scholarly journals Protective Role of Interleukin-10 in Ozone-Induced Pulmonary Inflammation

2010 ◽  
Vol 118 (12) ◽  
pp. 1721-1727 ◽  
Author(s):  
Gillian S. Backus ◽  
Reuben Howden ◽  
Jennifer Fostel ◽  
Alison K. Bauer ◽  
Hye-Youn Cho ◽  
...  
Keyword(s):  
Pulmonary Inflammation ◽  
Interleukin 10 ◽  
Protective Role

scholarly journals PROTECTIVE ROLE OF CORTISTATIN IN PULMONARY INFLAMMATION AND FIBROSIS

2021 ◽  
Author(s):  
Margarita Barriga ◽  
Raquel Benitez ◽  
Viviane Ferraz‐de‐Paula ◽  
Marina Garcia‐Frutos ◽  
Marta Caro ◽  
...  
Keyword(s):  
Pulmonary Inflammation ◽  
Protective Role

P0523PROTECTIVE ROLE OF REGULATORY B CELLS ON THE RENAL TISSUE REPAIRMEN AFTER ISCHEMIA REPERCUSSION INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yokota Yunosuke ◽  
Goh Kodama ◽  
Sakuya Itou ◽  
Yosuke Nakayama ◽  
Nobukazu Komatsu ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Renal Function ◽  
B Cells ◽  
Interleukin 10 ◽  
Renal Tissue ◽  
Protective Role ◽  
Regulatory B Cells ◽  
Tubulointerstitial Injury ◽  
Iri Model

Abstract Background and Aims Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end- stage renal disease. It has been postulated that interleukin-10 (IL-10)-producing Regulatory B cells (Breg) play an important role for the tissue repairment in several tissues and organs. Basically, protective role of Breg has been reported in inflammatory bowel disease. In the kidney, it has been shown that IL-10 suppresses renal function decline and improves renal prognosis in IRI model, a typical model of AKI. However, the identity of Breg in the kidney and their origin have not been clarified. Further, how the Breg works during the transition from AKI to CKD is not known. Therefore, first we investigated whether Breg existed in renal tissue on the progression from AKI to CKD in IRI model mice. Further, we performed splenectomy, and examined the renal injury, Breg, and plasma IL-10 levels in this model. Method To examine the existence of Breg in the kidney of IRI model, we used 8-10 weeks-old GFP / IL-10 mice based on C57BL / 6J mice. They are reporter mice for IL-10 producing cells, and can visualize IL-10 producing cells under a fluorescence microscope without fluorescent immunostaining. We prepared following three groups, sham, IRI (unilateral), and IRI + SN (splenectomy) groups. Mice were anesthetized with chloral hydrate (4 g/kg,, intraperitoneal). After making a midline incision, exposed a blood vessel of the left renal pedicles and clamped it for 30 min by clips. one day, 7 days, and 14 days after the surgery, mice were sacrificed, and renal function and plasma IL-10 levels as well as tissue damages by PAS and Masson’s Trichrome staining were assessed. Tissue IL-10-producing cells were detected by flow cytometry. Results There was no difference of plasma IL-10 levels and renal tubulointerstitial injury in IRI group and IRI+SN group on day 1 after IRI. However, on day 7 and day 14, plasma IL-10 levels became gradually higher in IRI group, and SN decreased the increase in IL-10 levels. Tubulointerstitial injury was induced by IRI and SN further worsened tubular damages. Serum Cr and BUN levels were not different in three groups due to normal right kidney. On day 1, number of IL-10-producing B cells increased in the spleen and renal medulla in IRI group confirmed by flow cytometry, which was completely diminished by SN, suggesting that origin of the infiltrated Breg might be spleen, thereby being involved in the protective role in IRI injury in the kidney. Conclusion We report for the first time that Breg might be recruited from spleen by AKI, which may be one of the mechanisms to prevent the progression to CKD.

scholarly journals A Contemporary View of Natriuretic Peptides in the SARS-CoV-2 Era

2021 ◽  
Vol 12 ◽  
Author(s):  
Speranza Rubattu ◽  
Giovanna Gallo ◽  
Massimo Volpe
Keyword(s):  
Viral Infection ◽  
Natriuretic Peptides ◽  
Pulmonary Inflammation ◽  
Protective Role ◽  
Protective Effects ◽  
Cardiac Damage ◽  
Protective Function ◽  
Therapeutic Benefits ◽  
Prognostic Implications

The heart releases natriuretic peptides (NPs) which represent an important hormonal axis with cardiorenal protective effects. In view of their properties, NPs have pathophysiologic, diagnostic and prognostic implications in several cardiovascular diseases (CVDs). Severe pulmonary inflammation, as induced by the SARS-COV2, may increase pulmonary pressure with potential influence on NPs release, whereby normal cardiovascular integrity becomes impaired. Moreover, pre-existing CVDs are strong negative prognostic factors since they exacerbate the effects of the viral infection and lead to worse outcomes. In this context, it may be expected that NPs exert a key protective role toward the virus infection whereas an impairment of NPs release contributes to the virus deleterious effects. In this review article we explore the potential involvement of NPs in the COVID-19 disease. To this aim, we will first focus on the interactions between NPs and the Ang II/ATIR arm of the renin-angiotensin-aldosterone system (RAAS) as well as with the protective ACE2/Ang (1-7) arm of the RAAS. Subsequently, we will review evidence that strongly supports the role of increased NT-proBNP level as a marker of cardiac damage and of worse prognosis in the COVID-19 affected patients. Finally, we will discuss the potential therapeutic benefits of these protective hormones toward the viral infection through their endothelial protective function, anti-inflammatory and anti-thrombotic effects. In conclusion, the potential implications of NPs in the SARS-CoV-2 infection, as discussed in our article, represent an important issue that deserves to be fully investigated.

scholarly journals Protective Role of Interleukin-10 in Atherosclerosis

1999 ◽  
Vol 85 (8) ◽  
Author(s):  
Ziad Mallat ◽  
Sandrine Besnard ◽  
Micheline Duriez ◽  
Virginie Deleuze ◽  
Florence Emmanuel ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Protective Role

Protective role of interleukin-10-producing regulatory dendritic cells against murine autoimmune gastritis

2008 ◽  
Vol 43 (2) ◽  
pp. 100-107 ◽  
Author(s):  
Masamoto Torisu ◽  
Hidehiro Murakami ◽  
Fazle Akbar ◽  
Hidetaka Matsui ◽  
Yoichi Hiasa ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Interleukin 10 ◽  
Protective Role ◽  
Autoimmune Gastritis ◽  
Regulatory Dendritic Cells

scholarly journals The Correlation Between Interleukin-10 1082G/A Gene Polimorphism Late Onset with Nephrotoxicity Secondary to Antituberculosis Treatment in Multidrug Resistant Tuberculosis Patients

2019 ◽  
Vol 39 (4) ◽  
pp. 215-219
Author(s):  
Harsini Harsini ◽  
Reviono Reviono ◽  
Umarudin Umarudin
Keyword(s):  
Late Onset ◽  
Interleukin 10 ◽  
Multidrug Resistant ◽  
Protective Role ◽  
Tuberculosis Patients ◽  
Resistant Tuberculosis ◽  
Multidrug Resistant Tuberculosis ◽  
Antituberculosis Treatment ◽  
Mdr Tb

Backgrounds: Tuberculosis controlling programme has become more complex with MDR-TB problem. Interleukin 10 (IL-10) 1082G/A gene polimorphism correlates with IL-10 secretion as anti-inflammatory cytokine which plays important role in pathogenesis of MDR-TB infection. The management of MDR-TB which used aminoglycosides could cause nephrotoxic effect to the patients. The protective role of IL-10 from IL-10 1082 G/A genotype to nephrotoxicity due to kanamycin still becomes a prolem nowadays. Methods: This study was a retorspective cohort study of MDR-TB patients who underwent treatment in Dr. Moewardi Hospital in 2011-2015. Results: Subjects of the study were 89 MDR-TB patients with IL-10 1082 G/A genotype polimorphism. The proportions of IL-10 1082 G/A genotype were AA genotype of 13.48%, GG of 4.49%, and GA of 82.2%. Statistic test showed that the onset of nephrotoxicity in GG genotype was faster than GA and AA genotype Conclusions: Interleukin 10 1082 G/A gene polymorphism had no significant correlation with nephrotoxicity onset in MDR-TB patients treated with kanamycin in Dr. Moewardi hospital. (J Respir Indo. 2019; 39(4): 215-9)

scholarly journals Interleukin-4 and Interleukin-10 Are Involved in Host Resistance to Staphylococcus aureus Infection through Regulation of Gamma Interferon

2000 ◽  
Vol 68 (5) ◽  
pp. 2424-2430 ◽  
Author(s):  
Sanae Sasaki ◽  
Shinsuke Nishikawa ◽  
Tomisato Miura ◽  
Mayuko Mizuki ◽  
Kyogo Yamada ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Survival Rates ◽  
Interleukin 10 ◽  
Protective Role ◽  
Gamma Interferon ◽  
Interleukin 4 ◽  
T Helper 1 ◽  
Th2 Response ◽  
Ifn Γ

ABSTRACT Our previous study showed that gamma interferon (IFN-γ), a T-helper 1 (Th1)-type cytokine, plays a detrimental role inStaphylococcus aureus infection in mice. In this study, the role of Th2-type cytokines such as interleukin-4 (IL-4) and IL-10 inS. aureus infection was investigated. IL-10 mRNA was induced in parallel with IFN-γ in the spleens and kidneys of mice during S. aureus infection, whereas IL-4 mRNA was induced in the spleens but not in the kidneys of these animals. Spleen cells obtained from S. aureus-infected mice produced lower titers of IFN-γ and higher titers of IL-4 and IL-10 in response to heat-killed S. aureus than did those from uninfected mice. Administration of anti-IL-4 monoclonal antibody (MAb) or anti-IL-10 MAb inhibited the elimination of S. aureus cells from the kidneys of mice. IFN-γ mRNA expression was enhanced in the spleens of anti-IL-4 MAb- or anti-IL-10 MAb-treated mice and also in the kidneys of anti-IL-4 MAb-treated animals. Next, we evaluated the role of IFN-γ in S. aureus infection in IFN-γ−/−mice. An increase in survival rates, a decrease in bacterial numbers in the kidneys, and an amelioration of histologic abnormalities in these organs were observed in IFN-γ−/− mice compared with those in IFN-γ+/+ mice. Administration of MAb against IL-4 or IL-10 failed to affect bacterial growth in the spleens and kidneys of IFN-γ−/− mice irrespective of the expression of Th2 response. These results suggest that S. aureusinfection induced a Th2 response and that IL-4 and IL-10 might play a protective role through the regulation of IFN-γ in S. aureus infection.

scholarly journals The Role of IgG4 in the Fine Tuning of Tolerance in IgE-Mediated Allergy and Cancer

2020 ◽  
Vol 21 (14) ◽  
pp. 5017
Author(s):  
Rodolfo Bianchini ◽  
Sophia N. Karagiannis ◽  
Galateja Jordakieva ◽  
Erika Jensen-Jarolim
Keyword(s):  
Interleukin 10 ◽  
Structural Features ◽  
Protective Role ◽  
Fine Tuning ◽  
Healthy Human ◽  
Chronic Antigenic Stimulation ◽  
Cell Class ◽  
Serum Igg4 ◽  
Ige Mediated

Among the four immunoglobulin G (IgG) subclasses, IgG4 is the least represented in serum of a healthy human and it is considered an “odd” antibody. The IgG4 antibody has unique structural features that affect its biological function. These include the ability to undergo antigen-binding fragment (Fab)-arm exchange, to create fragment crystallizable (Fc) – Fc binding with other IgG4 and other IgG subclass antibodies, have a unique affinity profile for Fc gamma receptors (FcγRs) and no binding to complement component C1q. Altogether, these characteristics support anti-inflammatory roles of IgG4 leading to immune tolerance. Under conditions of chronic antigenic stimulation and Th2-type inflammation, both tissue and serum IgG4 levels are increased. This review seeks to highlight how in allergen immunotherapy IgG4 can confer a protective role as a “blocking” antibody and safeguard from subsequent allergen exposure, while IgG4 can confer immunomodulatory functions to support malignancy. While Th2 conditions drive polarization of macrophages to the M2a subtype, chronic antigen stimulation drives B cell class switching to IgG4 to further support phenotypical macrophage changes towards an M2b-like state. M2b-like macrophages can secrete chemokine (C-C motif) ligand 1 (CCL1) and interleukin-10 (IL-10) to support regulatory cell recruitment and to further shape a tolerogenic microenvironment. Thereby, IgG4 have a Janus-faced role, favorable in allergy but detrimental in cancer.

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