scholarly journals Immunostimulants in respiratory diseases: focus on Pidotimod

Author(s):  
Francesca Puggioni ◽  
Magna Alves-Correia ◽  
Manar-Farouk Mohamed ◽  
Niccolò Stomeo ◽  
Riccardo Mager ◽  
...  

Usefulness of Pidotimod and its role as immunostimulant, has been discussed, we know, for several decades. Nevertheless, there is still much to know. Understanding its mechanisms and its potential usefulness in airway infections and its prevention, asthma both Th2 and non Th2 type, bronchiectasis, as adjuvant in vaccination and in allergen immunotherapy still remains to clearly unveil. The aim of this paper was to provide a useful updated review of the role of the main available immunostimulants, giving particular focus on Pidotimod use and its potentials utility in respiratory diseases. Pidotimod showed its usefulness in reducing need for antibiotics in airway infections, increasing the level of immunoglobulins (IgA, IgM, IgG) and T-lymphocyte subsets (CD3+, CD4+) endowed with immunomodulatory activity that affect both innate and adaptive immune responses. Higher expression of TLR2 and of HLA-DR molecules, induction of dendritic cell maturation and release of pro-inflammatory molecules, stimulation of T lymphocyte proliferation and differentiation toward a Th1 phenotype, as well as an increase of the phagocytosis have been demonstrated to be associated with Pidotimod in in vitro studies. All these activities are potentially useful for several respiratory conditions such as asthma, COPD, and recurrent respiratory tract infections.

Apmis ◽  
1994 ◽  
Vol 102 (1-6) ◽  
pp. 371-380 ◽  
Author(s):  
RUBHANA Raqib ◽  
FINN P. Reinholt ◽  
PRADEEP KUMAR Bardhan ◽  
ANDERS KÄRnell ◽  
ALF A. Lindberg

LASER THERAPY ◽  
1998 ◽  
Vol 10 (4) ◽  
pp. 153-158 ◽  
Author(s):  
Atif Agaiby ◽  
Lucy Ghali ◽  
Mary Dyson

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5378-5378
Author(s):  
Minoo Battiwalla ◽  
Yiyuan Wu ◽  
Ryotaro Nakamura ◽  
Marija Radovic ◽  
Rajinder P.S. Bajwa ◽  
...  

Abstract Clinically significant cytomegalovirus (CMV) infection in allogeneic blood or marrow transplant recipients has dramatically declined in recent years by the strategy of early detection of reactivation and pre-emptive therapy with Ganciclovir (GCV). We have previously shown that even in the absence of overt CMV disease, persisting post-transplant antigenemia predicts for increased late relapse and treatment failure. (Nakamura, et al BBMT 2004) In other words, frequent CMV reactivation serves as a surrogate for impaired post-transplant immune reconstitution. To explain the observed association between CMV reactivation and relapse we also raised the possibility that several weeks of GCV therapy could exert a deleterious effect on a fragile immune system. Clinical association between GCV administration and impaired lymphocyte function has not received attention previously; perhaps because of confounding effects from the underlying conditions (HIV or post-transplant) that induce CMV reactivation. We examined the effect of GCV in vitro on normal human PBMCs. Human PBMCs were extracted from normal volunteers and subjected to mitogenic stimulation (PHA) in the absence or presence of varying concentrations of GCV. PHA-induced proliferation, measured by uptake of 3[H]-thymidine after 5 days incubation in RPMI-10% AB serum, was reduced by 35% at peak therapeutic concentrations (10mg/ml) of GCV as opposed to 73% by Tacrolimus (10ng/ml). GCV did not induce lymphocyte apoptosis in the presence or absence of stimulation. Flow cytometry-based BrdU incorporation assays show that GCV exerts a time-dependent impairment of DNA synthesis in lymphocytes. Collectively, these results show that GCV suppresses T-lymphocyte proliferation in vitro at therapeutic concentrations and the likely mechanism of action is inhibition of DNA synthesis. Further work is ongoing to evaluate the effect of GCV on proliferative responses to specific antigens and to confirm these effects in comparison to other drugs used in the transplant setting. Figure Figure


Medicine ◽  
2015 ◽  
Vol 94 (44) ◽  
pp. e1902 ◽  
Author(s):  
Jang-Hee Cho ◽  
Young-Deuk Yoon ◽  
Hye Min Jang ◽  
Eugene Kwon ◽  
Hee-Yeon Jung ◽  
...  

1983 ◽  
Vol 26 (1) ◽  
pp. 126-136 ◽  
Author(s):  
David S. Chudwin ◽  
Morton J. Cowan ◽  
Diane W. Wara ◽  
Arthur J. Ammann

1983 ◽  
Vol 157 (6) ◽  
pp. 1736-1745 ◽  
Author(s):  
W J Britt ◽  
B Chesebro

A Friend virus (FV)-specific T lymphocyte proliferation assay was used to compare the T lymphocyte responses of H-2 congenic mice that differed in their ability to recover from FV leukemia after inoculation of high virus doses. Gene(s) of the H-2D region influenced the kinetics of this response such that H-2Db/b homozygous mice were positive 6-8 d earlier than H-2Dd/b mice. This correlated with the Rfv-1, H-2D-linked influence on recovery from FV by these mice, and also appeared to explain the prominent effect of virus dose on recovery incidence. These findings were supported by the ability of passively transferred immune splenic T lymphocytes to induce recovery from leukemia at 6 d after FV inoculation, but not at 16 d. H-2a/a mice were found to be unresponsive in the FV-specific T lymphocyte proliferation assay. This effect mapped to the left of H-2D, possibly in the H-2I region, and may be an in vitro manifestation of the Rfv-2 gene. No evidence for nonspecific immunosuppression of the T lymphocyte response to concanavalin A was observed in any of the H-2 congenic F1 mice studied.


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