival. Serial measurement of cytokines can help allocate the patients to adequate treatment strategies. Further study of the underlying mechanism may shed light on cytokine therapies as novel approaches.


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