scholarly journals Detection of Cytokines and Collectins in Bronchoalveolar Fluid Samples of Patients Infected with Histoplasma capsulatum and Pneumocystis jirovecii

2021 ◽  
Vol 7 (11) ◽  
pp. 938
Author(s):  
Laura E. Carreto-Binaghi ◽  
Eda P. Tenorio ◽  
Fernando R. Morales-Villarreal ◽  
El Moukhtar Aliouat ◽  
Edgar Zenteno ◽  
...  
Keyword(s):  
Histoplasma Capsulatum ◽  
Fungal Infections ◽  
Protein A ◽  
Immunological Response ◽  
Surfactant Protein ◽  
Pneumocystis Jirovecii ◽  
Hiv Patients ◽  
Tnf Α ◽  
Bronchoalveolar Fluid ◽  
Ifn Γ

Histoplasmosis and pneumocystosis co-infections have been reported mainly in immunocompromised humans and in wild animals. The immunological response to each fungal infection has been described primarily using animal models; however, the host response to concomitant infection is unknown. The present work aimed to evaluate the pulmonary immunological response of patients with pneumonia caused either by Histoplasma capsulatum, Pneumocystis jirovecii, or their co-infection. We analyzed the pulmonary collectin and cytokine patterns of 131 bronchoalveolar lavage samples, which included HIV and non-HIV patients infected with H. capsulatum, P. jirovecii, or both fungi, as well as healthy volunteers and HIV patients without the studied fungal infections. Our results showed an increased production of the surfactant protein-A (SP-A) in non-HIV patients with H. capsulatum infection, contrasting with HIV patients (p < 0.05). Significant differences in median values of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, IL-33, IL-13, and CXCL8 were found among all the groups studied, suggesting that these cytokines play a role in the local inflammatory processes of histoplasmosis and pneumocystosis. Interestingly, non-HIV patients with co-infection and pneumocystosis alone showed lower levels of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, and IL-23 than histoplasmosis patients, suggesting an immunomodulatory ability of P. jirovecii over H. capsulatum response.

scholarly journals The Significance of KL-6 as Prognosis Monitoring Biomarker in Patients With Severe COVID-19 From Stabilized Stage Toward Convalescence

2021 ◽  
Author(s):  
Long He ◽  
Liu Lu ◽  
Ming Zong ◽  
Huang Zhou ◽  
Lan Wang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protein A ◽  
Alveolar Epithelium ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Monocyte Count ◽  
Type Ii ◽  
Tnf Α ◽  
Ifn Γ ◽  
Blood Routine

Abstract Background: This study aims to identify some biomarkers for monitoring the recovery of lung injury in severe COVID-19 patients from stabilized stage toward convalescence.Methods: We enrolled participants who diagnosed with severe COVID-19 (n = 28) and health volunteers (n = 25) from Taikang Tongji (Wuhan) Hospital. The patients were in a stabilized stage and had a course of 48.1±12.8 days. We followed these patients for 90 days. The blood routine, cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-17A, TNF-α, IFN-α, IFN-γ), type II alveolar epithelium injury indicators (Surfactant protein A (SP-A), Krebs von den Lungen-6 (KL-6)) and chest CT were tested on the 1, 30, 60, and 90 days after enrollment. Results: In stabilized stage, the parameters of blood routine and some cytokines (IL-1β, IL-2, IL-4, IL-12p70, TNF-α) had bounced back to normal (p>0.05). Some cytokines (IL-5, IL-6, IL-10, IL-17A, IFN-α, IFN-γ) and type II alveolar epithelium injury indicators (SP-A and KL-6) were still higher than normal (p<0.05). During the stabilized stage to convalescence, in spite of the variation of monocyte count, monocyte/lymphocyte ratio, IL-5, IL-10, IL-12p70, IL-17A, IFN-γ, IFN-α, SP-A and KL-6 were downward trend (p<0.05), only KL-6 level (p<0.05) could simultaneously reflect the lung injury volume which be measured by CT. Conclusions: Our preliminary data indicated that KL-6 could be an effective prognostic biomarker for monitoring the recovery of lung function in patients with severe COVID-19 from stabilized stage toward convalescence.

scholarly journals High Levels of TNF-α and TIM-3 as a Biomarker of Immune Reconstitution Inflammatory Syndrome in People with HIV Infection

Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 527
Author(s):  
Lucero A. Ramon-Luing ◽  
Ranferi Ocaña-Guzman ◽  
Norma A. Téllez-Navarrete ◽  
Mario Preciado-García ◽  
Dámaris P. Romero-Rodríguez ◽  
...  
Keyword(s):  
Immune Reconstitution Inflammatory Syndrome ◽  
Immune Reconstitution ◽  
Control Group ◽  
Hiv Patients ◽  
Art Initiation ◽  
Tnf Α ◽  
Ifn Γ ◽  
Α Level ◽  
Inflammatory Syndrome

Immune reconstitution inflammatory syndrome (IRIS) is an exacerbated immune response that can occur to HIV+ patients after initiating antiretroviral therapy (ART). IRIS pathogenesis is unclear, but dysfunctional and exhausted cells have been reported in IRIS patients, and the TIM-3/Gal-9 axis has been associated with chronic phases of viral infection. This study aimed to evaluate the soluble levels of TIM-3 and Gal-9 and their relationship with IRIS development. TIM-3, Gal-9, TNF-α, IFN-γ, IL-6, TNFR1, TNFR2, E-cadherin, ADAM10, and ADAM17 were measured to search for IRIS-associated biomarkers in plasma samples from 0-, 4-, 8-, 12-, and 24-weeks after ART initiation of 61 HIV+ patients (15 patients developed IRIS, and 46 did not). We found that patients who developed IRIS had higher levels of TIM-3 [median 4806, IQR: 3206–6182] at the time of the IRIS events, compared to any other follow-up time evaluated in these patients or compared with a control group of patients who did not develop IRIS. Similarly, IRIS patients had a higher TNF-α level [median 10.89, IQR: 8.36–12.34] at IRIS events than any other follow-up time evaluated. Other molecules related to the TIM-3 and TNF-α pathway (Gal-9, IL-6, IFN-γ, TNFR1, TNFR2, ADAM-10, and ADAM-17) did not change during the IRIS events. In conclusion, our data suggest that a high level of soluble TIM-3 and TNF-α could be used as an IRIS biomarker.

scholarly journals Distinguishable Immunologic Characteristics of COVID-19 Patients with Comorbid Type 2 Diabetes Compared with Nondiabetic Individuals

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ruxing Zhao ◽  
Yujing Sun ◽  
Yongyuan Zhang ◽  
Weili Wang ◽  
Shouyu Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immunological Response ◽  
Clinical Severity ◽  
Blood Levels ◽  
Immunological Parameters ◽  
Global Pandemic ◽  
Tnf Α ◽  
Significant Difference ◽  
Ifn Γ

Background. COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has threatened every civilian as a global pandemic. The immune system poses the critical interactive chain between the human body and the virus. Here, we make efforts to examine whether comorbidity with type 2 diabetes (T2D) affects the immunological response in COVID-19 patients. Methods. We conducted a retrospective pilot study investigating immunological characteristics of confirmed cases of COVID-19 with or without comorbid T2D. Two subcohorts of sex- and age-matched participants were eligible for data analysis, of which 33 participants were with T2D and the remaining 37 were nondiabetic (NDM). Cellular immunity was assessed by flow cytometric determination of surface markers including CD3, CD4, CD8, CD19, CD16, and CD56 in peripheral blood. Levels of C reactive protein, immunoglobulin (IgG, IgM, IgA, and IgE), and complements (C3, C4) were detected by rate nephelometry immunoassay. And Th1/Th2 cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, and IFN-γ) were detected by Cytometric Bead Array. Results. Neutrophil counts were found to be significantly higher in the T2D group than in the NDM group and had a significant relevance with clinical severity. Lymphocyte frequencies showed no significant differences in the two groups. However, the proportions and absolute counts of T, Tc, Th, and NK cells decreased in both groups to different degrees. An abnormal increase in neutrophil count and a decrease in lymphocyte subpopulations may represent risk factors of COVID-19 severity. The level of IgG, IgM, IgA, C3, and C4 showed no significant difference between the two groups, while the IgE levels were higher in the T2D group than in the NDM group ( p < 0.05 ). Th1 cytokines including IFN-γ, TNF-α, and IL-6, as well as CRP, appeared significantly higher in the T2D group. Conclusions. The COVID-19 patients comorbid with T2D demonstrated distinguishable immunological parameters, which represented clinical relevancies with the predisposed disease severity in T2D.

Comparison of SP-A and LPS effects on the THP-1 monocytic cell line

2000 ◽  
Vol 279 (1) ◽  
pp. L110-L117 ◽  
Author(s):  
Mingchen Song ◽  
David S. Phelps
Keyword(s):  
Protein A ◽  
Surfactant Protein ◽  
Polymyxin B ◽  
Inhibitory Effects ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Monocytic Cells ◽  
Similar Treatment ◽  
Tnf Α ◽  
Factor Α

Surfactant protein A (SP-A) increases production of proinflammatory cytokines by monocytic cells, including THP-1 cells, as does lipopolysaccharide (LPS). Herein we report differences in responses to these agents. First, polymyxin B inhibits the LPS response but not the SP-A response. Second, SP-A-induced increases in tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-8 are reduced by >60% if SP-A is preincubated with Survanta (200 μg/ml) for 15 min before addition to THP-1 cells. However, the LPS effects on TNF-α and IL-8 are inhibited by <20% and the effect on IL-1β by <50%. Third, at Survanta levels of 1 mg/ml, SP-A-induced responses are reduced by >90%, and although the inhibitory effects on LPS action increase, they still do not reach those seen with SP-A. Finally, we tested whether SP-A could induce tolerance as LPS does. Pretreatment of THP-1 cells with LPS inhibits their response to subsequent LPS treatment 24 h later, including TNF-α, IL-1β, and IL-8. Similar treatment with SP-A reduces TNF-α, but IL-1β and IL-8 are further increased by the second treatment with SP-A rather than inhibited as with LPS. Thus, whereas both SP-A and LPS stimulate cytokine production, their mechanisms differ with respect to inhibition by surfactant lipids and in ability to induce tolerance.

scholarly journals Histoplasma capsulatum and Pneumocystis jirovecii coinfection in hospitalized HIV and non-HIV patients from a tertiary care hospital in Mexico

2019 ◽  
Vol 86 ◽  
pp. 65-72 ◽  
Author(s):  
Laura E. Carreto-Binaghi ◽  
Fernando R. Morales-Villarreal ◽  
Guadalupe García-de la Torre ◽  
Tania Vite-Garín ◽  
Jose-Antonio Ramirez ◽  
...  
Keyword(s):  
Histoplasma Capsulatum ◽  
Tertiary Care Hospital ◽  
Tertiary Care ◽  
Pneumocystis Jirovecii ◽  
Care Hospital ◽  
Hiv Patients

scholarly journals Pulmonary surfactant protein A and surfactant lipids upregulate IRAK-M, a negative regulator of TLR-mediated inflammation in human macrophages

2012 ◽  
Vol 303 (7) ◽  
pp. L608-L616 ◽  
Author(s):  
Huy A. Nguyen ◽  
Murugesan V. S. Rajaram ◽  
Douglas A. Meyer ◽  
Larry S. Schlesinger
Keyword(s):  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Protein A ◽  
Surfactant Protein ◽  
Negative Regulator ◽  
Surfactant Protein A ◽  
Proinflammatory Cytokine Production ◽  
Human Macrophages ◽  
Tnf Α

Alveolar macrophages (AMs) are exposed to frequent challenges from inhaled particulates and microbes and function as a first line of defense with a highly regulated immune response because of their unique biology as prototypic alternatively activated macrophages. Lung collectins, particularly surfactant protein A (SP-A), contribute to this activation state by fine-tuning the macrophage inflammatory response. During short-term (10 min–2 h) exposure, SP-A's regulation of human macrophage responses occurs through decreased activity of kinases required for proinflammatory cytokine production. However, AMs are continuously exposed to surfactant, and the biochemical pathways underlying long-term reduction of proinflammatory cytokine activity are not known. We investigated the molecular mechanism(s) underlying SP-A- and surfactant lipid-mediated suppression of proinflammatory cytokine production in response to Toll-like receptor (TLR) 4 (TLR4) activation over longer time periods. We found that exposure of human macrophages to SP-A for 6–24 h upregulates expression of IL-1 receptor-associated kinase M (IRAK-M), a negative regulator of TLR-mediated NF-κB activation. Exposure to Survanta, a natural bovine lung extract lacking SP-A, also enhances IRAK-M expression, but at lower magnitude and for a shorter duration than SP-A. Surfactant-mediated upregulation of IRAK-M in macrophages suppresses TLR4-mediated TNF-α and IL-6 production in response to LPS, and IRAK-M knockdown by small interfering RNA reverses this suppression. In contrast to TNF-α and IL-6, the surfactant components upregulate LPS-mediated immunoregulatory IL-10 production, an effect reversed by IRAK-M knockdown. In conclusion, these data identify an important signaling regulator in human macrophages that is used by surfactant to control the long-term alveolar inflammatory response, i.e., enhanced IRAK-M activity.

scholarly journals Surfactant Protein A Prevents IFN-γ/IFN-γ Receptor Interaction and Attenuates Classical Activation of Human Alveolar Macrophages

2016 ◽  
Vol 197 (2) ◽  
pp. 590-598 ◽  
Author(s):  
Carlos M. Minutti ◽  
Belén García-Fojeda ◽  
Alejandra Sáenz ◽  
Mateo de las Casas-Engel ◽  
Raquel Guillamat-Prats ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Receptor Interaction ◽  
Classical Activation ◽  
Human Alveolar Macrophages ◽  
Ifn Γ

Phytic acid modulates the morphology, immunological response of cytokines and β-defensins in porcine intestine exposed to deoxynivalenol and fumonisin B1

2021 ◽  
pp. 1-10
Author(s):  
E.O. da Silva ◽  
J.P. Santos ◽  
A.T. Morey ◽  
L.M. Yamauchi ◽  
A.P.F.R. Loureiro Bracarense
Keyword(s):  
Phytic Acid ◽  
Morphological Changes ◽  
Animal Health ◽  
Fumonisin B1 ◽  
Immunological Response ◽  
Beneficial Effects ◽  
Intestinal Lesions ◽  
Tnf Α ◽  
Ifn Γ ◽  
Necrosis Factor

Occurrence of mycotoxins in agricultural products represents a risk for human and animal health. Therefore, there is a requirement of strategies to mitigate their harmful impacts. This study investigated the effects of phytic acid (IP6) on the immunological response of pro-(interleukin (IL)-1β, IL-6, IL-8, IL-10, interferon (IFN)-γ, tumour necrosis factor (TNF)-α) and anti-inflammatory (IL-10) cytokines and β-defensins 1 (pBD-1) and 2 (pBD-2) in porcine jejunal explants exposed to deoxynivalenol (DON) and fumonisin B1 (FB1). The explants were exposed to the following treatments: control, DON (10 μM), DON plus IP6 2.5 mM or 5 mM, FB1 (70 μM), FB1 IP6 plus 2.5 or 5 mM. The expression levels of the cytokines were measured by RT-qPCR. The exposure to FB1 and DON induced intestinal lesions. The presence of 2.5 and 5 mM IP6 inhibited the morphological changes induced by the mycotoxins. The explants exposed to DON showed an increase in the expression of IL-1β and IL-8 and a decrease in the levels of IL-6, IFN-γ, IL-10 and pBD-2. IP6 (5 mM) decreased the expression of IL-8 and increased the expression in pBD-1 and 2 compared to DON alone. FB1 induced a significant decrease in the levels of most of the pro-inflammatory cytokines, IL-10 and pBD-1, and an increase in IL-1β expression. The addition of IP6 5 mM induced significant increase in TNF-α expression compared to FB1. Taken together, the results suggest IP6 modulates immunological changes induced by DON and FB1 on intestinal mucosa resulting in beneficial effects that contribute to intestinal homeostasis and health.

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