Evidence map›Paper›PMID 37667129›Full record

ReviewWorld journal of microbiology & biotechnology2023

Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.

Vinaya Krishnan, Sreemoye Nath, Preetha Nair, Bannhi Das

Abstract readReview
PubMed Publisher
In one paragraph

Review in World journal of microbiology & biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Article
  7. Article
  8. The PE/PPE family proteins ofFrontiers in immunology · 2025
    Review
  9. Review
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Vinaya KrishnanDepartment of Biotechnology, Mount Carmel College Autonomous, Bengaluru, 560052, India.
Sreemoye NathUniversity of North Texas, Denton, TX, 76201, USA.
Preetha NairDepartment of Biotechnology, Mount Carmel College Autonomous, Bengaluru, 560052, India.
Bannhi DasDepartment of Biotechnology, Mount Carmel College Autonomous, Bengaluru, 560052, India. bannhi.das@gmail.com.ORCID http://orcid.org/0000-0001-7674-0046
Department of Biotechnology · INUniversity of North Texas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mt.b), a deadly disease causer, is a facultative parasite. This microorganism has developed several methods to defend itself, once internalized within specialised vacuoles in the macrophages. A wide array of receptors like the complement receptor mannose receptors, scavenger receptor assists the entry of the microbe within the phagocytic macrophages. However, Mt.b is clever enough to protect itself from the hostile environment of the macrophage thereby prevailing within it. The microbe can efficiently inhibit processes like phagosome-lysosome fusion, acidification of phagosomes, release of proinflammatory cytokines and stop crucial events like apoptosis. Additionally, it also adopts resistance to killing by reactive oxygen intermediates and reactive nitrogen intermediates. There are multiple genes both in host and the pathogen which are involved in this successful survival of Mt.b. The regulation of phagolysosome fusion is mediated by proteins such as Coronin, TlyA, SapM, PnkG, EsxH. The microbe has certain mechanisms to even acquire iron from the host cell, to withstand iron deprivation as a mode of host's defence mechanism. This review focuses on the various defensive adaptations acquired by Mt.b for fighting against the deprived conditions existing within the macrophages and their capability of proliferating successfully within it, thereby resulting in a diseased condition.

Indexed as

Mycobacterium tuberculosisAcclimatizationApoptosisIronMacrophagesIronCoroninMacrophageMycobacterium tuberculosisPhagolysosomeReactive nitrogen intermediateReactive oxygen species

Identifiers

PMID37667129
OpenAlexW4386413033

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.