scholarly journals The Mycobacterium tuberculosis PE_PGRS Protein Family Acts as an Immunological Decoy to Subvert Host Immune Response

2022 ◽  
Vol 23 (1) ◽  
pp. 525
Author(s):  
Tarina Sharma ◽  
Anwar Alam ◽  
Aquib Ehtram ◽  
Anshu Rani ◽  
Sonam Grover ◽  
...  

Mycobacterium tuberculosis (M.tb) is a successful pathogen that can reside within the alveolar macrophages of the host and can survive in a latent stage. The pathogen has evolved and developed multiple strategies to resist the host immune responses. M.tb escapes from host macrophage through evasion or subversion of immune effector functions. M.tb genome codes for PE/PPE/PE_PGRS proteins, which are intrinsically disordered, redundant and antigenic in nature. These proteins perform multiple functions that intensify the virulence competence of M.tb majorly by modulating immune responses, thereby affecting immune mediated clearance of the pathogen. The highly repetitive, redundant and antigenic nature of PE/PPE/PE_PGRS proteins provide a critical edge over other M.tb proteins in terms of imparting a higher level of virulence and also as a decoy molecule that masks the effect of effector molecules, thereby modulating immuno-surveillance. An understanding of how these proteins subvert the host immunological machinery may add to the current knowledge about M.tb virulence and pathogenesis. This can help in redirecting our strategies for tackling M.tb infections.

Author(s):  
Sebastian Wawrocki ◽  
Magdalena Druszczynska

The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.


2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Alessandra Siracusano ◽  
Antonella Teggi ◽  
Elena Ortona

Cystic echinococcosis (CE) is a widespread chronic endemic helminthic disease caused by infection with metacestodes of the tapewormEchinococcus granulosus. CE affects humans and has a worldwide prevalence of approximately six million. In this review, we discuss current findings in diagnosis and clinical management of CE and new concepts relating toE. granulosusmolecules that directly modulate the host immune responses favouring a strong anti-inflammatory response and perpetuating parasite survival in the host. New insights into the molecular biology ofE. granulosuswill improve considerably our knowledge of the disease and will provide new potential therapeutic applications to treat or prevent inflammatory immune-mediated disease.


2012 ◽  
Vol 109 (20) ◽  
pp. 7729-7734 ◽  
Author(s):  
K. H. Kim ◽  
D. R. An ◽  
J. Song ◽  
J. Y. Yoon ◽  
H. S. Kim ◽  
...  

2019 ◽  
Author(s):  
Gabriele Pollara ◽  
Carolin T Turner ◽  
Gillian S Tomlinson ◽  
Lucy CK Bell ◽  
Ayesha Khan ◽  
...  

AbstractHost immune responses at the site of Mycobacterium tuberculosis (Mtb) infection serve to contain the pathogen, but also mediate the pathogenesis of tuberculosis (TB) and onward transmission of infection. Interferon gamma (IFNγ) responses do not discriminate between protection and pathogenicity, but IL-17A/F responses, known to drive pathology in diverse chronic inflammatory diseases, have also been associated with TB pathogenesis in animal models. At the site of in vivo immune recall responses to Mtb modelled by the tuberculin skin test, we show for the first time that active TB in humans is also associated with exaggerated IL-17A/F expression, accumulation of Th17 cells and IL-17A/F bioactivity, including increased neutrophil recruitment and matrix metalloproteinase-1 expression directly implicated in TB pathogenesis. These features discriminate recall responses in patients with active TB from those with cured or latent infection and are also evident at the site of TB disease. Our data support targeting of this pathway in host-directed therapy for TB.


2016 ◽  
Vol 7 ◽  
Author(s):  
Mohd Khubaib ◽  
Javaid A. Sheikh ◽  
Saurabh Pandey ◽  
Battu Srikanth ◽  
Manish Bhuwan ◽  
...  

2020 ◽  
Vol 8 (11) ◽  
pp. 1840
Author(s):  
Souvik Ghosh ◽  
Yashpal S. Malik

The COVID-19 pandemic, caused by a novel zoonotic coronavirus (CoV), SARS-CoV-2, has infected 46,182 million people, resulting in 1,197,026 deaths (as of 1 November 2020), with devastating and far-reaching impacts on economies and societies worldwide. The complex origin, extended human-to-human transmission, pathogenesis, host immune responses, and various clinical presentations of SARS-CoV-2 have presented serious challenges in understanding and combating the pandemic situation. Human CoVs gained attention only after the SARS-CoV outbreak of 2002–2003. On the other hand, animal CoVs have been studied extensively for many decades, providing a plethora of important information on their genetic diversity, transmission, tissue tropism and pathology, host immunity, and therapeutic and prophylactic strategies, some of which have striking resemblance to those seen with SARS-CoV-2. Moreover, the evolution of human CoVs, including SARS-CoV-2, is intermingled with those of animal CoVs. In this comprehensive review, attempts have been made to compare the current knowledge on evolution, transmission, pathogenesis, immunopathology, therapeutics, and prophylaxis of SARS-CoV-2 with those of various animal CoVs. Information on animal CoVs might enhance our understanding of SARS-CoV-2, and accordingly, benefit the development of effective control and prevention strategies against COVID-19.


mBio ◽  
2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anil A. Panackal ◽  
Kim C. Williamson ◽  
Diederik van de Beek ◽  
David R. Boulware ◽  
Peter R. Williamson

ABSTRACTThe host damage-response framework states that microbial pathogenesis is a product of microbial virulence factors and collateral damage from host immune responses. Immune-mediated host damage is particularly important within the size-restricted central nervous system (CNS), where immune responses may exacerbate cerebral edema and neurological damage, leading to coma and death. In this review, we compare human host and therapeutic responses in representative nonviral generalized CNS infections that induce archetypal host damage responses: cryptococcal menigoencephalitis and tuberculous meningitis in HIV-infected and non-HIV-infected patients, pneumococcal meningitis, and cerebral malaria. Consideration of the underlying patterns of host responses provides critical insights into host damage and may suggest tailored adjunctive therapeutics to improve disease outcome.


AIDS ◽  
2008 ◽  
Vol 22 (17) ◽  
pp. 2241-2250 ◽  
Author(s):  
Lingyun Shao ◽  
Wenhong Zhang ◽  
Shu Zhang ◽  
Crystal Y Chen ◽  
Weimin Jiang ◽  
...  

2021 ◽  
Vol SP (2) ◽  
Author(s):  
Uzma A. Jilani ◽  
Zulhabri Othman ◽  
Syed A. Jilani

The coronavirus disease 2019 (COVID‐19) has created a worldwide crisis, raising fears and concerns regarding clinical outcomes in patients with comorbidities. Some of the highly prevalent communicable and non-communicable diseases worldwide are cardiovascular diseases, diabetes, HIV/AIDS, and hepatitis B and C, which reduce the host immune responses to concurrent acute infections. Despite over 170 million confirmed cases of COVID‐19 worldwide as of 24 June 2021, insufficient data is reporting the prognosis of HIV and SARS-CoV-2 co‐infection. This narrative review aims to present current knowledge on the impact of SARS-CoV-2 on people living with HIV/AIDS, in terms of immunological responses and clinical outcome. Although some studies have been performed and are in progress to determine the impact of SARS-CoV-2 infection on patients living with HIV/AIDS, controversies still exist whether COVID-19 severity and mortality are higher among this special subgroup or similar to the general population.


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