Rabaptin5 acts as a key regulator for Rab7l1‐mediated phagosome maturation process

Immunology ◽  
2021 ◽  
Author(s):  
Rohini Shrivastava ◽  
Gourango Pradhan ◽  
Sudip Ghosh ◽  
Sangita Mukhopadhyay
Keyword(s):  
Maturation Process ◽  
Phagosome Maturation

scholarly journals Mycobacterium's Arrest of Phagosome Maturation in Macrophages Requires Rab5 Activity and Accessibility to Iron

2003 ◽  
Vol 14 (8) ◽  
pp. 3366-3377 ◽  
Author(s):  
Victoria A. Kelley ◽  
Jeffrey S. Schorey
Keyword(s):  
Mycobacterium Avium ◽  
Dominant Negative ◽  
Late Endosome ◽  
Maturation Process ◽  
Phagosome Maturation ◽  
Retroviral Transduction ◽  
Murine Macrophages ◽  
Late Endosomes ◽  
Early Endosomes ◽  
Insight Into

Many mycobacteria are intramacrophage pathogens that reside within nonacidified phagosomes that fuse with early endosomes but do not mature to phagolysosomes. The mechanism by which mycobacteria block this maturation process remains elusive. To gain insight into whether fusion with early endosomes is required for mycobacteria-mediated inhibition of phagosome maturation, we investigated how perturbing the GTPase cycles of Rab5 and Rab7, GTPases that regulate early and late endosome fusion, respectively, would affect phagosome maturation. Retroviral transduction of the constitutively activated forms of both GTPases into primary murine macrophages had no effect on Mycobacterium avium retention in an early endosomal compartment. Interestingly, expression of dominant negative Rab5, Rab5(S34N), but not dominant negative Rab7, resulted in a significant increase in colocalization of M. avium with markers of late endosomes/lysosomes and increased mycobacterial killing. This colocalization was specific to mycobacteria since Rab5(S34N) expressing cells showed diminished trafficking of endocytic tracers to lysosomes. We further demonstrated that maturation of M. avium phagosomes was halted in Rab5(S34N) expressing macrophages supplemented with exogenous iron. These findings suggest that fusion with early endosomes is required for mycobacterial retention in early phagosomal compartments and that an inadequate supply of iron is one factor in mycobacteria's inability to prevent the normal maturation process in Rab5(S34N)-expressing macrophages.

Calcium Signaling Commands Phagosome Maturation Process

2019 ◽  
Vol 38 (2) ◽  
pp. 57-69 ◽  
Author(s):  
Gourango Pradhan ◽  
Philip Raj Abraham ◽  
Rohini Shrivastava ◽  
Sangita Mukhopadhyay
Keyword(s):  
Calcium Signaling ◽  
Maturation Process ◽  
Phagosome Maturation

scholarly journals From infection niche to therapeutic target: the intracellular lifestyle of Mycobacterium tuberculosis

Microbiology ◽  
2021 ◽  
Vol 167 (4) ◽  
Author(s):  
Leah Isobella Rankine-Wilson ◽  
Tirosh Shapira ◽  
Carine Sao Emani ◽  
Yossef Av-Gay
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Side Effects ◽  
Type Species ◽  
Life Stage ◽  
Maturation Process ◽  
Human Pathogen ◽  
Phagosome Maturation ◽  
Content Type ◽  
The Past ◽  
Multiple Drugs

Mycobacterium tuberculosis (Mtb) is an obligate human pathogen killing millions of people annually. Treatment for tuberculosis is lengthy and complicated, involving multiple drugs and often resulting in serious side effects and non-compliance. Mtb has developed numerous complex mechanisms enabling it to not only survive but replicate inside professional phagocytes. These mechanisms include, among others, overcoming the phagosome maturation process, inhibiting the acidification of the phagosome and inhibiting apoptosis. Within the past decade, technologies have been developed that enable a more accurate understanding of Mtb physiology within its intracellular niche, paving the way for more clinically relevant drug-development programmes. Here we review the molecular biology of Mtb pathogenesis offering a unique perspective on the use and development of therapies that target Mtb during its intracellular life stage.

Phagosome maturation and modulation of macrophage effector function by intracellular pathogens: target for therapeutics

2021 ◽  
Author(s):  
Brahmaji Sontyana ◽  
Rohini Shrivastava ◽  
Srikanth Battu ◽  
Sudip Ghosh ◽  
Sangita Mukhopadhyay
Keyword(s):  
Antigen Presentation ◽  
Effector Function ◽  
Intracellular Pathogens ◽  
Maturation Process ◽  
Phagosome Maturation ◽  
Immune Effector ◽  
Effector Functions ◽  
Intracellular Infections

Macrophages are important cells that regulate various innate functions. Macrophages after engulfment of pathogens proceed for phagosome maturation and finally fuse with lysosomes to kill pathogens. Although pathogen degradation is one of the important functions of phagosomes, various immune-effector functions of macrophages are also dependent on the phagosome maturation process. This review discusses signaling processes regulating phagosome maturation as well as various effector functions of macrophages such as apoptosis, antigen presentation, autophagy and inflammasome that are dependent on the phagosome maturation process. It also discusses strategies adopted by various intracellular pathogens to counteract these functions to evade intracellular destruction mechanisms. These studies may give direction for the development of new therapeutics to control various intracellular infections.

ENDOCRINE CHANGES BEFORE AND AFTER THE MENARCHE

1973 ◽  
Vol 74 (4) ◽  
pp. 685-694 ◽  
Author(s):  
B.-A. Lamberg ◽  
R.-L. Kantero ◽  
P. Saarinen ◽  
O. Widholm
Keyword(s):  
Binding Proteins ◽  
Maturation Process ◽  
Hormone Binding ◽  
Maximal Level ◽  
Continuous Increase ◽  
Mean Values ◽  
Thyroxine Binding Globulin ◽  
Before And After ◽  
Free Thyroxine Index ◽  
Level 1

ABSTRACT In an endocrine survey of healthy girls aged 8 to 20 years before and after the menarche, the serum thyroxine (T4), uptake of triiodothyronine by Sephadex (T3U), and the binding capacities of thyroxine binding globulin (TBG) and pre-albumin (TBPA) were measured, and a free thyroxine index (FTI = T4 × T3U) was calculated. The subjects were grouped according to skeletal age (SA) until the menarche and after this in the post-menarcheal age (PMA), expressed in years. T4 and FTI increased concomitantly and reached peak values of 8.40 μg/100 ml and 8.40, respectively, at 2–3 years PMA. The corresponding mean values for post-menarcheal girls (7.74 μg/100 ml and 7.51) differed statistically significantly from the means before the menarche (7.03 μg/ 100 ml and 6.75). The TBG remained virtually unchanged during the whole period, whereas the TBPA showed a continuous increase and reached a maximal level 1–2 years after the menarche. The maturation process in girls in some way involves an increase in the total and free T4 level which is not dependent on hormone binding proteins.

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